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Human genetics – Wikipedia

Human genetics is the study of inheritance as it occurs in human beings. Human genetics encompasses a variety of overlapping fields including: classical genetics, cytogenetics, molecular genetics, biochemical genetics, genomics, population genetics, developmental genetics, clinical genetics, and genetic counseling.

Genes can be the common factor of the qualities of most human-inherited traits. Study of human genetics can be useful as it can answer questions about human nature, understand the diseases and development of effective disease treatment, and understand genetics of human life. This article describes only basic features of human genetics; for the genetics of disorders please see: medical genetics.

Inheritance of traits for humans are based upon Gregor Mendel’s model of inheritance. Mendel deduced that inheritance depends upon discrete units of inheritance, called factors or genes.[1]

Autosomal traits are associated with a single gene on an autosome (non-sex chromosome)they are called “dominant” because a single copyinherited from either parentis enough to cause this trait to appear. This often means that one of the parents must also have the same trait, unless it has arisen due to an unlikely new mutation. Examples of autosomal dominant traits and disorders are Huntington’s disease and achondroplasia.

Autosomal recessive traits is one pattern of inheritance for a trait, disease, or disorder to be passed on through families. For a recessive trait or disease to be displayed two copies of the trait or disorder needs to be presented. The trait or gene will be located on a non-sex chromosome. Because it takes two copies of a trait to display a trait, many people can unknowingly be carriers of a disease. From an evolutionary perspective, a recessive disease or trait can remain hidden for several generations before displaying the phenotype. Examples of autosomal recessive disorders are albinism, cystic fibrosis.

X-linked genes are found on the sex X chromosome. X-linked genes just like autosomal genes have both dominant and recessive types. Recessive X-linked disorders are rarely seen in females and usually only affect males. This is because males inherit their X chromosome and all X-linked genes will be inherited from the maternal side. Fathers only pass on their Y chromosome to their sons, so no X-linked traits will be inherited from father to son. Men cannot be carriers for recessive X linked traits, as they only have one X chromosome, so any X linked trait inherited from the mother will show up.

Females express X-linked disorders when they are homozygous for the disorder and become carriers when they are heterozygous. X-linked dominant inheritance will show the same phenotype as a heterozygote and homozygote. Just like X-linked inheritance, there will be a lack of male-to-male inheritance, which makes it distinguishable from autosomal traits. One example of an X-linked trait is CoffinLowry syndrome, which is caused by a mutation in ribosomal protein gene. This mutation results in skeletal, craniofacial abnormalities, mental retardation, and short stature.

X chromosomes in females undergo a process known as X inactivation. X inactivation is when one of the two X chromosomes in females is almost completely inactivated. It is important that this process occurs otherwise a woman would produce twice the amount of normal X chromosome proteins. The mechanism for X inactivation will occur during the embryonic stage. For people with disorders like trisomy X, where the genotype has three X chromosomes, X-inactivation will inactivate all X chromosomes until there is only one X chromosome active. Males with Klinefelter syndrome, who have an extra X chromosome, will also undergo X inactivation to have only one completely active X chromosome.

Y-linked inheritance occurs when a gene, trait, or disorder is transferred through the Y chromosome. Since Y chromosomes can only be found in males, Y linked traits are only passed on from father to son. The testis determining factor, which is located on the Y chromosome, determines the maleness of individuals. Besides the maleness inherited in the Y-chromosome there are no other found Y-linked characteristics.

A pedigree is a diagram showing the ancestral relationships and transmission of genetic traits over several generations in a family. Square symbols are almost always used to represent males, whilst circles are used for females. Pedigrees are used to help detect many different genetic diseases. A pedigree can also be used to help determine the chances for a parent to produce an offspring with a specific trait.

Four different traits can be identified by pedigree chart analysis: autosomal dominant, autosomal recessive, x-linked, or y-linked. Partial penetrance can be shown and calculated from pedigrees. Penetrance is the percentage expressed frequency with which individuals of a given genotype manifest at least some degree of a specific mutant phenotype associated with a trait.

Inbreeding, or mating between closely related organisms, can clearly be seen on pedigree charts. Pedigree charts of royal families often have a high degree of inbreeding, because it was customary and preferable for royalty to marry another member of royalty. Genetic counselors commonly use pedigrees to help couples determine if the parents will be able to produce healthy children.

A karyotype is a very useful tool in cytogenetics. A karyotype is picture of all the chromosomes in the metaphase stage arranged according to length and centromere position. A karyotype can also be useful in clinical genetics, due to its ability to diagnose genetic disorders. On a normal karyotype, aneuploidy can be detected by clearly being able to observe any missing or extra chromosomes.[1]

Giemsa banding, g-banding, of the karyotype can be used to detect deletions, insertions, duplications, inversions, and translocations. G-banding will stain the chromosomes with light and dark bands unique to each chromosome. A FISH, fluorescent in situ hybridization, can be used to observe deletions, insertions, and translocations. FISH uses fluorescent probes to bind to specific sequences of the chromosomes that will cause the chromosomes to fluoresce a unique color.[1]

Genomics refers to the field of genetics concerned with structural and functional studies of the genome.[1] A genome is all the DNA contained within an organism or a cell including nuclear and mitochondrial DNA. The human genome is the total collection of genes in a human being contained in the human chromosome, composed of over three billion nucleotides.[2] In April 2003, the Human Genome Project was able to sequence all the DNA in the human genome, and to discover that the human genome was composed of around 20,000 protein coding genes.

Medical genetics is the branch of medicine that involves the diagnosis and management of hereditary disorders. Medical genetics is the application of genetics to medical care. It overlaps human genetics, for example, research on the causes and inheritance of genetic disorders would be considered within both human genetics and medical genetics, while the diagnosis, management, and counseling of individuals with genetic disorders would be considered part of medical genetics.

Population genetics is the branch of evolutionary biology responsible for investigating processes that cause changes in allele and genotype frequencies in populations based upon Mendelian inheritance.[3] Four different forces can influence the frequencies: natural selection, mutation, gene flow (migration), and genetic drift. A population can be defined as a group of interbreeding individuals and their offspring. For human genetics the populations will consist only of the human species. The Hardy-Weinberg principle is a widely used principle to determine allelic and genotype frequencies.

In addition to nuclear DNA, humans (like almost all eukaryotes) have mitochondrial DNA. Mitochondria, the “power houses” of a cell, have their own DNA. Mitochondria are inherited from one’s mother, and their DNA is frequently used to trace maternal lines of descent (see mitochondrial Eve). Mitochondrial DNA is only 16kb in length and encodes for 62 genes.

The XY sex-determination system is the sex-determination system found in humans, most other mammals, some insects (Drosophila), and some plants (Ginkgo). In this system, the sex of an individual is determined by a pair of sex chromosomes (gonosomes). Females have two of the same kind of sex chromosome (XX), and are called the homogametic sex. Males have two distinct sex chromosomes (XY), and are called the heterogametic sex.

Sex linkage is the phenotypic expression of an allele related to the chromosomal sex of the individual. This mode of inheritance is in contrast to the inheritance of traits on autosomal chromosomes, where both sexes have the same probability of inheritance. Since humans have many more genes on the X than the Y, there are many more X-linked traits than Y-linked traits.However, females carry two or more copies of the X chromosome, resulting in a potentially toxic dose of X-linked genes.[4]

To correct this imbalance, mammalian females have evolved a unique mechanism of dosage compensation. In particular, by way of the process called X-chromosome inactivation (XCI), female mammals transcriptionally silence one of their two Xs in a complex and highly coordinated manner.[4]

GeneticChromosomal

[35]

Here is the original post:

Human genetics – Wikipedia

Human genetics – Wikipedia

Human genetics is the study of inheritance as it occurs in human beings. Human genetics encompasses a variety of overlapping fields including: classical genetics, cytogenetics, molecular genetics, biochemical genetics, genomics, population genetics, developmental genetics, clinical genetics, and genetic counseling.

Genes can be the common factor of the qualities of most human-inherited traits. Study of human genetics can be useful as it can answer questions about human nature, understand the diseases and development of effective disease treatment, and understand genetics of human life. This article describes only basic features of human genetics; for the genetics of disorders please see: medical genetics.

Inheritance of traits for humans are based upon Gregor Mendel’s model of inheritance. Mendel deduced that inheritance depends upon discrete units of inheritance, called factors or genes.[1]

Autosomal traits are associated with a single gene on an autosome (non-sex chromosome)they are called “dominant” because a single copyinherited from either parentis enough to cause this trait to appear. This often means that one of the parents must also have the same trait, unless it has arisen due to an unlikely new mutation. Examples of autosomal dominant traits and disorders are Huntington’s disease and achondroplasia.

Autosomal recessive traits is one pattern of inheritance for a trait, disease, or disorder to be passed on through families. For a recessive trait or disease to be displayed two copies of the trait or disorder needs to be presented. The trait or gene will be located on a non-sex chromosome. Because it takes two copies of a trait to display a trait, many people can unknowingly be carriers of a disease. From an evolutionary perspective, a recessive disease or trait can remain hidden for several generations before displaying the phenotype. Examples of autosomal recessive disorders are albinism, cystic fibrosis.

X-linked genes are found on the sex X chromosome. X-linked genes just like autosomal genes have both dominant and recessive types. Recessive X-linked disorders are rarely seen in females and usually only affect males. This is because males inherit their X chromosome and all X-linked genes will be inherited from the maternal side. Fathers only pass on their Y chromosome to their sons, so no X-linked traits will be inherited from father to son. Men cannot be carriers for recessive X linked traits, as they only have one X chromosome, so any X linked trait inherited from the mother will show up.

Females express X-linked disorders when they are homozygous for the disorder and become carriers when they are heterozygous. X-linked dominant inheritance will show the same phenotype as a heterozygote and homozygote. Just like X-linked inheritance, there will be a lack of male-to-male inheritance, which makes it distinguishable from autosomal traits. One example of an X-linked trait is CoffinLowry syndrome, which is caused by a mutation in ribosomal protein gene. This mutation results in skeletal, craniofacial abnormalities, mental retardation, and short stature.

X chromosomes in females undergo a process known as X inactivation. X inactivation is when one of the two X chromosomes in females is almost completely inactivated. It is important that this process occurs otherwise a woman would produce twice the amount of normal X chromosome proteins. The mechanism for X inactivation will occur during the embryonic stage. For people with disorders like trisomy X, where the genotype has three X chromosomes, X-inactivation will inactivate all X chromosomes until there is only one X chromosome active. Males with Klinefelter syndrome, who have an extra X chromosome, will also undergo X inactivation to have only one completely active X chromosome.

Y-linked inheritance occurs when a gene, trait, or disorder is transferred through the Y chromosome. Since Y chromosomes can only be found in males, Y linked traits are only passed on from father to son. The testis determining factor, which is located on the Y chromosome, determines the maleness of individuals. Besides the maleness inherited in the Y-chromosome there are no other found Y-linked characteristics.

A pedigree is a diagram showing the ancestral relationships and transmission of genetic traits over several generations in a family. Square symbols are almost always used to represent males, whilst circles are used for females. Pedigrees are used to help detect many different genetic diseases. A pedigree can also be used to help determine the chances for a parent to produce an offspring with a specific trait.

Four different traits can be identified by pedigree chart analysis: autosomal dominant, autosomal recessive, x-linked, or y-linked. Partial penetrance can be shown and calculated from pedigrees. Penetrance is the percentage expressed frequency with which individuals of a given genotype manifest at least some degree of a specific mutant phenotype associated with a trait.

Inbreeding, or mating between closely related organisms, can clearly be seen on pedigree charts. Pedigree charts of royal families often have a high degree of inbreeding, because it was customary and preferable for royalty to marry another member of royalty. Genetic counselors commonly use pedigrees to help couples determine if the parents will be able to produce healthy children.

A karyotype is a very useful tool in cytogenetics. A karyotype is picture of all the chromosomes in the metaphase stage arranged according to length and centromere position. A karyotype can also be useful in clinical genetics, due to its ability to diagnose genetic disorders. On a normal karyotype, aneuploidy can be detected by clearly being able to observe any missing or extra chromosomes.[1]

Giemsa banding, g-banding, of the karyotype can be used to detect deletions, insertions, duplications, inversions, and translocations. G-banding will stain the chromosomes with light and dark bands unique to each chromosome. A FISH, fluorescent in situ hybridization, can be used to observe deletions, insertions, and translocations. FISH uses fluorescent probes to bind to specific sequences of the chromosomes that will cause the chromosomes to fluoresce a unique color.[1]

Genomics refers to the field of genetics concerned with structural and functional studies of the genome.[1] A genome is all the DNA contained within an organism or a cell including nuclear and mitochondrial DNA. The human genome is the total collection of genes in a human being contained in the human chromosome, composed of over three billion nucleotides.[2] In April 2003, the Human Genome Project was able to sequence all the DNA in the human genome, and to discover that the human genome was composed of around 20,000 protein coding genes.

Medical genetics is the branch of medicine that involves the diagnosis and management of hereditary disorders. Medical genetics is the application of genetics to medical care. It overlaps human genetics, for example, research on the causes and inheritance of genetic disorders would be considered within both human genetics and medical genetics, while the diagnosis, management, and counseling of individuals with genetic disorders would be considered part of medical genetics.

Population genetics is the branch of evolutionary biology responsible for investigating processes that cause changes in allele and genotype frequencies in populations based upon Mendelian inheritance.[3] Four different forces can influence the frequencies: natural selection, mutation, gene flow (migration), and genetic drift. A population can be defined as a group of interbreeding individuals and their offspring. For human genetics the populations will consist only of the human species. The Hardy-Weinberg principle is a widely used principle to determine allelic and genotype frequencies.

In addition to nuclear DNA, humans (like almost all eukaryotes) have mitochondrial DNA. Mitochondria, the “power houses” of a cell, have their own DNA. Mitochondria are inherited from one’s mother, and their DNA is frequently used to trace maternal lines of descent (see mitochondrial Eve). Mitochondrial DNA is only 16kb in length and encodes for 62 genes.

The XY sex-determination system is the sex-determination system found in humans, most other mammals, some insects (Drosophila), and some plants (Ginkgo). In this system, the sex of an individual is determined by a pair of sex chromosomes (gonosomes). Females have two of the same kind of sex chromosome (XX), and are called the homogametic sex. Males have two distinct sex chromosomes (XY), and are called the heterogametic sex.

Sex linkage is the phenotypic expression of an allele related to the chromosomal sex of the individual. This mode of inheritance is in contrast to the inheritance of traits on autosomal chromosomes, where both sexes have the same probability of inheritance. Since humans have many more genes on the X than the Y, there are many more X-linked traits than Y-linked traits.However, females carry two or more copies of the X chromosome, resulting in a potentially toxic dose of X-linked genes.[4]

To correct this imbalance, mammalian females have evolved a unique mechanism of dosage compensation. In particular, by way of the process called X-chromosome inactivation (XCI), female mammals transcriptionally silence one of their two Xs in a complex and highly coordinated manner.[4]

GeneticChromosomal

[35]

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Human genetics – Wikipedia

Human Genetics – medschool.ucla.edu

A hub of deep expertise, the Department of Human Genetics helps partners across UCLA interpret data and leverage genomic technology to improve study design and solve medical problems.

We demystify genetic complexities to provide vital insights for a range of clinical and research applications. We strive to improve the care of as many patients as possible by pushing our capabilities, developing novel ways to address unanswered questions.

Your next collaboration is right down the street.

Our enviable proximity to the worlds brightest scientific minds enables both thriving scheduled events and impromptu sidewalk powwows. A casual conversation during your coffee run could lead to your next big publication.

Come find out why innovation lives here.

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Jonathan Flint, MDPsychiatrist Dr. Jonathan Flint has been named a fellow of the Royal Society, an academy that includes some of the worlds most eminent scientists.Learn More

Bogdan Pasaniuc, PhDA team of researchers from UCLA, Cedars-Sinai Cancer and Dana-Farber Cancer Institute has identified 34 genes that are associated with an increased risk for developing the earliest stages of ovarian cancer.Learn More

Deborah Krakow, MDNamed to Los Angeles Magazines 2019 list of Top Doctors in Los Angeles specializing in Genetics. The list identifies doctors considered to be at the top of their fields.Learn More

Julian Martinez, MD, PhD Named to Los Angeles Magazines 2019 list of Top Doctors in Los Angeles specializing in Genetics. The list identifies doctors considered to be at the top of their fields.Learn More

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Human Genetics – medschool.ucla.edu

Department of Human Genetics | The University of Chicago

The Department of Human Genetics is the home within the Division of Biological Sciences for the study of basic principles of genetics and genomics as applied to human disease. We provide broad training in experimental genetics and genomics, statistical and population genetics, bioinformatics, and clinical genetics. A common theme throughout our research is the application of basic genetic principles and strategies to the study of disease mechanism, disease susceptibility, and the genetic architecture of complex traits. Our faculty bridge between basic and clinical research and train students for careers in academia, industry, and medicine.

The Department of Human Genetics has an unwavering commitment to diversity, inclusion, free expression, and open discourse.These values are at the core of our roles as scientists, as teachers, and as citizens of a free society.

Science, including genetics, plays a central role in many crucial issues of our time. We are committed to generating rigorous scientific knowledge, training future scientists, and preparing our students to be well-informed citizens in a democratic society.

Excerpt from:

Department of Human Genetics | The University of Chicago

Human genetics – Wikipedia

Human genetics is the study of inheritance as it occurs in human beings. Human genetics encompasses a variety of overlapping fields including: classical genetics, cytogenetics, molecular genetics, biochemical genetics, genomics, population genetics, developmental genetics, clinical genetics, and genetic counseling.

Genes can be the common factor of the qualities of most human-inherited traits. Study of human genetics can be useful as it can answer questions about human nature, understand the diseases and development of effective disease treatment, and understand genetics of human life. This article describes only basic features of human genetics; for the genetics of disorders please see: medical genetics.

Inheritance of traits for humans are based upon Gregor Mendel’s model of inheritance. Mendel deduced that inheritance depends upon discrete units of inheritance, called factors or genes.[1]

Autosomal traits are associated with a single gene on an autosome (non-sex chromosome)they are called “dominant” because a single copyinherited from either parentis enough to cause this trait to appear. This often means that one of the parents must also have the same trait, unless it has arisen due to an unlikely new mutation. Examples of autosomal dominant traits and disorders are Huntington’s disease and achondroplasia.

Autosomal recessive traits is one pattern of inheritance for a trait, disease, or disorder to be passed on through families. For a recessive trait or disease to be displayed two copies of the trait or disorder needs to be presented. The trait or gene will be located on a non-sex chromosome. Because it takes two copies of a trait to display a trait, many people can unknowingly be carriers of a disease. From an evolutionary perspective, a recessive disease or trait can remain hidden for several generations before displaying the phenotype. Examples of autosomal recessive disorders are albinism, cystic fibrosis.

X-linked genes are found on the sex X chromosome. X-linked genes just like autosomal genes have both dominant and recessive types. Recessive X-linked disorders are rarely seen in females and usually only affect males. This is because males inherit their X chromosome and all X-linked genes will be inherited from the maternal side. Fathers only pass on their Y chromosome to their sons, so no X-linked traits will be inherited from father to son. Men cannot be carriers for recessive X linked traits, as they only have one X chromosome, so any X linked trait inherited from the mother will show up.

Females express X-linked disorders when they are homozygous for the disorder and become carriers when they are heterozygous. X-linked dominant inheritance will show the same phenotype as a heterozygote and homozygote. Just like X-linked inheritance, there will be a lack of male-to-male inheritance, which makes it distinguishable from autosomal traits. One example of an X-linked trait is CoffinLowry syndrome, which is caused by a mutation in ribosomal protein gene. This mutation results in skeletal, craniofacial abnormalities, mental retardation, and short stature.

X chromosomes in females undergo a process known as X inactivation. X inactivation is when one of the two X chromosomes in females is almost completely inactivated. It is important that this process occurs otherwise a woman would produce twice the amount of normal X chromosome proteins. The mechanism for X inactivation will occur during the embryonic stage. For people with disorders like trisomy X, where the genotype has three X chromosomes, X-inactivation will inactivate all X chromosomes until there is only one X chromosome active. Males with Klinefelter syndrome, who have an extra X chromosome, will also undergo X inactivation to have only one completely active X chromosome.

Y-linked inheritance occurs when a gene, trait, or disorder is transferred through the Y chromosome. Since Y chromosomes can only be found in males, Y linked traits are only passed on from father to son. The testis determining factor, which is located on the Y chromosome, determines the maleness of individuals. Besides the maleness inherited in the Y-chromosome there are no other found Y-linked characteristics.

A pedigree is a diagram showing the ancestral relationships and transmission of genetic traits over several generations in a family. Square symbols are almost always used to represent males, whilst circles are used for females. Pedigrees are used to help detect many different genetic diseases. A pedigree can also be used to help determine the chances for a parent to produce an offspring with a specific trait.

Four different traits can be identified by pedigree chart analysis: autosomal dominant, autosomal recessive, x-linked, or y-linked. Partial penetrance can be shown and calculated from pedigrees. Penetrance is the percentage expressed frequency with which individuals of a given genotype manifest at least some degree of a specific mutant phenotype associated with a trait.

Inbreeding, or mating between closely related organisms, can clearly be seen on pedigree charts. Pedigree charts of royal families often have a high degree of inbreeding, because it was customary and preferable for royalty to marry another member of royalty. Genetic counselors commonly use pedigrees to help couples determine if the parents will be able to produce healthy children.

A karyotype is a very useful tool in cytogenetics. A karyotype is picture of all the chromosomes in the metaphase stage arranged according to length and centromere position. A karyotype can also be useful in clinical genetics, due to its ability to diagnose genetic disorders. On a normal karyotype, aneuploidy can be detected by clearly being able to observe any missing or extra chromosomes.[1]

Giemsa banding, g-banding, of the karyotype can be used to detect deletions, insertions, duplications, inversions, and translocations. G-banding will stain the chromosomes with light and dark bands unique to each chromosome. A FISH, fluorescent in situ hybridization, can be used to observe deletions, insertions, and translocations. FISH uses fluorescent probes to bind to specific sequences of the chromosomes that will cause the chromosomes to fluoresce a unique color.[1]

Genomics refers to the field of genetics concerned with structural and functional studies of the genome.[1] A genome is all the DNA contained within an organism or a cell including nuclear and mitochondrial DNA. The human genome is the total collection of genes in a human being contained in the human chromosome, composed of over three billion nucleotides.[2] In April 2003, the Human Genome Project was able to sequence all the DNA in the human genome, and to discover that the human genome was composed of around 20,000 protein coding genes.

Medical genetics is the branch of medicine that involves the diagnosis and management of hereditary disorders. Medical genetics is the application of genetics to medical care. It overlaps human genetics, for example, research on the causes and inheritance of genetic disorders would be considered within both human genetics and medical genetics, while the diagnosis, management, and counseling of individuals with genetic disorders would be considered part of medical genetics.

Population genetics is the branch of evolutionary biology responsible for investigating processes that cause changes in allele and genotype frequencies in populations based upon Mendelian inheritance.[3] Four different forces can influence the frequencies: natural selection, mutation, gene flow (migration), and genetic drift. A population can be defined as a group of interbreeding individuals and their offspring. For human genetics the populations will consist only of the human species. The Hardy-Weinberg principle is a widely used principle to determine allelic and genotype frequencies.

In addition to nuclear DNA, humans (like almost all eukaryotes) have mitochondrial DNA. Mitochondria, the “power houses” of a cell, have their own DNA. Mitochondria are inherited from one’s mother, and their DNA is frequently used to trace maternal lines of descent (see mitochondrial Eve). Mitochondrial DNA is only 16kb in length and encodes for 62 genes.

The XY sex-determination system is the sex-determination system found in humans, most other mammals, some insects (Drosophila), and some plants (Ginkgo). In this system, the sex of an individual is determined by a pair of sex chromosomes (gonosomes). Females have two of the same kind of sex chromosome (XX), and are called the homogametic sex. Males have two distinct sex chromosomes (XY), and are called the heterogametic sex.

Sex linkage is the phenotypic expression of an allele related to the chromosomal sex of the individual. This mode of inheritance is in contrast to the inheritance of traits on autosomal chromosomes, where both sexes have the same probability of inheritance. Since humans have many more genes on the X than the Y, there are many more X-linked traits than Y-linked traits.However, females carry two or more copies of the X chromosome, resulting in a potentially toxic dose of X-linked genes.[4]

To correct this imbalance, mammalian females have evolved a unique mechanism of dosage compensation. In particular, by way of the process called X-chromosome inactivation (XCI), female mammals transcriptionally silence one of their two Xs in a complex and highly coordinated manner.[4]

GeneticChromosomal

[35]

Original post:

Human genetics – Wikipedia

Human genetics | biology | Britannica.com

Human genetics, study of the inheritance of characteristics by children from parents. Inheritance in humans does not differ in any fundamental way from that in other organisms.

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genetics: Human genetics

Some geneticists specialize in the hereditary processes of human genetics. Most of the emphasis is on understanding and treating genetic

The study of human heredity occupies a central position in genetics. Much of this interest stems from a basic desire to know who humans are and why they are as they are. At a more practical level, an understanding of human heredity is of critical importance in the prediction, diagnosis, and treatment of diseases that have a genetic component. The quest to determine the genetic basis of human health has given rise to the field of medical genetics. In general, medicine has given focus and purpose to human genetics, so the terms medical genetics and human genetics are often considered synonymous.

A new era in cytogenetics, the field of investigation concerned with studies of the chromosomes, began in 1956 with the discovery by Jo Hin Tjio and Albert Levan that human somatic cells contain 23 pairs of chromosomes. Since that time the field has advanced with amazing rapidity and has demonstrated that human chromosome aberrations rank as major causes of fetal death and of tragic human diseases, many of which are accompanied by mental retardation. Since the chromosomes can be delineated only during mitosis, it is necessary to examine material in which there are many dividing cells. This can usually be accomplished by culturing cells from the blood or skin, since only the bone marrow cells (not readily sampled except during serious bone marrow disease such as leukemia) have sufficient mitoses in the absence of artificial culture. After growth, the cells are fixed on slides and then stained with a variety of DNA-specific stains that permit the delineation and identification of the chromosomes. The Denver system of chromosome classification, established in 1959, identified the chromosomes by their length and the position of the centromeres. Since then the method has been improved by the use of special staining techniques that impart unique light and dark bands to each chromosome. These bands permit the identification of chromosomal regions that are duplicated, missing, or transposed to other chromosomes.

Micrographs showing the karyotypes (i.e., the physical appearance of the chromosome) of a male and a female have been produced. In a typical micrograph the 46 human chromosomes (the diploid number) are arranged in homologous pairs, each consisting of one maternally derived and one paternally derived member. The chromosomes are all numbered except for the X and the Y chromosomes, which are the sex chromosomes. In humans, as in all mammals, the normal female has two X chromosomes and the normal male has one X chromosome and one Y chromosome. The female is thus the homogametic sex, as all her gametes normally have one X chromosome. The male is heterogametic, as he produces two types of gametesone type containing an X chromosome and the other containing a Y chromosome. There is good evidence that the Y chromosome in humans, unlike that in Drosophila, is necessary (but not sufficient) for maleness.

A human individual arises through the union of two cells, an egg from the mother and a sperm from the father. Human egg cells are barely visible to the naked eye. They are shed, usually one at a time, from the ovary into the oviducts (fallopian tubes), through which they pass into the uterus. Fertilization, the penetration of an egg by a sperm, occurs in the oviducts. This is the main event of sexual reproduction and determines the genetic constitution of the new individual.

Human sex determination is a genetic process that depends basically on the presence of the Y chromosome in the fertilized egg. This chromosome stimulates a change in the undifferentiated gonad into that of the male (a testicle). The gonadal action of the Y chromosome is mediated by a gene located near the centromere; this gene codes for the production of a cell surface molecule called the H-Y antigen. Further development of the anatomic structures, both internal and external, that are associated with maleness is controlled by hormones produced by the testicle. The sex of an individual can be thought of in three different contexts: chromosomal sex, gonadal sex, and anatomic sex. Discrepancies between these, especially the latter two, result in the development of individuals with ambiguous sex, often called hermaphrodites. The phenomenon of homosexuality is of uncertain cause and is unrelated to the above sex-determining factors. It is of interest that in the absence of a male gonad (testicle) the internal and external sex anatomy is always female, even in the absence of a female ovary. A female without ovaries will, of course, be infertile and will not experience any of the female developmental changes normally associated with puberty. Such a female will often have Turners syndrome.

If X-containing and Y-containing sperm are produced in equal numbers, then according to simple chance one would expect the sex ratio at conception (fertilization) to be half boys and half girls, or 1 : 1. Direct observation of sex ratios among newly fertilized human eggs is not yet feasible, and sex-ratio data are usually collected at the time of birth. In almost all human populations of newborns, there is a slight excess of males; about 106 boys are born for every100 girls. Throughout life, however, there is a slightly greater mortality of males; this slowly alters the sex ratio until, beyond the age of about 50 years, there is an excess of females. Studies indicate that male embryos suffer a relatively greater degree of prenatal mortality, so the sex ratio at conception might be expected to favour males even more than the 106 : 100 ratio observed at birth would suggest. Firm explanations for the apparent excess of male conceptions have not been established; it is possible that Y-containing sperm survive better within the female reproductive tract, or they may be a little more successful in reaching the egg in order to fertilize it. In any case, the sex differences are small, the statistical expectation for a boy (or girl) at any single birth still being close to one out of two.

During gestationthe period of nine months between fertilization and the birth of the infanta remarkable series of developmental changes occur. Through the process of mitosis, the total number of cells changes from 1 (the fertilized egg) to about 2 1011. In addition, these cells differentiate into hundreds of different types with specific functions (liver cells, nerve cells, muscle cells, etc.). A multitude of regulatory processes, both genetically and environmentally controlled, accomplish this differentiation. Elucidation of the exquisite timing of these processes remains one of the great challenges of human biology.

Immunity is the ability of an individual to recognize the self molecules that make up ones own body and to distinguish them from such nonself molecules as those found in infectious microorganisms and toxins. This process has a prominent genetic component. Knowledge of the genetic and molecular basis of the mammalian immune system has increased in parallel with the explosive advances made in somatic cell and molecular genetics.

There are two major components of the immune system, both originating from the same precursor stem cells. The bursa component provides B lymphocytes, a class of white blood cells that, when appropriately stimulated, differentiate into plasma cells. These latter cells produce circulating soluble proteins called antibodies or immunoglobulins. Antibodies are produced in response to substances called antigens, most of which are foreign proteins or polysaccharides. An antibody molecule can recognize a specific antigen, combine with it, and initiate its destruction. This so-called humoral immunity is accomplished through a complicated series of interactions with other molecules and cells; some of these interactions are mediated by another group of lymphocytes, the T lymphocytes, which are derived from the thymus gland. Once a B lymphocyte has been exposed to a specific antigen, it remembers the contact so that future exposure will cause an accelerated and magnified immune reaction. This is a manifestation of what has been called immunological memory.

The thymus component of the immune system centres on the thymus-derived T lymphocytes. In addition to regulating the B cells in producing humoral immunity, the T cells also directly attack cells that display foreign antigens. This process, called cellular immunity, is of great importance in protecting the body against a variety of viruses as well as cancer cells. Cellular immunity is also the chief cause of the rejection of organ transplants. The T lymphocytes provide a complex network consisting of a series of helper cells (which are antigen-specific), amplifier cells, suppressor cells, and cytotoxic (killer) cells, all of which are important in immune regulation.

One of the central problems in understanding the genetics of the immune system has been in explaining the genetic regulation of antibody production. Immunobiologists have demonstrated that the system can produce well over one million specific antibodies, each corresponding to a particular antigen. It would be difficult to envisage that each antibody is encoded by a separate gene; such an arrangement would require a disproportionate share of the entire human genome. Recombinant DNA analysis has illuminated the mechanisms by which a limited number of immunoglobulin genes can encode this vast number of antibodies.

Each antibody molecule consists of several different polypeptide chainsthe light chains (L) and the longer heavy chains (H). The latter determine to which of five different classes (IgM, IgG, IgA, IgD, or IgE) an immunoglobulin belongs. Both the L and H chains are unique among proteins in that they contain constant and variable parts. The constant parts have relatively identical amino acid sequences in any given antibody. The variable parts, on the other hand, have different amino acid sequences in each antibody molecule. It is the variable parts, then, that determine the specificity of the antibody.

Recombinant DNA studies of immunoglobulin genes in mice have revealed that the light-chain genes are encoded in four separate parts in germ-line DNA: a leader segment (L), a variable segment (V), a joining segment (J), and a constant segment (C). These segments are widely separated in the DNA of an embryonic cell, but in a mature B lymphocyte they are found in relative proximity (albeit separated by introns). The mouse has more than 200 light-chain variable region genes, only one of which will be incorporated into the proximal sequence that codes for the antibody production in a given B lymphocyte. Antibody diversity is greatly enhanced by this system, as the V and J segments rearrange and assort randomly in each B-lymphocyte precursor cell. The mechanisms by which this DNA rearrangement takes place are not clear, but transposons are undoubtedly involved. Similar combinatorial processes take place in the genes that code for the heavy chains; furthermore, both the light-chain and heavy-chain genes can undergo somatic mutations to create new antibody-coding sequences. The net effect of these combinatorial and mutational processes enables the coding of millions of specific antibody molecules from a limited number of genes. It should be stressed, however, that each B lymphocyte can produce only one antibody. It is the B lymphocyte population as a whole that produces the tremendous variety of antibodies in humans and other mammals.

Plasma cell tumours (myelomas) have made it possible to study individual antibodies, since these tumours, which are descendants of a single plasma cell, produce one antibody in abundance. Another method of obtaining large amounts of a specific antibody is by fusing a B lymphocyte with a rapidly growing cancer cell. The resultant hybrid cell, known as a hybridoma, multiplies rapidly in culture. Since the antibodies obtained from hybridomas are produced by clones derived from a single lymphocyte, they are called monoclonal antibodies.

As has been stated, cellular immunity is mediated by T lymphocytes that can recognize infected body cells, cancer cells, and the cells of a foreign transplant. The control of cellular immune reactions is provided by a linked group of genes, known as the major histocompatibility complex (MHC). These genes code for the major histocompatibility antigens, which are found on the surface of almost all nucleated somatic cells. The major histocompatibility antigens were first discovered on the leukocytes (white blood cells) and are therefore usually referred to as the HLA (human leukocyte group A) antigens.

The advent of the transplantation of human organs in the 1950s made the question of tissue compatibility between donor and recipient of vital importance, and it was in this context that the HLA antigens and the MHC were elucidated. Investigators found that the MHC resides on the short arm of chromosome 6, on four closely associated sites designated HLA-A, HLA-B, HLA-C, and HLA-D. Each locus is highly polymorphic; i.e., each is represented by a great many alleles within the human gene pool. These alleles, like those of the ABO blood group system, are expressed in codominant fashion. Because of the large number of alleles at each HLA locus, there is an extremely low probability of any two individuals (other than siblings) having identical HLA genotypes. (Since a person inherits one chromosome 6 from each parent, siblings have a 25 percent probability of having received the same paternal and maternal chromosomes 6 and thus of being HLA matched.)

Although HLA antigens are largely responsible for the rejection of organ transplants, it is obvious that the MHC did not evolve to prevent the transfer of organs from one person to another. Indeed, information obtained from the histocompatibility complex in the mouse (which is very similar in its genetic organization to that of the human) suggests that a primary function of the HLA antigens is to regulate the number of specific cytotoxic T killer cells, which have the ability to destroy virus-infected cells and cancer cells.

More is known about the genetics of the blood than about any other human tissue. One reason for this is that blood samples can be easily secured and subjected to biochemical analysis without harm or major discomfort to the person being tested. Perhaps a more cogent reason is that many chemical properties of human blood display relatively simple patterns of inheritance.

Certain chemical substances within the red blood cells (such as the ABO and MN substances noted above) may serve as antigens. When cells that contain specific antigens are introduced into the body of an experimental animal such as a rabbit, the animal responds by producing antibodies in its own blood.

In addition to the ABO and MN systems, geneticists have identified about 14 blood-type gene systems associated with other chromosomal locations. The best known of these is the Rh system. The Rh antigens are of particular importance in human medicine. Curiously, however, their existence was discovered in monkeys. When blood from the rhesus monkey (hence the designation Rh) is injected into rabbits, the rabbits produce so-called Rh antibodies that will agglutinate not only the red blood cells of the monkey but the cells of a large proportion of human beings as well. Some people (Rh-negative individuals), however, lack the Rh antigen; the proportion of such persons varies from one human population to another. Akin to data concerning the ABO system, the evidence for Rh genes indicates that only a single chromosome locus (called r) is involved and is located on chromosome 1. At least 35 Rh alleles are known for the r location; basically the Rh-negative condition is recessive.

A medical problem may arise when a woman who is Rh-negative carries a fetus that is Rh-positive. The first such child may have no difficulty, but later similar pregnancies may produce severely anemic newborn infants. Exposure to the red blood cells of the first Rh-positive fetus appears to immunize the Rh-negative mother, that is, she develops antibodies that may produce permanent (sometimes fatal) brain damage in any subsequent Rh-positive fetus. Damage arises from the scarcity of oxygen reaching the fetal brain because of the severe destruction of red blood cells. Measures are available for avoiding the severe effects of Rh incompatibility by transfusions to the fetus within the uterus; however, genetic counselling before conception is helpful so that the mother can receive Rh immunoglobulin immediately after her first and any subsequent pregnancies involving an Rh-positive fetus. This immunoglobulin effectively destroys the fetal red blood cells before the mothers immune system is stimulated. The mother thus avoids becoming actively immunized against the Rh antigen and will not produce antibodies that could attack the red blood cells of a future Rh-positive fetus.

Human serum, the fluid portion of the blood that remains after clotting, contains various proteins that have been shown to be under genetic control. Study of genetic influences has flourished since the development of precise methods for separating and identifying serum proteins. These move at different rates under the impetus of an electrical field (electrophoresis), as do proteins from many other sources (e.g., muscle or nerve). Since the composition of a protein is specified by the structure of its corresponding gene, biochemical studies based on electrophoresis permit direct study of tissue substances that are only a metabolic step or two away from the genes themselves.

Electrophoretic studies have revealed that at least one-third of the human serum proteins occur in variant forms. Many of the serum proteins are polymorphic, occurring as two or more variants with a frequency of not less than 1 percent each in a population. Patterns of polymorphic serum protein variants have been used to determine whether twins are identical (as in assessing compatibility for organ transplants) or whether two individuals are related (as in resolving paternity suits). Whether the different forms have a selective advantage is not generally known.

Much attention in the genetics of substances in the blood has been centred on serum proteins called haptoglobins, transferrins (which transport iron), and gamma globulins (a number of which are known to immunize against infectious diseases). Haptoglobins appear to relate to two common alleles at a single chromosome locus; the mode of inheritance of the other two seems more complicated, about 18 kinds of transferrins having been described. Like blood-cell antigen genes, serum-protein genes are distributed worldwide in the human population in a way that permits their use in tracing the origin and migration of different groups of people.

Hundreds of variants of hemoglobin have been identified by electrophoresis, but relatively few are frequent enough to be called polymorphisms. Of the polymorphisms, the alleles for sickle-cell and thalassemia hemoglobins produce serious disease in homozygotes, whereas others (hemoglobins C, D, and E) do not. The sickle-cell polymorphism confers a selective advantage on the heterozygote living in a malarial environment; the thalassemia polymorphism provides a similar advantage.

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Human genetics | biology | Britannica.com

Department of Human Genetics | The University of Chicago

The Department of Human Genetics is the home within the Division of Biological Sciences for the study of basic principles of genetics and genomics as applied to human disease. We provide broad training in experimental genetics and genomics, statistical and population genetics, bioinformatics, and clinical genetics. A common theme throughout our research is the application of basic genetic principles and strategies to the study of disease mechanism, disease susceptibility, and the genetic architecture of complex traits. Our faculty bridge between basic and clinical research and train students for careers in academia, industry, and medicine.

The Department of Human Genetics has an unwavering commitment to diversity, inclusion, free expression, and open discourse.These values are at the core of our roles as scientists, as teachers, and as citizens of a free society.

Science, including genetics, plays a central role in many crucial issues of our time. We are committed to generating rigorous scientific knowledge, training future scientists, and preparing our students to be well-informed citizens in a democratic society.

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What is Bitcoin Cash? – finance.yahoo.com

For many newcomers, cryptocurrencies can be confusing at the best of times. Not only are they extremely complex, but there are also so many of them to choose from.

Bitcoin itself is no stranger to this. There are multiple iterations of Bitcoin, from the original BTC to Bitcoin Gold and Bitcoin Private. The biggest competitor to Bitcoin though is Bitcoin Cash (BCH). BCH is a hard fork of Bitcoin that aims to solve the issue of scaling through the use of bigger blocks.

Bitcoin Cash arose due to a large scaling debate that happened within the Bitcoin community. Debates began to arise when the Bitcoin mempool began to fill up due to the amount of transactions taking place on the network. This caused Bitcoin to become slower and more expensive to send than it had been in the past.

There were two options depending on your viewpoint. The first was to scale by increasing the block size of Bitcoin, and the second was to scale via a second-layer solution such as the Lightning Network. When neither side could come to a compromise, a fork took place and led to the creation of what became known as Bitcoin Cash.

Bitcoin Cash was backed by evangelist Roger Ver and mining giant Jihan Wu along with many other industry leaders and experts. They disagreed with the idea of implementing SegWit onto Bitcoin and wanted to see Bitcoin scale to 8MB blocks.

Bigger blocks allow for more transactions to take place. However, this comes with the downside of creating a larger blockchain. Those who believe in BTC argue that bigger blocks will eventually lead to mining centralisation.

BCH supporters argue that through Moores Law technology will eventually catch up, allowing for bigger blocks to be possible without these centralisation issues.

Bigger blocks are believed to be necessary due to the fees associated with Bitcoin. When the network became extremely popular in the bull run of 2017, fees and transaction times began to rise considerably. This made it clear that Bitcoin needed to scale.

Bitcoin Cash believes that it has solved these problems through bigger blocks, which it argues allows for much lower fees.

It is impossible to discuss Bitcoin Cash without mentioning evangelist Roger Ver. Ver was one of the first people to promote Bitcoin to the world. He was an early investor in the cryptocurrency and many major cryptocurrency companies today were helped by his funding. As the owner of the bitcoin.com domain, he holds a powerful position.

Ver argues that the direction that BTC has taken has limited the cryptocurrency and allowed other altcoins to rise in prominence. He argues that Bitcoin Cash is the true Bitcoin as it is a form of peer-to-peer electronic cash, as stated in the white paper.

This has not been without controversy, and resulted in much antagonism directed towards Ver. Some have argued that Ver has misled the public in his promotion of Bitcoin Cash as the real Bitcoin an accusation he vehemently denies.

BCH went through its own drama in late 2018. After the split from BTC, BCH was led by Roger Ver, Jihan Wu, and development teams including Bitcoin Unlimited and Bitcoin ABC. They were also supported by Craig Wright of nChain and his partner Calvin Ayre.

However, their relationship soured, and another fork took place splitting Bitcoin Cash into BCH and Bitcoin Satoshis Vision (BSV).

Many members of the Bitcoin Cash community are on the r/btc subreddit. The r/btc subreddit is another split from the original r/bitcoin subreddit. The drama began when users argued that the r/bitcoin subreddit was too heavily moderated, therefore limiting free speech.

This led to the creation of r/btc, and this is where you can find the most up-to-date news on Bitcoin Cash and debates surrounding the cryptocurrency. If you want the latest news and to join the community, this is the place to start.

There are many fervent supporters of Bitcoin Cash who believe that on-chain scaling is the main solution to the current scaling issues. Although it has yet to make a dent in overtaking the original Bitcoin chain, their beliefs have not diminished. This is the main difference between Bitcoin Cash and Bitcoin the debate over scaling on-chain or via a second layer.

Arguments over the split still rage on to this day, with both sides not conceding any ground. Whilst many deride Bitcoin Cash, there is an argument to be made that the testing of an on-chain scaling solution is a good experiment for the whole of cryptocurrency.

The post What is Bitcoin Cash? appeared first on Coin Rivet.

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What is Bitcoin Cash? – finance.yahoo.com

Bitcoin Soars As Ethereum, Ripple’s XRP, Bitcoin Cash, And …

Bitcoin has continued its march higher after shooting up at the beginning of the month and now appears to be pulling away from the likes ethereum, Ripple’s XRP, bitcoin cash, EOS, and other major cryptocurrencies.

The bitcoin price has hit another year-to-date high in the past 24 hours, climbing to $5,622, according to prices from the Luxembourg-based Bitstamp exchange.

Now, a bullish technical indicator is giving investors heart that the recent rally will be held after bitcoin’s moving averages showed a pattern known as a golden cross.

The bitcoin price has been outperforming smaller cryptocurrencies after so-called altcoins made strong gains previously.

The golden crossoccurs when the average bitcoin price in the short term rises above its long term average price. Bitcoin’s 50-day moving average rose above its 200-day moving average for the first time since 2015yesterday.

Alternatively, when an assets short-term moving average crosses below the long-term moving average, it indicates the potential for a major selloff and is known as a death cross.

The bitcoin price has risen almost 2% over the last 24 hour trading period, according to data from CoinMarketCap, which tracks most major cryptocurrencies.

Elsewhere, ethereum and Ripple’s XRP lost 2%, while bitcoin cash, an offshoot of bitcoin itself, was down more than 5%. EOS was off by 3% over the last 24 hour trading period.

Binance coin, which increasingly seems to be deciding the direction of the bitcoin and cryptocurrency market, lost the most of the top ten cryptocurrencies over the last 24 hours, dropping almost 6%.

The bitcoin price has recorded another year-to-date high this week.

Bitcoin and cryptocurrency industry insiders have said bitcoin, the original cryptocurrency, is still very important to the wider market.

“If I had to pick one [cryptocurrency], I would pick bitcoin. We need bitcoin to succeed in order for the market to do well and for innovations to keep happening,” Hany Rashwan, the founder and chief executive of cryptocurrency trading tools company Amun, this week told the Crypto for Earthlings podcast.

“Bitcoin is the largest and most well support asset today and we shouldn’t dismiss it. There are a number of technical innovations on their way to make bitcoin more transactional. We should focus on that and keep investing in bitcoin more than anything else.”

Meanwhile, analysts and traders were keen to find any sign of what was pushing bitcoin higher while other coins, like ethereum, Ripple’s XRP, bitcoin cash, and EOS, fell.

The cryptocurrency market has been divided by bitcoin’s recent gains.

“Another strong surge during the Asian session[yesterday]brought us to a new high of $5,622 a coin, the highest level since November’s capitulation,” eToro senior market analyst Mati Greenspan wrote in a note to clients.

“There are a load of bullish signs right now but if you’re asking what caused this morning’s movement, you might be slightly disappointed as there doesn’t seem to be any specific catalyst for this. It seems simply to be a shift in outlook.

“During the bear market, there were a lot of people who sold their crypto in fear of lower prices. Those people didn’t really go away though, they’re simply standing on the sidelines waiting for the return of a bull market.”

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Bitcoin Soars As Ethereum, Ripple’s XRP, Bitcoin Cash, And …

Bitcoin Cash – finance.yahoo.com

Bitcoin Cash ABC Slides Again

Bitcoin Cash ABC slid by 3.14% on Friday. Following on from a 6.72% tumble on Thursday, Bitcoin Cash ABC ended the day at $255.02.

A relatively bullish start to the day saw Bitcoin Cash ABC rise to an intraday high $269.27 before hitting reverse.

Falling short of the first major resistance level at $279.15, Bitcoin Cash ABC fell to a late afternoon intraday low $251.34.

In spite of the reversal, Bitcoin Cash ABC steered clear of the first major support level at $249.92 to recover to $255 levels.

At the time of writing, Bitcoin Cash ABC was up by 2.28% to $260.85. Bucking the trend from the broader market, Bitcoin Cash ABC rose from $255.02 to a morning high $261.

In spite of the early move, Bitcoin Cash ABC left the major support and resistance levels untested.

For the day ahead, a move through to $262 levels would support a run at the first major resistance level at $265.75.

Barring a broad-based crypto rally, Bitcoin Cash ABC would likely come up short of $270 levels and the second major resistance level at $276.47. Fridays high $269.27 would likely pin Bitcoin Cash ABC back on the day.

In the event of a breakout, Bitcoin Cash ABC would likely fall short of $280 levels on the day.

Failure to move through to $262 levels could see Bitcoin Cash ABC hit reverse later in the day. A fall a pullback through $258.54 would bring $251 levels into play before any recovery.

Barring a crypto sell-off, Bitcoin Cash ABC would likely steer clear of sub-$250 levels and the first major support level at $247.82.

Litecoin rose by 1.49% on Friday. Partially reversing a 3.39% slide from Thursday, Litecoin ended the day at $71.64.

A choppy start to the day saw Litecoin slide to an intraday low $68.88 before striking an intraday high $73.5.

The moves through the early hours saw Litecoin leave the major support and resistance levels untested.

Easing back from the early intraday high, Litecoin fell to an afternoon low $69.5 before finding support late in the day.

At the time of writing, Litecoin was down by 0.61% to $71.20. A bearish start to the day saw Litecoin fall from a morning high $71.83 to a low $71.13 before steadying.

Litecoin left the major support and resistance levels untested in the early hours.

For the day ahead, a move through to $71.40 levels would bring $72 levels back into play before any pullback. Support from the broader market would be needed, however, for Litecoin to take a run at $73 levels and the first major resistance level at $73.80.

Failure to move through to $71.40 levels could see Litecoin slide further into the red before any recovery.

A fall through to $70 levels would bring the first major support level at $69.18 into play. Barring a crypto meltdown, Litecoin would likely avoid a return to sub-$69 levels on the day.

Story continues

Ripples XRP rallied by 6.34% on Friday. Reversing a 3.93% slide from Thursday, Ripples XRP ended the day at $0.3092.

Bullish through the day, Ripples XRP rallied from a start of a day intraday low $0.28799 to a late intraday high $0.31149.

Steering clear of the major support levels, Ripples XRP broke through the first major resistance level at $0.3060. In spite of the day-long rally, Ripples XRP came up short of $0.32 levels and the second major resistance level at $0.3209. More modest gains elsewhere likely capped the upside on the day.

At the time of writing, Ripples XRP was down by 0.38% to $0.30802. A relatively range-bound start to the day saw Ripples XRP fall from a morning high $0.31097 to a low $0.30757.

The early moves saw Ripples XRP leave the major support and resistance levels untested.

For the day ahead, a move through to $0.31 levels would support a run at the first major resistance level at $0.3178. Following Fridays breakout, support from the broader market would be needed for return to $0.32 levels.

Barring a broad-based crypto rally, Ripples XRP would likely come up short of the second major resistance level at $0.3264.

Failure to move through to $0.31 levels could see Ripples XRP take another hit on the day. A fall through $0.3030 levels would bring the first major support level at $0.2943 into play.

Barring a crypto meltdown, Ripples XRP would likely avoid a return to $0.28 levels on the day.

Please let us know what you think in the comments below

Thanks, Bob

This article was originally posted on FX Empire

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Bitcoin Cash – finance.yahoo.com

What is Bitcoin Cash? – Coin Rivet

For many newcomers, cryptocurrencies can be confusing at the best of times. Not only are they extremely complex, but there are also so many of them to choose from.

Bitcoin itself is no stranger to this. There are multiple iterations of Bitcoin, from the original BTC to Bitcoin Gold and Bitcoin Private. The biggest competitor to Bitcoin though is Bitcoin Cash (BCH). BCH is a hard fork of Bitcoin that aims to solve the issue of scaling through the use of bigger blocks.

Bitcoin Cash arose due to a large scaling debate that happened within the Bitcoin community. Debates began to arise when the Bitcoin mempool began to fill up due to the amount of transactions taking place on the network. This caused Bitcoin to become slower and more expensive to send than it had been in the past.

There were two options depending on your viewpoint. The first was to scale by increasing the block size of Bitcoin, and the second was to scale via a second-layer solution such as the Lightning Network. When neither side could come to a compromise, a fork took place and led to the creation of what became known as Bitcoin Cash.

Bitcoin Cash was backed by evangelist Roger Ver and mining giant Jihan Wu along with many other industry leaders and experts. They disagreed with the idea of implementing SegWit onto Bitcoin and wanted to see Bitcoin scale to 8MB blocks.

Bigger blocks allow for more transactions to take place. However, this comes with the downside of creating a larger blockchain. Those who believe in BTC argue that bigger blocks will eventually lead to mining centralisation.

BCH supporters argue that through Moores Law technology will eventually catch up, allowing for bigger blocks to be possible without these centralisation issues.

Bigger blocks are believed to be necessary due to the fees associated with Bitcoin. When the network became extremely popular in the bull run of 2017, fees and transaction times began to rise considerably. This made it clear that Bitcoin needed to scale.

Bitcoin Cash believes that it has solved these problems through bigger blocks, which it argues allows for much lower fees.

It is impossible to discuss Bitcoin Cash without mentioning evangelist Roger Ver. Ver was one of the first people to promote Bitcoin to the world. He was an early investor in the cryptocurrency and many major cryptocurrency companies today were helped by his funding. As the owner of the bitcoin.com domain, he holds a powerful position.

Ver argues that the direction that BTC has taken has limited the cryptocurrency and allowed other altcoins to rise in prominence. He argues that Bitcoin Cash is the true Bitcoin as it is a form of peer-to-peer electronic cash, as stated in the white paper.

This has not been without controversy, and resulted in much antagonism directed towards Ver. Some have argued that Ver has misled the public in his promotion of Bitcoin Cash as the real Bitcoin an accusation he vehemently denies.

BCH went through its own drama in late 2018. After the split from BTC, BCH was led by Roger Ver, Jihan Wu, and development teams including Bitcoin Unlimited and Bitcoin ABC. They were also supported by Craig Wright of nChain and his partner Calvin Ayre.

However, their relationship soured, and another fork took place splitting Bitcoin Cash into BCH and Bitcoin Satoshis Vision (BSV).

Many members of the Bitcoin Cash community are on the r/btc subreddit. The r/btc subreddit is another split from the original r/bitcoin subreddit. The drama began when users argued that the r/bitcoin subreddit was too heavily moderated, therefore limiting free speech.

This led to the creation of r/btc, and this is where you can find the most up-to-date news on Bitcoin Cash and debates surrounding the cryptocurrency. If you want the latest news and to join the community, this is the place to start.

There are many fervent supporters of Bitcoin Cash who believe that on-chain scaling is the main solution to the current scaling issues. Although it has yet to make a dent in overtaking the original Bitcoin chain, their beliefs have not diminished. This is the main difference between Bitcoin Cash and Bitcoin the debate over scaling on-chain or via a second layer.

Arguments over the split still rage on to this day, with both sides not conceding any ground. Whilst many deride Bitcoin Cash, there is an argument to be made that the testing of an on-chain scaling solution is a good experiment for the whole of cryptocurrency.

Read more:

What is Bitcoin Cash? – Coin Rivet

Moon Cash | Free bitcoin cash faucet

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Cash App – Bitcoin

Cash App is already the easiest way to send and receive money with friends and family. Weve made it just as easy to buy and sell BTC straight from your Cash App balance. Unlike other apps, most of our buys and sells happen in seconds. You can even spend your proceeds from a free Visa debit card.

Bitcoins price is volatile and unpredictable, so please make wise financial decisions. Dont spend more than you can afford, and review the FAQ and risks to buying Bitcoin before you buy.

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Cash App – Bitcoin

Bitcoin Cash (BCH) price, chart, and fundamentals info …

Bitcoin Cash (BCH) is a cryptocurrency or a form of digital asset. Bitcoin Cash (BCH) price for today is $237.77 with a 24-hour trading volume of $1,276,996,758. Price is down -6.6% in the last 24 hours. It has a circulating supply of 17.8 Million coins and a max supply of 21 Million coins. The most active exchange that is trading Bitcoin Cash is OEX. Explore the address and transactions of Bitcoin Cash on block explorers such as blockchair.com and bch.tokenview.com. Additional information about Bitcoin Cash coin can be found at https://www.bitcoincash.org/.

-0.23%

-6.6%

-18%

-18%

40%

-83%

PriceMarket CapTradingView

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Bitcoin Cash (BCH) price, chart, and fundamentals info …

Bitcoin Cash – Wikipedia

cryptocurrency

Bitcoin Cash is a cryptocurrency.[2] In mid-2017, a group of developers wanting to increase bitcoin’s block size limit prepared a code change. The change, called a hard fork, took effect on 1 August 2017. As a result, the bitcoin ledger called the blockchain and the cryptocurrency split in two.[3] At the time of the fork anyone owning bitcoin was also in possession of the same number of Bitcoin Cash units.[3] The technical difference between Bitcoin Cash and bitcoin is that Bitcoin Cash allows larger blocks in its blockchain than bitcoin, which in theory allows it to process more transactions per second.[4]

On 15 November 2018 Bitcoin Cash split into two cryptocurrencies.[5]

Bitcoin Cash is a cryptocurrency[6] and a payment network.[7] In relation to bitcoin it is characterized variously as a spin-off,[6] a strand,[8] a product of a hard fork,[9] an offshoot,[10] a clone,[11] a second version[12] or an altcoin.[13]

The naming of Bitcoin Cash is contentious; it is sometimes referred to as Bcash.[14]

Rising fees on the bitcoin network contributed to a push by some in the community to create a hard fork to increase the blocksize.[15] This push came to a head in July 2017 when some members of the Bitcoin community including Roger Ver felt that adopting BIP 91 without increasing the block-size limit favored people who wanted to treat Bitcoin as a digital investment rather than as a transactional currency.[16][17] This push by some to increase the block size met a resistance. Since its inception up to July 2017, bitcoin users had maintained a common set of rules for the cryptocurrency.[16] Eventually, a group of bitcoin activists,[12] investors, entrepreneurs, developers[16] and largely China based miners were unhappy with bitcoin’s proposed SegWit improvement plans meant to increase capacity and pushed forward alternative plans for a split which created Bitcoin Cash.[11] The proposed split included a plan to increase the number of transactions its ledger can process by increasing the block size limit to eight megabytes.[16][17]

The would-be hard fork with an expanded block size limit was described by hardware manufacturer Bitmain in June 2017 as a “contingency plan” should the Bitcoin community decide to fork; the first implementation of the software was proposed under the name Bitcoin ABC at a conference that month. In July 2017, the Bitcoin Cash name was proposed by mining pool ViaBTC.

On 1 August 2017 Bitcoin Cash began trading at about $240, while Bitcoin traded at about $2,700.[3]

In 2018 Bitcoin Core developer Cory Fields found a bug in the Bitcoin ABC software that would have allowed an attacker to create a block causing a chain split. Fields notified the development team about it and the bug was fixed.[18]

In November 2018, a hard-fork chain split of Bitcoin Cash occurred between two rival factions called Bitcoin ABC and Bitcoin SV.[19] On 15 November 2018 Bitcoin Cash ABC traded at about $289 and Bitcoin SV traded at about $96.50, down from $425.01 on 14 November for the un-split Bitcoin Cash.[5]

The split originated from what was described as a “civil war” in two competing bitcoin cash camps.[20][21] The first camp, led by entrepreneur Roger Ver and Jihan Wu of Bitmain, promoted the software entitled Bitcoin ABC (short for Adjustable Blocksize Cap) which would maintain the block size at 32MB.[21] The second camp led by Craig Steven Wright and billionaire Calvin Ayre put forth a competing software version Bitcoin SV, short for “Bitcoin Satoshi’s Vision,” that would increase the blocksize to 128MB.[19][21]

Controversy

The arguments have devolved over three or four years of bitter debate, the principles are real and they are important to preserve, but a lot of the drama has nothing to do with principles anymore. A lot of this debate is now more about hurt feelings. Its about bruised egos. Its about things that were said that cant be unsaid, insults that were exchanged, and personalities and ego.

Andreas Antonopoulos, “The Verge”

There are two factions of bitcoin supporters, that support large blocks or small blocks.[4] The Bitcoin Cash faction favors the use of its currency as a medium of exchange for commerce while the bitcoin supporting faction view Bitcoin’s primary use as that of a store of value.[4] Some bitcoin supporters like to call Bitcoin Cash Bcash, Btrash, or simply, a scam, while Bitcoin Cash advocates insist that their implementation is the pure form of Bitcoin.[4]

Bitcoin Cash trades on digital currency exchanges including Bitstamp,[22] Coinbase,[23] Gemini,[24] Kraken,[25] and ShapeShift using the Bitcoin Cash name and the BCH ticker symbol for the cryptocurrency. A few other exchanges use the BCC ticker symbol, though BCC is commonly used for Bitconnect. On 26 March 2018, OKEx removed all Bitcoin Cash trading pairs except for BCH/BTC, BCH/ETH and BCH/USDT due to “inadequate liquidity”.[6] As of May2018[update], daily transaction numbers for Bitcoin Cash are about one-tenth of those of bitcoin.[6]

By November 2017 the value of Bitcoin Cash, which had been as high as $900, had fallen to around $300, much of that due to people who had originally held Bitcoin selling off the Bitcoin Cash they received at the hard fork.[15] On 20 December 2017 it reached an intraday high of $4,355.62 and then fell 88% to $519.12 on 23 August 2018.[26]

As of August 2018, Bitcoin Cash payments are supported by payment service providers such as BitPay, Coinify and GoCoin.[27] The research firm Chainanalysis noted that in May 2018, 17 largest payment processing services such as BitPay, Coinify, and GoCoin processed Bitcoin Cash payments worth of US$3.7 million, down from US$10.5 million processed in March.[27]

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Bitcoin Cash – Wikipedia

Bitcoincash price | index, chart and news | WorldCoinIndex

About

Bitcoin Cash was launched in August 2017, as a direct response to small block sizes on the Bitcoin code. 1MB block sizes were not meeting the demand of the growing community, so a group of dissatisfied crypto enthusiasts decided to create a hard fork of the Bitcoin blockchain, with an increased 8MB block size. No one person currently takes credit for the tokens creation; rather it is attributed to a de-centralized group of developers.

Bitcoin Cash was the first hard fork of Bitcoin, and it inherited and replicated the Bitcoin ledger records up until the point of creation. This means holders of Bitcoin (BTC) received the same amount of Bitcoin Cash (BCH) immediately upon launch. All transactions from that point on are separate, and do not affect each other.

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Bitcoincash price | index, chart and news | WorldCoinIndex

Bitcoin Cash (BCH) Price, View BCH Live Value & Buy Bitcoin …

BCH will be open for investment with a limit placed on the daily invested amount. When it reaches its daily limit, it will be closed to new investors and reopened the following day. Closing the investment can be done at any time. Created in August 2017, Bitcoin Cash was diverged from the original Bitcoin blockchain as a result of a hard fork …

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Bitcoin Cash (BCH) Price, View BCH Live Value & Buy Bitcoin …

Ripple Price Forecast: XRP vs SWIFT, SEC Updates, and More

Ripple vs SWIFT: The War Begins
While most criticisms of XRP do nothing to curb my bullish Ripple price forecast, there is one obstacle that nags at my conscience. Its name is SWIFT.

The Society for Worldwide Interbank Financial Telecommunication (SWIFT) is the king of international payments.

It coordinates wire transfers across 11,000 banks in more than 200 countries and territories, meaning that in order for XRP prices to ascend to $10.00, Ripple needs to launch a successful coup. That is, and always has been, an unwritten part of Ripple’s story.

We’ve seen a lot of progress on that score. In the last three years, Ripple wooed more than 100 financial firms onto its.

The post Ripple Price Forecast: XRP vs SWIFT, SEC Updates, and More appeared first on Profit Confidential.

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Ripple Price Forecast: XRP vs SWIFT, SEC Updates, and More


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