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Category Archives: Transhuman News

Portal:Libertarianism – Wikipedia

Posted: October 20, 2016 at 11:31 pm

The Ludwig von Mises Institute (LvMI), based in Auburn, Alabama, is a libertarian academic organization engaged in research and scholarship in the fields of economics, philosophy and political economy. Its scholarship is inspired by the work of Austrian School economist Ludwig von Mises. Anarcho-capitalist thinkers such as Murray Rothbard have also had a strong influence on the Institute's work. The Institute is funded entirely through private donations.

The Institute does not consider itself a traditional think tank. While it has working relationships with individuals such as U.S. Representative Ron Paul and organizations like the Foundation for Economic Education, it does not seek to implement public policy. It has no formal affiliation with any political party (including the Libertarian Party), nor does it receive funding from any. The Institute also has a formal policy of not accepting contract work from corporations or other organizations.

The Institute's official motto is Tu ne cede malis sed contra audentior ito, which comes from Virgil's Aeneid, Book VI; the motto means "do not give in to evil but proceed ever more boldly against it." Early in his life, Mises chose this sentence to be his guiding principle in life. It is prominently displayed throughout the Institute's campus, on their website and on memorabilia.

Lysander Spooner (19 January 1808 14 May 1887) was a libertarian,[1]individualist anarchist, entrepreneur, political philosopher, abolitionist, supporter of the labor movement, and legal theorist of the 19th century. He is also known for competing with the U.S. Post Office with his American Letter Mail Company, which was forced out of business by the United States government. He has been identified by some contemporary writers as an anarcho-capitalist,[2][3] while other writers and activists believe he was anti-capitalist for vocalizing opposition to wage labor.[4]

Later known as an early individualist anarchist, Spooner advocated what he called Natural Law or the "Science of Justice" wherein acts of initiatory coercion against individuals and their property were considered "illegal" but the so-called criminal acts that violated only man-made legislation were not.

He believed that the price of borrowing capital could be brought down by competition of lenders if the government de-regulated banking and money. This he believed would stimulate entrepreneurship. In his Letter to Cleveland, Spooner argued, "All the great establishments, of every kind, now in the hands of a few proprietors, but employing a great number of wage labourers, would be broken up; for few or no persons, who could hire capital and do business for themselves would consent to labour for wages for another."[5] Spooner took his own advice and started his own business called American Letter Mail Company which competed with the U.S. Post Office.

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Space station – Wikipedia

Posted: October 19, 2016 at 4:08 am

A space station, also known as an orbital station or an orbital space station, is a spacecraft capable of supporting a crew, which is designed to remain in space (most commonly as an artificial satellite in low Earth orbit) for an extended period of time and for other spacecraft to dock. A space station is distinguished from other spacecraft used for human spaceflight by lack of major propulsion or landing systems. Instead, other vehicles transport people and cargo to and from the station. As of September 2016[update] three space stations are in orbit: the International Space Station, which is permanently manned, China's Tiangong-1 (defunct) and Tiangong-2 (launched 15 September 2016, unmanned most of the time).[1][2] Previous stations include the Almaz and Salyut series, Skylab, and most recently Mir.

Today's space stations are research platforms, used to study the effects of long-term space flight on the human body as well as to provide platforms for greater number and length of scientific studies than available on other space vehicles. Each crew member stays aboard the station for weeks or months, but rarely more than a year. Most of the time crew remain inside the space station but its not necessary that crew should have to be stay inside the station. Since the ill-fated flight of Soyuz 11 to Salyut 1, all manned spaceflight duration records have been set aboard space stations. The duration record for a single spaceflight is 437.7 days, set by Valeriy Polyakov aboard Mir from 1994 to 1995. As of 2013[update], three astronauts have completed single missions of over a year, all aboard Mir.

Space stations have also been used for both military and civilian purposes. The last military-use space station was Salyut 5, which was used by the Almaz program of the Soviet Union in 1976 and 1977.[3]

Space stations have been envisaged since at least as early as 1869 when Edward Everett Hale wrote "The Brick Moon".[4] The first to give serious consideration to space stations were Konstantin Tsiolkovsky in the early 20th century and Hermann Oberth about two decades later.[4] In 1929 Herman Potonik's The Problem of Space Travel was published, the first to envision a "rotating wheel" space station to create artificial gravity.

During the Second World War, German scientists researched the theoretical concept of an orbital weapon based on a space station. Pursuing Oberth's idea of a space-based weapon, the so-called "sun gun" was a concept of a space station orbiting Earth at a height of 8,200 kilometres (5,100mi), with a weapon that was to utilize the sun's energy.[5]

In 1951, in Collier's weekly, Wernher von Braun published his design for a rotating wheel space station, which referenced Potonik's idea however these concepts would never leave the concept stage during the 20th century.[4]

During the same time as von Braun pursued Potonik's ideas, the Soviet design bureaus chiefly Vladimir Chelomey's OKB-52 were pursuing Tsiolkovsky's ideas for space stations. The work by OKB-52 would lead to the Almaz programme and (together with OKB-1) to the first space station: Salyut 1. The developed hardware laid the ground for the Salyut and Mir space stations, and is even today a considerable part of the ISS space station.

The first space station was Salyut 1, which was launched by the Soviet Union on April 19, 1971. Like all the early space stations, it was "monolithic", intended to be constructed and launched in one piece, and then manned by a crew later. As such, monolithic stations generally contained all their supplies and experimental equipment when launched, and were considered "expended", and then abandoned, when these were used up.

The earlier Soviet stations were all designated "Salyut", but among these there were two distinct types: civilian and military. The military stations, Salyut 2, Salyut 3, and Salyut 5, were also known as Almaz stations.

The civilian stations Salyut 6 and Salyut 7 were built with two docking ports, which allowed a second crew to visit, bringing a new spacecraft with them; the Soyuz ferry could spend 90 days in space, after which point it needed to be replaced by a fresh Soyuz spacecraft.[6] This allowed for a crew to man the station continually. Skylab was also equipped with two docking ports, like second-generation stations, but the extra port was never utilized. The presence of a second port on the new stations allowed Progress supply vehicles to be docked to the station, meaning that fresh supplies could be brought to aid long-duration missions. This concept was expanded on Salyut 7, which "hard docked" with a TKS tug shortly before it was abandoned; this served as a proof-of-concept for the use of modular space stations. The later Salyuts may reasonably be seen as a transition between the two groups.

Unlike previous stations, the Soviet space station Mir had a modular design; a core unit was launched, and additional modules, generally with a specific role, were later added to that. This method allows for greater flexibility in operation, as well as removing the need for a single immensely powerful launch vehicle. Modular stations are also designed from the outset to have their supplies provided by logistical support, which allows for a longer lifetime at the cost of requiring regular support launches.

The core module of the International Space Station was launched in 1998.

The ISS is divided into two main sections, the Russian orbital segment (ROS), and the United States operational segment (USOS).

USOS modules were brought to the station by the Space Shuttle and manually attached to the ISS by crews during EVAs. Connections are made manually for electrical, data, propulsion and cooling fluids. This results in a single piece which is not designed for disassembly.[7]

The Russian orbital segment's modules are able to launch, fly and dock themselves without human intervention using Proton rockets.[8] Connections are automatically made for power, data and propulsion fluids and gases. The Russian approach allows assembly of space stations orbiting other worlds in preparation for manned missions. The Nauka module of the ISS will be used in the 12th Russian/Soviet space station, OPSEK, whose main goal is supporting manned deep space exploration.

Russian Modular or 'next generation' space stations differ from 'Monolithic' single piece stations by allowing reconfiguration of the station to suit changing needs. According to a 2009 report, RKK Energia is considering methods to remove from the station some modules of the Russian Orbital Segment when the end of mission is reached for the ISS and use them as a basis for a new station, known as the Orbital Piloted Assembly and Experiment Complex. None of these modules would have reached the end of their useful lives in 2016 or 2020. The report presents a statement from an unnamed Russian engineer who believes that, based on the experience from Mir, a thirty-year life should be possible, except for micrometeorite damage, because the Russian modules have been built with on-orbit refurbishment in mind.[9]

China's first space laboratory, Tiangong-1 was launched in September 2011. The unmanned Shenzhou 8 then successfully performed an automatic rendezvous and docking in November 2011. The manned Shenzhou 9 then docked with Tiangong-1 in June 2012, the manned Shenzhou 10 in 2013. Tiangong 2 was launched in September 2016 and another space laboratory, Tiangong 3, is expected to be launched in subsequent years, paving the way for the construction of a larger space station around 2020.

In September 2016 it was reported that the Tiangong-1 is falling back to earth and will burn in the atmosphere during 2017.

These stations have various issues that limit their long-term habitability, such as very low recycling rates, relatively high radiation levels and a lack of weight. Some of these problems cause discomfort and long-term health effects. In the case of solar flares, all current habitats are protected by the Earth's magnetic field, and are below the Van Allen belts.

Future space habitats may attempt to address these issues, and could be intended for long-term occupation. Some designs might even accommodate large numbers of people, essentially "cities in space" where people would make their homes. No such design has yet been constructed, since even for a small station, the current (2016) launch costs are not economically or politically viable.

Possible ways to deal with these costs would be to build a large number of rockets (economies of scale), employ reusable rockets, In Situ Resource Utilisation, or non-rocket spacelaunch methods such as space elevators. For example, in 1975, proposing to seek long-term habitability through artificial gravity and enough mass in space to allow high radiation shielding, the most ambitious historical NASA study, a conceptual 10000-person spacestation, envisioned a future mass driver base launching 600 times its own mass in lunar material cumulatively over years.[10]

A space station is a complex system with many interrelated subsystems:

Molds that develop aboard space stations can produce acids that degrade metal, glass and rubber [11]

The Soviet space stations came in two types, the civilian Durable Orbital Station (DOS), and the military Almaz stations. (dates refer to periods when stations were inhabited by crews)

The business arrangement for developing and marketing the station was recently clarified by Russian firm Orbital Technologies, who is collaborating to develop the station with the Rocket and Space Technology Corporation Energia (RSC Energia). [22]

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Human genetics – An Introduction to Genetic Analysis …

Posted: at 4:08 am

In the study of rare disorders, four general patterns of inheritance are distinguishable by pedigree analysis: autosomal recessive, autosomal dominant, X-linked recessive, and X-linked dominant.

The affected phenotype of an autosomal recessive disorder is determined by a recessive allele, and the corresponding unaffected phenotype is determined by a dominant allele. For example, the human disease phenylketonuria is inherited in a simple Mendelian manner as a recessive phenotype, with PKU determined by the allele p and the normal condition by P . Therefore, sufferers from this disease are of genotype p /p , and people who do not have the disease are either P /P or P /p . What patterns in a pedigree would reveal such an inheritance? The two key points are that (1) generally the disease appears in the progeny of unaffected parents and (2) the affected progeny include both males and females. When we know that both male and female progeny are affected, we can assume that we are dealing with simple Mendelian inheritance, not sex-linked inheritance. The following typical pedigree illustrates the key point that affected children are born to unaffected parents:

From this pattern, we can immediately deduce simple Mendelian inheritance of the recessive allele responsible for the exceptional phenotype (indicated in black). Furthermore, we can deduce that the parents are both heterozygotes, say A /a ; both must have an a allele because each contributed an a allele to each affected child, and both must have an A allele because they are phenotypically normal. We can identify the genotypes of the children (in the order shown) as A /, a /a , a /a , and A /. Hence, the pedigree can be rewritten as follows:

Note that this pedigree does not support the hypothesis of X-linked recessive inheritance, because, under that hypothesis, an affected daughter must have a heterozygous mother (possible) and a hemizygous father, which is clearly impossible, because he would have expressed the phenotype of the disorder.

Notice another interesting feature of pedigree analysis: even though Mendelian rules are at work, Mendelian ratios are rarely observed in families, because the sample size is too small. In the preceding example, we see a 1:1 phenotypic ratio in the progeny of a monohybrid cross. If the couple were to have, say, 20 children, the ratio would be something like 15 unaffected children and 5 with PKU (a 3:1 ratio); but, in a sample of 4 children, any ratio is possible, and all ratios are commonly found.

The pedigrees of autosomal recessive disorders tend to look rather bare, with few black symbols. A recessive condition shows up in groups of affected siblings, and the people in earlier and later generations tend not to be affected. To understand why this is so, it is important to have some understanding of the genetic structure of populations underlying such rare conditions. By definition, if the condition is rare, most people do not carry the abnormal allele. Furthermore, most of those people who do carry the abnormal allele are heterozygous for it rather than homozygous. The basic reason that heterozygotes are much more common than recessive homozygotes is that, to be a recessive homozygote, both parents must have had the a allele, but, to be a heterozygote, only one parent must carry the a allele.

Geneticists have a quantitative way of connecting the rareness of an allele with the commonness or rarity of heterozygotes and homozygotes in a population. They obtain the relative frequencies of genotypes in a population by assuming that the population is in Hardy-Weinberg equilibrium, to be fully discussed in Chapter 24 . Under this simplifying assumption, if the relative proportions of two alleles A and a in a population are p and q , respectively, then the frequencies of the three possible genotypes are given by p 2 for A /A , 2pq for A /a , and q 2 for a /a . A numerical example illustrates this concept. If we assume that the frequency q of a recessive, disease-causing allele is 1/50, then p is 49/50, the frequency of homozygotes with the disease is q 2 =(1/50)2 =1/250, and the frequency of heterozygotes is 2pq =249/501/50 , or approximately 1/25. Hence, for this example, we see that heterozygotes are 100 times as frequent as disease sufferers, and, as this ratio increases, the rarer the allele becomes. The relation between heterozygotes and homozygotes recessive for a rare allele is shown in the following illustration. Note that the allele frequencies p and q can be used as the gamete frequencies in both sexes.

The formation of an affected person usually depends on the chance union of unrelated heterozygotes. However, inbreeding (mating between relatives) increases the chance that a mating will be between two heterozygotes. An example of a marriage between cousins is shown in . Individuals III-5 and III-6 are first cousins and produce two homozygotes for the rare allele. You can see from that an ancestor who is a heterozygote may produce many descendants who also are heterozygotes. Hence two cousins can carry the same rare recessive allele inherited from a common ancestor. For two unrelated persons to be heterozygous, they would have to inherit the rare allele from both their families. Thus matings between relatives generally run a higher risk of producing abnormal phenotypes caused by homozygosity for recessive alleles than do matings between nonrelatives. For this reason, first-cousin marriages contribute a large proportion of the sufferers of recessive diseases in the population.

Pedigree of a rare recessive phenotype determined by a recessive allele a . Gene symbols are normally not included in pedigree charts, but genotypes are inserted here for reference. Note that individuals II-1 and II-5 marry into the family; they are assumed (more...)

What are some examples of human recessive disorders? PKU has already served as an example of pedigree analysis, but what kind of phenotype is it? PKU is a disease of processing of the amino acid phenylalanine, a component of all proteins in the food that we eat. Phenylalanine is normally converted into tyrosine by the enzyme phenylalanine hydroxylase:

However, if a mutation in the gene encoding this enzyme alters the amino acid sequence in the vicinity of the enzymes active site, the enzyme cannot bind or convert phenylalanine (its substrate). Therefore phenylalanine builds up in the body and is converted instead into phenylpyruvic acid, a compound that interferes with the development of the nervous system, leading to mental retardation.

Babies are now routinely tested for this processing deficiency at birth. If the deficiency is detected, phenylalanine can be withheld by use of a special diet, and the development of the disease can be arrested.

Cystic fibrosis is another disease inherited according to Mendelian rules as a recessive phenotype. The allele that causes cystic fibrosis was isolated in 1989, and the sequence of its DNA was determined. This has led to an understanding of gene function in affected and unaffected persons, giving hope for more effective treatment. Cystic fibrosis is a disease whose most important symptom is the secretion of large amounts of mucus into the lungs, resulting in death from a combination of effects but usually precipitated by upper respiratory infection. The mucus can be dislodged by mechanical chest thumpers, and pulmonary infection can be prevented by antibiotics; so, with treatment, cystic fibrosis patients can live to adulthood. The disorder is caused by a defective protein that transports chloride ions across the cell membrane. The resultant alteration of the salt balance changes the constitution of the lung mucus.

Albinism, which served as a model of allelic determination of contrasting phenotypes in Chapter 1 , also is inherited in the standard autosomal recessive manner. The molecular nature of an albino allele and its inheritance are diagrammed in . This diagram shows a simple autosomal recessive inheritance in a pedigree and shows the molecular nature of the alleles involved. In this example, the recessive allele a is caused by a base pair change that introduces a stop codon into the middle of the gene, resulting in a truncated polypeptide. The mutation, by chance, also introduces a new target site for a restriction enzyme. Hence, a probe for the gene detects two fragments in the case of a and only one in A . (Other types of mutations would produce different effects at the level detected by Southern, Northern, and Western analyses.)

The molecular basis of Mendelian inheritance in a pedigree.

In all the examples heretofore considered, the disorder is caused by an allele for a defective protein. In heterozygotes, the single functional allele provides enough active protein for the cells needs. This situation is called haplosufficiency.

In human pedigrees, an autosomal recessive disorder is revealed by the appearance of the disorder in the male and female progeny of unaffected persons.

Here the normal allele is recessive, and the abnormal allele is dominant. It may seem paradoxical that a rare disorder can be dominant, but remember that dominance and recessiveness are simply properties of how alleles act and are not defined in terms of how common they are in the population. A good example of a rare dominant phenotype with Mendelian inheritance is pseudo-achondroplasia, a type of dwarfism ( ). In regard to this gene, people with normal stature are genotypically d /d , and the dwarf phenotype in principle could be D /d or D /D . However, it is believed that the two doses of the D allele in the D /D genotype produce such a severe effect that this is a lethal genotype. If this is true, all the dwarf individuals are heterozygotes.

The human pseudoachondroplasia phenotype, illustrated by a family of five sisters and two brothers. The phenotype is determined by a dominant allele, which we can call D , that interferes with bone growth during development. Most members of the human population (more...)

In pedigree analysis, the main clues for identifying a dominant disorder with Mendelian inheritance are that the phenotype tends to appear in every generation of the pedigree and that affected fathers and mothers transmit the phenotype to both sons and daughters. Again, the equal representation of both sexes among the affected offspring rules out sex-linked inheritance. The phenotype appears in every generation because generally the abnormal allele carried by a person must have come from a parent in the preceding generation. Abnormal alleles can arise de novo by the process of mutation. This event is relatively rare but must be kept in mind as a possibility. A typical pedigree for a dominant disorder is shown in . Once again, notice that Mendelian ratios are not necessarily observed in families. As with recessive disorders, persons bearing one copy of the rare A allele (A /a ) are much more common than those bearing two copies (A /A ), so most affected people are heterozygotes, and virtually all matings concerning dominant disorders are A /a a /a . Therefore, when the progeny of such matings are totaled, a 1:1 ratio is expected of unaffected (a /a ) to affected (A /a ) persons.

Pedigree of a dominant phenotype determined by a dominant allele A . In this pedigree, all the genotypes have been deduced.

Huntington disease is an example of a disease inherited as a dominant phenotype determined by an allele of a single gene. The phenotype is one of neural degeneration, leading to convulsions and premature death. However, it is a late-onset disease, the symptoms generally not appearing until after the person has begun to have children ( ). Each child of a carrier of the abnormal allele stands a 50 percent chance of inheriting the allele and the associated disease. This tragic pattern has led to a great effort to find ways of identifying people who carry the abnormal allele before they experience the onset of the disease. The application of molecular techniques has resulted in a promising screening procedure.

The age of onset of Huntington disease. The graph shows that people carrying the allele generally do not express the disease until after child-bearing age.

Some other rare dominant conditions are polydactyly (extra digits) and brachydactyly (short digits), shown in , and piebald spotting, shown in .

Some rare dominant phenotypes of the human hand. (a) (right) Polydactyly, a dominant phenotype characterized by extra fingers, toes, or both, determined by an allele P . The numbers in the accompanying pedigree (left) give the number of fingers in the (more...)

Piebald spotting, a rare dominant human phenotype. Although the phenotype is encountered sporadically in all races, the patterns show up best in those with dark skin. (a) The photographs show front and back views of affected persons IV-1, IV-3, III-5, (more...)

Pedigrees of Mendelian autosomal dominant disorders show affected males and females in each generation; they also show that affected men and women transmit the condition to equal proportions of their sons and daughters.

Phenotypes with X-linked recessive inheritance typically show the following patterns in pedigrees:

Many more males than females show the phenotype under study. This is because a female showing the phenotype can result only from a mating in which both the mother and the father bear the allele (for example, XA Xa Xa Y), whereas a male with the phenotype can be produced when only the mother carries the allele. If the recessive allele is very rare, almost all persons showing the phenotype are male.

None of the offspring of an affected male are affected, but all his daughters are carriers, bearing the recessive allele masked in the heterozygous condition. Half of the sons of these carrier daughters are affected ( ). Note that, in common X-linked phenotypes, this pattern might be obscured by inheritance of the recessive allele from a heterozygous mother as well as the father.

None of the sons of an affected male show the phenotype under study, nor will they pass the condition to their offspring. The reason behind this lack of male-to-male transmission is that a son obtains his Y chromosome from his father, so he cannot normally inherit the fathers X chromosome too.

Pedigree showing that X-linked recessive alleles expressed in males are then carried unexpressed by their daughters in the next generation, to be expressed again in their sons. Note that III-3 and III-4 cannot be distinguished phenotypically.

In the pedigree analysis of rare X-linked recessives, a normal female of unknown genotype is assumed to be homo-zygous unless there is evidence to the contrary.

Perhaps the most familiar example of X-linked recessive inheritance is red-green colorblindness. People with this condition are unable to distinguish red from green and see them as the same. The genes for color vision have been characterized at the molecular level. Color vision is based on three different kinds of cone cells in the retina, each sensitive to red, green, or blue wavelengths. The genetic determinants for the red and green cone cells are on the X chromosome. As with any X-linked recessive, there are many more males with the phenotype than females.

Another familiar example is hemophilia, the failure of blood to clot. Many proteins must interact in sequence to make blood clot. The most common type of hemophilia is caused by the absence or malfunction of one of these proteins, called Factor VIII. The most well known cases of hemophilia are found in the pedigree of interrelated royal families in Europe ( ). The original hemophilia allele in the pedigree arose spontaneously (as a mutation) either in the reproductive cells of Queen Victorias parents or of Queen Victoria herself. The son of the last czar of Russia, Alexis, inherited the allele ultimately from Queen Victoria, who was the grandmother of his mother Alexandra. Nowadays, hemophilia can be treated medically, but it was formerly a potentially fatal condition. It is interesting to note that, in the Jewish Talmud, there are rules about exemptions to male circumcision that show clearly that the mode of transmission of the disease through unaffected carrier females was well understood in ancient times. For example, one exemption was for the sons of women whose sisters sons had bled profusely when they were circumcised.

The inheritance of the X-linked recessive condition hemophilia in the royal families of Europe. A recessive allele causing hemophilia (failure of blood clotting) arose in the reproductive cells of Queen Victoria, or one of her parents, through mutation. (more...)

Duchenne muscular dystrophy is a fatal X-linked recessive disease. The phenotype is a wasting and atrophy of muscles. Generally the onset is before the age of 6, with confinement to a wheelchair by 12, and death by 20. The gene for Duchenne muscular dystrophy has now been isolated and shown to encode the muscle protein dystrophin. This discovery holds out hope for a better understanding of the physiology of this condition and, ultimately, a therapy.

A rare X-linked recessive phenotype that is interesting from the point of view of sexual differentiation is a condition called testicular feminization syndrome, which has a frequency of about 1 in 65,000 male births. People afflicted with this syndrome are chromosomally males, having 44 autosomes plus an X and a Y, but they develop as females ( ). They have female external genitalia, a blind vagina, and no uterus. Testes may be present either in the labia or in the abdomen. Although many such persons marry, they are sterile. The condition is not reversed by treatment with the male hormone androgen, so it is sometimes called androgen insensitivity syndrome. The reason for the insensitivity is that the androgen receptor malfunctions, so the male hormone can have no effect on the target organs that contribute to maleness. In humans, femaleness results when the male-determining system is not functional.

Four siblings with testicular feminization syndrome (congenital insensitivity to androgens). All four subjects in this photograph have 44 autosomes plus an X and a Y chromosome, but they have inherited the recessive X-linked allele conferring insensitivity to (more...)

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Human Genome Project – Wikipedia

Posted: at 4:07 am

The Human Genome Project (HGP) is an international scientific research project with the goal of determining the sequence of chemical base pairs which make up human DNA, and of identifying and mapping all of the genes of the human genome from both a physical and a functional standpoint.[1] It remains the world's largest collaborative biological project.[2] After the idea was picked up in 1984 by the US government when the planning started, with the project formally launched in 1990, and finally declared complete in 2003. Funding came from the US government through the National Institutes of Health (NIH) as well as numerous other groups from around the world. A parallel project was conducted outside of government by the Celera Corporation, or Celera Genomics, which was formally launched in 1998. Most of the government-sponsored sequencing was performed in twenty universities and research centers in the United States, the United Kingdom, Japan, France, Germany, Canada, and China.[3]

The Human Genome Project originally aimed to map the nucleotides contained in a human haploid reference genome (more than three billion). The "genome" of any given individual is unique; mapping the "human genome" involves sequencing multiple variations of each gene.[4] In May 2016, scientists considered extending the HGP to include creating a synthetic human genome.[5] In June 2016, scientists formally announced HGP-Write, a plan to synthesize the human genome.[6][7]

The Human Genome Project was a 13-year-long, publicly funded project initiated in 1990 with the objective of determining the DNA sequence of the entire euchromatic human genome within 15 years.[8] In May 1985, Robert Sinsheimer organized a workshop to discuss sequencing the human genome,[9] but for a number of reasons the NIH was uninterested in pursuing the proposal. The following March, the Santa Fe Workshop was organized by Charles DeLisi and David Smith of the Department of Energy's Office of Health and Environmental Research (OHER).[10] At the same time Renato Dulbecco proposed whole genome sequencing in an essay in Science.[11] James Watson followed two months later with a workshop held at the Cold Spring Harbor Laboratory.

The fact that the Santa Fe workshop was motivated and supported by a Federal Agency opened a path, albeit a difficult and tortuous one,[12] for converting the idea into public policy. In a memo to the Assistant Secretary for Energy Research (Alvin Trivelpiece), Charles DeLisi, who was then Director of OHER, outlined a broad plan for the project.[13] This started a long and complex chain of events which led to approved reprogramming of funds that enabled OHER to launch the Project in 1986, and to recommend the first line item for the HGP, which was in President Regan's 1988 budget submission,[12] and ultimately approved by the Congress. Of particular importance in Congressional approval was the advocacy of Senator Peter Domenici, whom DeLisi had befriended.[14] Domenici chaired the Senate Committee on Energy and Natural Resources, as well as the Budget Committee, both of which were key in the DOE budget process. Congress added a comparable amount to the NIH budget, thereby beginning official funding by both agencies.

Alvin Trivelpiece sought and obtained the approval of DeLisi's proposal by Deputy Secretary William Flynn Martin. This chart[15] was used in the spring of 1986 by Trivelpiece, then Director of the Office of Energy Research in the Department of Energy, to brief Martin and Under Secretary Joseph Salgado regarding his intention to reprogram $4 million to initiate the project with the approval of Secretary Herrington. This reprogramming was followed by a line item budget of $16 million in the Reagan Administrations 1987 budget submission to Congress.[16] It subsequently passed both Houses. The Project was planned for 15 years.[17]

Candidate technologies were already being considered for the proposed undertaking at least as early as 1985.[18]

In 1990, the two major funding agencies, DOE and NIH, developed a memorandum of understanding in order to coordinate plans and set the clock for the initiation of the Project to 1990.[19] At that time, David Galas was Director of the renamed Office of Biological and Environmental Research in the U.S. Department of Energys Office of Science and James Watson headed the NIH Genome Program. In 1993, Aristides Patrinos succeeded Galas and Francis Collins succeeded James Watson, assuming the role of overall Project Head as Director of the U.S. National Institutes of Health (NIH) National Center for Human Genome Research (which would later become the National Human Genome Research Institute). A working draft of the genome was announced in 2000 and the papers describing it were published in February 2001. A more complete draft was published in 2003, and genome "finishing" work continued for more than a decade.

The $3-billion project was formally founded in 1990 by the US Department of Energy and the National Institutes of Health, and was expected to take 15 years.[20] In addition to the United States, the international consortium comprised geneticists in the United Kingdom, France, Australia, China and myriad other spontaneous relationships.[21]

Due to widespread international cooperation and advances in the field of genomics (especially in sequence analysis), as well as major advances in computing technology, a 'rough draft' of the genome was finished in 2000 (announced jointly by U.S. President Bill Clinton and the British Prime Minister Tony Blair on June 26, 2000).[22] This first available rough draft assembly of the genome was completed by the Genome Bioinformatics Group at the University of California, Santa Cruz, primarily led by then graduate student Jim Kent. Ongoing sequencing led to the announcement of the essentially complete genome on April 14, 2003, two years earlier than planned.[23][24] In May 2006, another milestone was passed on the way to completion of the project, when the sequence of the last chromosome was published in Nature.[25]

The project did not aim to sequence all the DNA found in human cells. It sequenced only "euchromatic" regions of the genome, which make up about 90% of the genome. The other regions, called "heterochromatic" are found in centromeres and telomeres, and were not sequenced under the project.[26]

The Human Genome Project was declared complete in April 2003. An initial rough draft of the human genome was available in June 2000 and by February 2001 a working draft had been completed and published followed by the final sequencing mapping of the human genome on April 14, 2003. Although this was reported to be 99% of the euchromatic human genome with 99.99% accuracy a major quality assessment of the human genome sequence was published on May 27, 2004 indicating over 92% of sampling exceeded 99.99% accuracy which was within the intended goal.[27] Further analyses and papers on the HGP continue to occur.[28]

The sequencing of the human genome holds benefits for many fields, from molecular medicine to human evolution. The Human Genome Project, through its sequencing of the DNA, can help us understand diseases including: genotyping of specific viruses to direct appropriate treatment; identification of mutations linked to different forms of cancer; the design of medication and more accurate prediction of their effects; advancement in forensic applied sciences; biofuels and other energy applications; agriculture, animal husbandry, bioprocessing; risk assessment; bioarcheology, anthropology and evolution. Another proposed benefit is the commercial development of genomics research related to DNA based products, a multibillion-dollar industry.

The sequence of the DNA is stored in databases available to anyone on the Internet. The U.S. National Center for Biotechnology Information (and sister organizations in Europe and Japan) house the gene sequence in a database known as GenBank, along with sequences of known and hypothetical genes and proteins. Other organizations, such as the UCSC Genome Browser at the University of California, Santa Cruz,[29] and Ensembl[30] present additional data and annotation and powerful tools for visualizing and searching it. Computer programs have been developed to analyze the data, because the data itself is difficult to interpret without such programs. Generally speaking, advances in genome sequencing technology have followed Moores Law, a concept from computer science which states that integrated circuits can increase in complexity at an exponential rate.[31] This means that the speeds at which whole genomes can be sequenced can increase at a similar rate, as was seen during the development of the above-mentioned Human Genome Project.

The process of identifying the boundaries between genes and other features in a raw DNA sequence is called genome annotation and is in the domain of bioinformatics. While expert biologists make the best annotators, their work proceeds slowly, and computer programs are increasingly used to meet the high-throughput demands of genome sequencing projects. Beginning in 2008, a new technology known as RNA-seq was introduced that allowed scientists to directly sequence the messenger RNA in cells. This replaced previous methods of annotation, which relied on inherent properties of the DNA sequence, with direct measurement, which was much more accurate. Today, annotation of the human genome and other genomes relies primarily on deep sequencing of the transcripts in every human tissue using RNA-seq. These experiments have revealed that over 90% of genes contain at least one and usually several alternative splice variants, in which the exons are combined in different ways to produce 2 or more gene products from the same locus.[citation needed]

The genome published by the HGP does not represent the sequence of every individual's genome. It is the combined mosaic of a small number of anonymous donors, all of European origin. The HGP genome is a scaffold for future work in identifying differences among individuals. Subsequent projects sequenced the genomes of multiple distinct ethnic groups, though as of today there is still only one "reference genome."[citation needed]

Key findings of the draft (2001) and complete (2004) genome sequences include:

The Human Genome Project was started in 1990 with the goal of sequencing and identifying all three billion chemical units in the human genetic instruction set, finding the genetic roots of disease and then developing treatments. It is considered a Mega Project because the human genome has approximately 3.3 billion base-pairs. With the sequence in hand, the next step was to identify the genetic variants that increase the risk for common diseases like cancer and diabetes.[19][36]

It was far too expensive at that time to think of sequencing patients whole genomes. So the National Institutes of Health embraced the idea for a "shortcut", which was to look just at sites on the genome where many people have a variant DNA unit. The theory behind the shortcut was that, since the major diseases are common, so too would be the genetic variants that caused them. Natural selection keeps the human genome free of variants that damage health before children are grown, the theory held, but fails against variants that strike later in life, allowing them to become quite common. (In 2002 the National Institutes of Health started a $138 million dollar project called the HapMap to catalog the common variants in European, East Asian and African genomes.)[37]

The genome was broken into smaller pieces; approximately 150,000 base pairs in length.[36] These pieces were then ligated into a type of vector known as "bacterial artificial chromosomes", or BACs, which are derived from bacterial chromosomes which have been genetically engineered. The vectors containing the genes can be inserted into bacteria where they are copied by the bacterial DNA replication machinery. Each of these pieces was then sequenced separately as a small "shotgun" project and then assembled. The larger, 150,000 base pairs go together to create chromosomes. This is known as the "hierarchical shotgun" approach, because the genome is first broken into relatively large chunks, which are then mapped to chromosomes before being selected for sequencing.[38][39]

Funding came from the US government through the National Institutes of Health in the United States, and a UK charity organization, the Wellcome Trust, as well as numerous other groups from around the world. The funding supported a number of large sequencing centers including those at Whitehead Institute, the Sanger Centre, Washington University in St. Louis, and Baylor College of Medicine.[20][40]

The United Nations Educational, Scientific and Cultural Organization (UNESCO) served as an important channel for the involvement of developing countries in the Human Genome Project.[41]

In 1998, a similar, privately funded quest was launched by the American researcher Craig Venter, and his firm Celera Genomics. Venter was a scientist at the NIH during the early 1990s when the project was initiated. The $300,000,000 Celera effort was intended to proceed at a faster pace and at a fraction of the cost of the roughly $3 billion publicly funded project. The Celera approach was able to proceed at a much more rapid rate, and at a lower cost than the public project because it relied upon data made available by the publicly funded project.[42]

Celera used a technique called whole genome shotgun sequencing, employing pairwise end sequencing,[43] which had been used to sequence bacterial genomes of up to six million base pairs in length, but not for anything nearly as large as the three billion base pair human genome.

Celera initially announced that it would seek patent protection on "only 200300" genes, but later amended this to seeking "intellectual property protection" on "fully-characterized important structures" amounting to 100300 targets. The firm eventually filed preliminary ("place-holder") patent applications on 6,500 whole or partial genes. Celera also promised to publish their findings in accordance with the terms of the 1996 "Bermuda Statement", by releasing new data annually (the HGP released its new data daily), although, unlike the publicly funded project, they would not permit free redistribution or scientific use of the data. The publicly funded competitors were compelled to release the first draft of the human genome before Celera for this reason. On July 7, 2000, the UCSC Genome Bioinformatics Group released a first working draft on the web. The scientific community downloaded about 500 GB of information from the UCSC genome server in the first 24 hours of free and unrestricted access.[44]

In March 2000, President Clinton announced that the genome sequence could not be patented, and should be made freely available to all researchers. The statement sent Celera's stock plummeting and dragged down the biotechnology-heavy Nasdaq. The biotechnology sector lost about $50 billion in market capitalization in two days.

Although the working draft was announced in June 2000, it was not until February 2001 that Celera and the HGP scientists published details of their drafts. Special issues of Nature (which published the publicly funded project's scientific paper)[45] and Science (which published Celera's paper[46]) described the methods used to produce the draft sequence and offered analysis of the sequence. These drafts covered about 83% of the genome (90% of the euchromatic regions with 150,000 gaps and the order and orientation of many segments not yet established). In February 2001, at the time of the joint publications, press releases announced that the project had been completed by both groups. Improved drafts were announced in 2003 and 2005, filling in to approximately 92% of the sequence currently.

In the IHGSC international public-sector Human Genome Project (HGP), researchers collected blood (female) or sperm (male) samples from a large number of donors. Only a few of many collected samples were processed as DNA resources. Thus the donor identities were protected so neither donors nor scientists could know whose DNA was sequenced. DNA clones from many different libraries were used in the overall project, with most of those libraries being created by Pieter J. de Jong's lab. Much of the sequence (>70%) of the reference genome produced by the public HGP came from a single anonymous male donor from Buffalo, New York (code name RP11).[47][48]

HGP scientists used white blood cells from the blood of two male and two female donors (randomly selected from 20 of each) each donor yielding a separate DNA library. One of these libraries (RP11) was used considerably more than others, due to quality considerations. One minor technical issue is that male samples contain just over half as much DNA from the sex chromosomes (one X chromosome and one Y chromosome) compared to female samples (which contain two X chromosomes). The other 22 chromosomes (the autosomes) are the same for both sexes.

Although the main sequencing phase of the HGP has been completed, studies of DNA variation continue in the International HapMap Project, whose goal is to identify patterns of single-nucleotide polymorphism (SNP) groups (called haplotypes, or haps). The DNA samples for the HapMap came from a total of 270 individuals: Yoruba people in Ibadan, Nigeria; Japanese people in Tokyo; Han Chinese in Beijing; and the French Centre dEtude du Polymorphisme Humain (CEPH) resource, which consisted of residents of the United States having ancestry from Western and Northern Europe.

In the Celera Genomics private-sector project, DNA from five different individuals were used for sequencing. The lead scientist of Celera Genomics at that time, Craig Venter, later acknowledged (in a public letter to the journal Science) that his DNA was one of 21 samples in the pool, five of which were selected for use.[49][50]

In 2007, a team led by Jonathan Rothberg published James Watson's entire genome, unveiling the six-billion-nucleotide genome of a single individual for the first time.[51]

The work on interpretation and analysis of genome data is still in its initial stages. It is anticipated that detailed knowledge of the human genome will provide new avenues for advances in medicine and biotechnology. Clear practical results of the project emerged even before the work was finished. For example, a number of companies, such as Myriad Genetics, started offering easy ways to administer genetic tests that can show predisposition to a variety of illnesses, including breast cancer, hemostasis disorders, cystic fibrosis, liver diseases and many others. Also, the etiologies for cancers, Alzheimer's disease and other areas of clinical interest are considered likely to benefit from genome information and possibly may lead in the long term to significant advances in their management.[37][52]

There are also many tangible benefits for biologists. For example, a researcher investigating a certain form of cancer may have narrowed down his/her search to a particular gene. By visiting the human genome database on the World Wide Web, this researcher can examine what other scientists have written about this gene, including (potentially) the three-dimensional structure of its product, its function(s), its evolutionary relationships to other human genes, or to genes in mice or yeast or fruit flies, possible detrimental mutations, interactions with other genes, body tissues in which this gene is activated, and diseases associated with this gene or other datatypes. Further, deeper understanding of the disease processes at the level of molecular biology may determine new therapeutic procedures. Given the established importance of DNA in molecular biology and its central role in determining the fundamental operation of cellular processes, it is likely that expanded knowledge in this area will facilitate medical advances in numerous areas of clinical interest that may not have been possible without them.[53]

The analysis of similarities between DNA sequences from different organisms is also opening new avenues in the study of evolution. In many cases, evolutionary questions can now be framed in terms of molecular biology; indeed, many major evolutionary milestones (the emergence of the ribosome and organelles, the development of embryos with body plans, the vertebrate immune system) can be related to the molecular level. Many questions about the similarities and differences between humans and our closest relatives (the primates, and indeed the other mammals) are expected to be illuminated by the data in this project.[37][54]

The project inspired and paved the way for genomic work in other fields, such as agriculture. For example, by studying the genetic composition of Tritium aestivum, the worlds most commonly used bread wheat, great insight has been gained into the ways that domestication has impacted the evolution of the plant.[55] Which loci are most susceptible to manipulation, and how does this play out in evolutionary terms? Genetic sequencing has allowed these questions to be addressed for the first time, as specific loci can be compared in wild and domesticated strains of the plant. This will allow for advances in genetic modification in the future which could yield healthier, more disease-resistant wheat crops.

At the onset of the Human Genome Project several ethical, legal, and social concerns were raised in regards to how increased knowledge of the human genome could be used to discriminate against people. One of the main concerns of most individuals was the fear that both employers and health insurance companies would refuse to hire individuals or refuse to provide insurance to people because of a health concern indicated by someone's genes.[56] In 1996 the United States passed the Health Insurance Portability and Accountability Act (HIPAA) which protects against the unauthorized and non-consensual release of individually identifiable health information to any entity not actively engaged in the provision of healthcare services to a patient.[57]

Along with identifying all of the approximately 20,00025,000 genes in the human genome, the Human Genome Project also sought to address the ethical, legal, and social issues that were created by the onset of the project. For that the Ethical, Legal, and Social Implications (ELSI) program was founded in 1990. Five percent of the annual budget was allocated to address the ELSI arising from the project.[20][58] This budget started at approximately $1.57 million in the year 1990, but increased to approximately $18 million in the year 2014. [59]

Whilst the project may offer significant benefits to medicine and scientific research, some authors have emphasised the need to address the potential social consequences of mapping the human genome. "Molecularising disease and their possible cure will have a profound impact on what patients expect from medical help and the new generation of doctors' perception of illness."[60]

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En Route to Mars, The Moon | Science Mission Directorate

Posted: October 17, 2016 at 1:20 am

En route to Mars, the Moon

Why colonize the Moon before going to Mars? NASA scientists give their reasons.

March 18, 2005: NASA has a new Vision for Space Exploration: in the decades ahead, humans will land on Mars and explore the red planet. Brief visits will lead to longer stays and, maybe one day, to colonies.

Why the Moon before Mars?

"The Moon is a natural first step," explains Philip Metzger, a physicist at NASA Kennedy Space Center. "It's nearby. We can practice living, working and doing science there before taking longer and riskier trips to Mars."

Right: The Moon, an alien world in Earth's backyard. Photo credit: International Space Station astronaut Leroy Chiao. [More]

The Moon and Mars have a lot in common. The Moon has only one-sixth Earth's gravity; Mars has one-third. The Moon has no atmosphere; the Martian atmosphere is highly rarefied. The Moon can get very cold, as low as -240o C in shadows; Mars varies between -20o and -100o C.

Even more important, both planets are covered with silt-fine dust, called "regolith." The Moon's regolith was created by the ceaseless bombardment of micrometeorites, cosmic rays and particles of solar wind breaking down rocks for billions of years. Martian regolith resulted from the impacts of more massive meteorites and even asteroids, plus ages of daily erosion from water and wind. There are places on both worlds where the regolith is 10+ meters deep.

Answering these questions on Earth isn't easy. Moondust and Mars dust is so ... alien.

Try this: Run your finger across the screen of your computer. You'll get a little residue of dust clinging to your fingertip. It's soft and fuzzy--that's Earth dust.

Lunar dust is different: "It's almost like fragments of glass or coral--odd shapes that are very sharp and interlocking," says Metzger. (

"Even after short moon walks, Apollo 17 astronauts found dust particles had jammed the shoulder joints of their spacesuits," says Masami Nakagawa, associate professor in the mining engineering department of the Colorado School of Mines. "Moondust penetrated into seals, causing the spacesuits to leak some air pressure."

Above: Dust flies from the tires of a moon buggy, driven by Apollo 17 astronaut Gene Cernan. These "rooster-tails" of dust caused problems, which the astronauts solved using duct tape. [More]

In sunlit areas, adds Nakagawa, fine dust levitated above the Apollo astronauts' knees and even above their heads, because individual particles were electrostatically charged by the Sun's ultraviolet light. Such dust particles, when tracked into the astronauts' habitat where they would become airborne, irritated their eyes and lungs. "It's a potentially serious problem."

Dust is also ubiquitous on Mars, although Mars dust is probably not as sharp as moondust. Weathering smooths the edges. Nevertheless, Martian duststorms whip these particles 50 m/s (100+ mph), scouring and wearing every exposed surface. As the rovers Spirit and Opportunity have revealed, Mars dust (like moondust) is probably electrically charged. It clings to solar panels, blocks sunlight and reduces the amount of power that can be generated for a surface mission.

For these reasons, NASA is funding Nakagawa's Project Dust, a four-year study dedicated to finding ways of mitigating the effects of dust on robotic and human exploration, ranging from designs of air filters to thin-film coatings that repel dust from spacesuits and machinery.

The Moon is also a good testing ground for what mission planners call "in-situ resource utilization" (ISRU)--a.k.a. "living off the land." Astronauts on Mars are going to want to mine certain raw materials locally: oxygen for breathing, water for drinking and rocket fuel (essentially hydrogen and oxygen) for the journey home. "We can try this on the Moon first," says Metzger.

Both the Moon and Mars are thought to harbor water frozen in the ground. The evidence for this is indirect. NASA and ESA spacecraft have detected hydrogen--presumably the H in H2O--in Martian soil. Putative icy deposits range from the Martian poles almost to the equator. Lunar ice, on the other hand, is localized near the Moon's north and south poles deep inside craters where the Sun never shines, according to similar data from Lunar Prospector and Clementine, two spacecraft that mapped the Moon in the mid-1990s.

If this ice could be excavated, thawed out and broken apart into hydrogen and oxygen ... Voila! Instant supplies. NASA's Lunar Reconnaissance Orbiter, due to launch in 2008, will use modern sensors to search for deposits and pinpoint possible mining sites.

"The lunar poles are a cold place, so we've been working with people who specialize in cold places to figure out how to land on the soils and dig into the permafrost to excavate water," Metzger says. Prime among NASA's partners are investigators from the Army Corps of Engineers' Cold Regions Research and Engineering Laboratory (CRREL). Key challenges include ways of landing rockets or building habitats on ice-rich soils without having their heat melt the ground so it collapses under their weight.

Testing all this technology on the Moon, which is only 2 or 3 days away from Earth, is going to be much easier than testing it on Mars, six months away.

So ... to Mars! But first, the Moon.

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Gaiam TV is now Gaia

Posted: at 1:20 am

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How to increase serotonin in the human brain without drugs

Posted: at 1:20 am

For the last 4 decades, the question of how to manipulate the serotonergic system with drugs has been an important area of research in biological psychiatry, and this research has led to advances in the treatment of depression. Research on the association between various polymorphisms and depression supports the idea that serotonin plays a role, not only in the treatment of depression but also in susceptibility to depression and suicide. The research focus here has been on polymorphisms of the serotonin transporter, but other serotonin-related genes may also be involved.15 In the future, genetic research will make it possible to predict with increasing accuracy who is susceptible to depression. Much less attention has been given to how this information will be used for the benefit of individuals with a serotonin-related susceptibility to depression, and little evidence exists concerning strategies to prevent depression in those with such a susceptibility. Various studies have looked at early intervention in those with prodromal symptoms as well as at population strategies for preventing depression.611 Obviously, prevention is preferable to early intervention; moreover, although population strategies are important, they are ideally supplemented with preventive interventions that can be used over long periods of time in targeted individuals who do not yet exhibit even nonclinical symptoms. Clearly, pharmacologic approaches are not appropriate, and given the evidence for serotonin's role in the etiology and treatment of depression, nonpharmacologic methods of increasing serotonin are potential candidates to test for their ability to prevent depression.

Another reason for pursuing nonpharmacologic methods of increasing serotonin arises from the increasing recognition that happiness and well-being are important, both as factors protecting against mental and physical disorders and in their own right.1214 Conversely, negative moods are associated with negative outcomes. For example, the negative mood hostility is a risk factor for many disorders. For the sake of brevity, hostility is discussed here mainly in relation to one of the biggest sources of mortality, coronary heart disease (CHD). A meta-analysis of 45 studies demonstrated that hostility is a risk factor for CHD and for all-cause mortality.15 More recent research confirms this. Hostility is associated not only with the development of CHD but also with poorer survival in coronary artery disease (CAD) patients.16 Hostility may lead to decreased social support and social isolation,17 and low perceived social support is associated with greater mortality in those with CAD.18 Effects are not just limited to CHD. For example, the opposite of hostility, agreeableness, was a significant protective factor against mortality in a sample of older, frail participants.19

The constitution of the WHO states Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.20 This may sound exaggerated but positive mood within the normal range is an important predictor of health and longevity. In a classic study, those in the lowest quartile for positive emotions, rated from autobiographies written at a mean age of 22 years, died on average 10 years earlier than those in the highest quartile.21 Even taking into account possible confounders, other studies found the same solid link between feeling good and living longer.12 In a series of recent studies, negative emotions were associated with increased disability due to mental and physical disorders,22 increased incidence of depression,23 increased suicide24 and increased mortality25 up to 2 decades later. Positive emotions protected against these outcomes. A recent review including meta-analyses assessed cross-sectional, longitudinal and experimental studies and concluded that happiness is associated with and precedes numerous successful outcomes.26 Mood may influence social behaviour, and social support is one of the most studied psychosocial factors in relation to health and disease.27 Low social support is associated with higher levels of stress, depression, dysthymia and posttraumatic stress disorder and with increased morbidity and mortality from a host of medical illnesses.27

Research confirms what might be intuitively expected, that positive emotions and agreeableness foster congenial relationships with others.28,29 This in turn will create the conditions for an increase in social support.

Several studies found an association between measures related to serotonin and mood in the normal range. Lower platelet serotonin2 receptor function was associated with lower mood in one study,30 whereas better mood was associated with higher blood serotonin levels in another.31 Two studies found that greater prolactin release in response to fenfluramine was associated with more positive mood.32,33 The idea that these associations indicate a causal association between serotonin function and mood within the normal range is consistent with a study demonstrating that, in healthy people with high trait irritability, tryptophan, relative to placebo, decreased quarrelsome behaviours, increased agreeable behaviours and improved mood.34 Serotonin may be associated with physical health as well as mood. In otherwise healthy individuals, a low prolactin response to the serotonin-releasing drug fenfluramine was associated with the metabolic syndrome, a risk factor for heart disease,35 suggesting that low serotonin may predispose healthy individuals to suboptimal physical as well as mental functioning.

Nonpharmacologic methods of raising brain serotonin may not only improve mood and social functioning of healthy people a worthwhile objective even without additional considerations but would also make it possible to test the idea that increases in brain serotonin may help protect against the onset of various mental and physical disorders. Four strategies that are worth further investigation are discussed below.

The article by Perreau-Linck and colleagues36 (page 430 of this issue) provides an initial lead about one possible strategy for raising brain serotonin. Using positron emission tomography, they obtained a measure of serotonin synthesis in the brains of healthy participants who underwent positive, negative and neutral mood inductions. Reported levels of happiness were positively correlated and reported levels of sadness were negatively correlated with serotonin synthesis in the right anterior cingulate cortex. The idea that alterations in thought, either self-induced or due to psychotherapy, can alter brain metabolism is not new. Numerous studies have demonstrated changes in blood flow in such circumstances. However, reports related to specific transmitters are much less common. In one recent study, meditation was reported to increase release of dopamine.37 The study by Perreau-Linck and colleagues36 is the first to report that self-induced changes in mood can influence serotonin synthesis. This raises the possibility that the interaction between serotonin synthesis and mood may be 2-way, with serotonin influencing mood and mood influencing serotonin. Obviously, more work is needed to answer questions in this area. For example, is the improvement in mood associated with psychotherapy accompanied by increases in serotonin synthesis? If more precise information is obtained about the mental states that increase serotonin synthesis, will this help to enhance therapy techniques?

Exposure to bright light is a second possible approach to increasing serotonin without drugs. Bright light is, of course, a standard treatment for seasonal depression, but a few studies also suggest that it is an effective treatment for nonseasonal depression38 and also reduces depressed mood in women with premenstrual dysphoric disorder39 and in pregnant women suffering from depression.40 The evidence relating these effects to serotonin is indirect. In human postmortem brain, serotonin levels are higher in those who died in summer than in those who died in winter.41 A similar conclusion came from a study on healthy volunteers, in which serotonin synthesis was assessed by measurements of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the venous outflow from the brain.42 There was also a positive correlation between serotonin synthesis and the hours of sunlight on the day the measurements were made, independent of season. In rats, serotonin is highest during the light part of the lightdark cycle, and this state is driven by the photic cycle rather than the circadian rhythm.43,44 The existence of a retinoraphe tract may help explain why, in experimental animals, neuronal firing rates, c-fos expression and the serotonin content in the raphe nuclei are responsive to retinal light exposure.4448 In humans, there is certainly an interaction between bright light and the serotonin system. The mood-lowering effect of acute tryptophan depletion in healthy women is completely blocked by carrying out the study in bright light (3000 lux) instead of dim light.49

Relatively few generations ago, most of the world population was involved in agriculture and was outdoors for much of the day. This would have resulted in high levels of bright light exposure even in winter. Even on a cloudy day, the light outside can be greater than 1000 lux, a level never normally achieved indoors. In a recent study carried out at around latitude 45 N, daily exposure to light greater than 1000 lux averaged about 30 minutes in winter and only about 90 minutes in summer50 among people working at least 30 hours weekly; weekends were included. In this group, summer bright light exposure was probably considerably less than the winter exposure of our agricultural ancestors. We may be living in a bright lightdeprived society. A large literature that is beyond the scope of this editorial exists on the beneficial effect of bright light exposure in healthy individuals. Lamps designed for the treatment of seasonal affective disorder, which provide more lux than is ever achieved by normal indoor lighting, are readily available, although incorporating their use into a daily routine may be a challenge for some. However, other strategies, both personal and institutional, exist. Light cafes pioneered in Scandinavia have come to the United Kingdom,51 and an Austrian village that receives no sunshine in the winter because of its surrounding mountains is building a series of giant mirrors to reflect sunlight into the valley.52 Better use of daylight in buildings is an issue that architects are increasingly aware of. Working indoors does not have to be associated with suboptimal exposure to bright light.

A third strategy that may raise brain serotonin is exercise. A comprehensive review of the relation between exercise and mood concluded that antidepressant and anxiolytic effects have been clearly demonstrated.53 In the United Kingdom the National Institute for Health and Clinical Excellence, which works on behalf of the National Health Service and makes recommendations on treatments according to the best available evidence, has published a guide on the treatment of depression.54 The guide recommends treating mild clinical depression with various strategies, including exercise rather than antidepressants, because the riskbenefit ratio is poor for antidepressant use in patients with mild depression. Exercise improves mood in subclinical populations as well as in patients. The most consistent effect is seen when regular exercisers undertake aerobic exercise at a level with which they are familiar.53 However, some skepticism remains about the antidepressant effect of exercise, and the National Institute of Mental Health in the United States is currently funding a clinical trial of the antidepressant effect of exercise that is designed to overcome sources of potential bias and threats to internal and external validity that have limited previous research.55

Several lines of research suggest that exercise increases brain serotonin function in the human brain. Post and colleagues56 measured biogenic amine metabolites in cerebrospinal fluid (CSF) of patients with depression before and after they increased their physical activity to simulate mania. Physical activity increased 5-HIAA, but it is not clear that this was due to increased serotonin turnover or to mixing of CSF from higher regions, which contain higher levels of 5-HIAA, with lumbar CSF (or to a combination of both mechanisms). Nonetheless, this finding stimulated many animal studies on the effects of exercise. For example, Chaouloff and colleagues57 showed that exercise increased tryptophan and 5-HIAA in rat ventricles. More recent studies using intracerebral dialysis have shown that exercise increases extracellular serotonin and 5-HIAA in various brain areas, including the hippocampus and cortex (for example, see5860). Two different mechanisms may be involved in this effect. As reviewed by Jacobs and Fornal,61 motor activity increases the firing rates of serotonin neurons, and this results in increased release and synthesis of serotonin.62 In addition, there is an increase in the brain of the serotonin precursor tryptophan that persists after exercise.63

The largest body of work in humans looking at the effect of exercise on tryptophan availability to the brain is concerned with the hypothesis that fatigue during exercise is associated with elevated brain tryptophan and serotonin synthesis. A large body of evidence supports the idea that exercise, including exercise to fatigue, is associated with an increase in plasma tryptophan and a decrease in the plasma level of the branched chain amino acids (BCAAs) leucine, isoleucine and valine (see64,65 for reviews). The BCAAs inhibit tryptophan transport into the brain.66 Because of the increase in plasma tryptophan and decrease in BCAA, there is a substantial increase in tryptophan availability to the brain. Tryptophan is an effective mild hypnotic,67 a fact that stimulated the hypothesis that it may be involved in fatigue. A full discussion of this topic is not within the scope of this editorial; however, it is notable that several clinical trials of BCAA investigated whether it was possible to counter fatigue by lowering brain tryptophan, with results that provided little support for the hypothesis. Further, exercise results in an increase in the plasma ratio of tryptophan to the BCAAs before the onset of fatigue.64,65 The conclusion of these studies is that, in humans, a rise in precursor availability should increase serotonin synthesis during and after exercise and that this is not related to fatigue, although it may be related to improved mood. Whether motor activity increases the firing rate of serotonin neurons in humans, as in animals, is not known. However, it is clear that aerobic exercise can improve mood.

As with exposure to bright light, there has been a large change in the level of vigorous physical exercise experienced since humans were hunter-gatherers or engaged primarily in agriculture.68 Lambert68 argued that the decline in vigorous physical exercise and, in particular, in effort-based rewards may contribute to the high level of depression in today's society. The effect of exercise on serotonin suggests that the exercise itself, not the rewards that stem from exercise, may be important. If trials of exercise to prevent depression are successful, then prevention of depression can be added to the numerous other benefits of exercise.

The fourth factor that could play a role in raising brain serotonin is diet. According to some evidence, tryptophan, which increases brain serotonin in humans as in experimental animals,69 is an effective antidepressant in mild-to-moderate depression.67,70 Further, in healthy people with high trait irritability, it increases agreeableness, decreases quarrelsomeness and improves mood.34 However, whether tryptophan should be considered primarily as a drug or a dietary component is a matter of some dispute. In the United States, it is classified as a dietary component, but Canada and some European countries classify it as a drug. Treating tryptophan as a drug is reasonable because, first, there is normally no situation in which purified tryptophan is needed for dietary reasons, and second, purified tryptophan and foods containing tryptophan have different effects on brain serotonin. Although purified tryptophan increases brain serotonin, foods containing tryptophan do not.71 This is because tryptophan is transported into the brain by a transport system that is active toward all the large neutral amino acids and tryptophan is the least abundant amino acid in protein. There is competition between the various amino acids for the transport system, so after the ingestion of a meal containing protein, the rise in the plasma level of the other large neutral amino acids will prevent the rise in plasma tryptophan from increasing brain tryptophan. The idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false. Another popular myth that is widespread on the Internet is that bananas improve mood because of their serotonin content. Although it is true that bananas contain serotonin, it does not cross the bloodbrain barrier.

-Lactalbumin, a minor constituent of milk, is one protein that contains relatively more tryptophan than most proteins. Acute ingestion of -lactalbumin by humans can improve mood and cognition in some circumstances, presumably owing to increased serotonin.72,73 Enhancing the tryptophan content of the diet chronically with -lactalbumin is probably not practical. However, increasing the tryptophan content of the diet relative to that of the other amino acids is something that possibly occurred in the past and could occur again in the future. Kerem and colleagues74 studied the tryptophan content of both wild chickpeas and the domesticated chickpeas that were bred from them in the Near East in neolithic times. The mean protein content (per mg dry seed) was similar for 73 cultivars and 15 wild varieties. In the cultivated group, however, the tryptophan content was almost twice that of the wild seeds. Interestingly, the greater part of the increase was due to an increase in the free tryptophan content (i.e., not part of the protein). In cultivated chickpeas, almost two-thirds of the tryptophan was in the free form. Kerem and colleagues74 argue that there was probably selection for seeds with a higher tryptophan content. This is plausible, given another example of an early strategy to increase the available tryptophan content of an important food source. Pellagra is a disorder caused by niacin deficiency, usually owing to poverty and a diet relying heavily on corn (maize), which has a low level of niacin and its precursor tryptophan. Cultures in the Americas that relied greatly on corn used alkali during its processing (e.g., boiling the corn in lime when making tortillas). This enhanced the nutritional quality of the corn by increasing the bioavailability of both niacin and tryptophan, a practice that prevented pellagra.75 The Europeans transported corn around the world but did not transport the traditional alkali-processing methods, thereby causing epidemics of pellagra in past centuries. Breeding corn with a higher tryptophan content was shown in the 1980s to prevent pellagra76; presumably, it also raised brain serotonin. In a recent issue of Nature Biotechnology, Morris and Sands77 argue that plant breeders should be focusing more on nutrition than on yield. They ask, Could consumption of tryptophan-rich foods play a role in reducing the prevalence of depression and aggression in society? Cross-national studies have reported a positive association between corn consumption and homicide rates78 and a negative association between dietary tryptophan and suicide rates.79 Although the idea behind such studies is interesting, any causal attribution must remain speculative, given the possible confounds. Nonetheless, the possibility that the mental health of a population could be improved by increasing the dietary intake of tryptophan relative to the dietary intake of other amino acids remains an interesting idea that should be explored.

The primary purpose of this editorial is to point out that pharmacologic strategies are not the only ones worthy of study when devising strategies to increase brain serotonin function. The effect of nonpharmacologic interventions on brain serotonin and the implications of increased serotonin for mood and behaviour need to be studied more. The amount of money and effort put into research on drugs that alter serotonin is very much greater than that put into non-pharmacologic methods. The magnitude of the discrepancy is probably neither in tune with the wishes of the public nor optimal for progress in the prevention and treatment of mental disorders.

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A friend asked me about population structure, and methods to ferret it out and classify it. So here is a quick survey on the major methods Im familiar with/utilize now and then. Ill go roughly in chronological order.

First, you have trees. These are pretty popular from macroevolutionary relationships, but on the population genetic scale (intraspecific, microevolutionary) youre mostly talking about representing distances between groups in a tree format. You saw this in History and Geography of Genes, where genetic distances in the form of Fst values (proportion of genetic variation unique to between two groups) were used as distance inputs.

A problem with trees is that they dont model gene flow, a major dynamic on a microevolutionary scale. Also, complex relationships can get elided in tree frameworks, and as you add more and more populations you often end up with an incomprehensible fan-like topology.

Then you have principle component analyses (PCA) and related methods (e.g., multidimensional scaling, which is very different in the sausage-making but generates a similar output). Like trees, this is a visualization of the variation, in this case on a two dimensional plot (please dont bring up three dimensional PCA, theres no such thing until holograms show up).

The problem with PCA is that different types of dynamics can lead to the same result. For example, someone who is an F1 of two distinct groups occupies the same position as a population which happens to occupy a genetic position between two groups. Additionally, by constraining the variation into two dimensions, one can mislead in terms of relationships. There are many dimensions, but operationally you focus on on two at a time.

A paper of interest, Population Structure and Eigenanalysis.

Next you have model-based clustering introduced in Jonathan Pritchards Inference of Population Structure Using Multilocus Genotype Data. There are many flavors of this, but they operate under the same framework. You have a model of population dynamics, and see how the genotype data can be explained by parameters of the model. Of particular interest is assignment to one of K populations, which can be combined to explain the variation in the data.

Unlike PCA these model-based methods are rather good at identifying people who are first generation mixes, as opposed to those from stabilized groups along a cline. But, they also produce artifacts, because they are quite sensitive to the input data, and lend themselves to cherry-picking.

Earlier I said that one problem with the tree methods is that they dont model gene flow. Joe Pickrells TreeMix does so. Like the original tree methods, and unlike PCA or unsupervised model-based clustering, you specify a set of populations. Then you compare the populations in terms of their genetic distance, and fit them to a tree, but add migration parameters to that tree where the fit between the tree and the data is the most tenuous fit.

All visualizations are deformations of reality. TreeMix attempts to mitigate this somewhat by introducing another representation, that of migration.

Next we have local ancestry methods. By local ancestry, basically we mean methods which can assign ancestry to particular regions of the genome. While tree methods measure differences across pooled populations, PCA and model-based methods compare genotypes between individuals (this is a simplification, but bear with me). Local ancestry methods, like RFMix, compare regions of the genome with each other.

Related to, but not exactly the same, as local ancestry methods are haplotype based methods. In particular, Im thinking of the FineStructure and its related methods. These leverage variation across the genome in terms of haplotypes, rather than just looking at genotypes. They also tend to benefit from phasing, for obvious methods. FineStructure and its relatives tend to need more marker density than model-based methods, which require more marker density than PCA, which requires more marker density that tree based methods. These haplotype based methods allow for correction of and accounting for forces such as genetic drift, which tend to skew results in other methods.

Finally, there is the AdmixTools framework which is good for testing very explicit hypotheses. While many of the above methods, such as TreeMix and unsupervised model-based clustering, explore an almost open-ended space of structure possibilities, the methods in AdmixTools exists in large part to test narrow delimited models. This goes to the fact that many of these methods are complementary, and you should use them together to arrive at a robust result. For example, if you are assigning populations for TreeMix, you should use PCA and model-based clustering to make sure that the populations are clear and distinct, and outliers are removed.

Theres a lot I left out, but many of the other methods are just twists on the ones above.

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Tamil Siddar BHOGAR – Kundalini Yoga and Spiritual Alchemy

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Click on pictures at right to visit: The Life of Bhogar in Pictures.

Patanjali Raja Yoga was his student.

All these we teach in Energy Enhancement.

Bhoganthar or Bhogar, the Jna Guru of Babaji, in the poem Bhogar Jna Sagarama (Bhogars Oceanic Life Story, consisting of 557 verses, verse number 2, lines number 3 and 4), identifies himself as a Tamilian, (Ramaiah, 1979; 1982. p. 17).[1] In the same verse he states that the great Siddha Klangi Nthar initiated him in Jna Yoga (supreme self-knowledge).

Klangi Nthar was born in Kai (Benares). He attained the immortal state of swarpa samdhi at the ago of 315, and then made China the center of his teaching activities. He belonged to the ancient tradition of Nava (nine) Nth sadhus (holy ascetics), tracing their tradition to Lord Shiva. There are nine important shrines associated with this tradition, five of which are in the Himlaya Mountains: Amarnth (where Shiva first taught Kriya Yoga to his Shakti partner, Parvati Devi), Kedarnth, Badrinth (India), Kailsanth, (Tibet) and Paupatinth (Nepal).

Meanwhile, Bhoganthar practiced Kundalini Yoga in four stages. The first three stages arc described in a later chapter on The Psychophysiology of Kriya Kundalini Pranayama. Bhoganthar chose the Palani Malai (mountain) in what is now southwestern Tamil Nadu as the site for intensive yogic practice (tapas) for the final stage. He attained swarpa samdhi at Palani, through the grace of Lord Muruga, or the eternal youth, Kumra Swmi. The Kumraswmi temple at Palani became the epicenter of his activities.

He visited many countries astrally, and physically and through transmigration leaving his body to enter into the body of another.

In one of his songs Bhoganthar claims to have flown to China at one point in a sort of airplane which he built: he held discussions with Chinese Siddhas before returning to India (Kailasapathy, 1969, p. 197-211). His visit to South America has been confirmed by accounts left by the Muycas of Chile:

He convened a meeting of many siddhas just before the beginning of the present Kali Yuga, in 3102 BC, to determine the best way for humanity to progress along the spiritual path during the coming period of darkness.

The Yoga of love and devotion, Bhakti Yoga, was chosen as being the best means. Bhoganthar was entrusted by the siddhas with the task of defining the rituals for the worship of their favorite deity Palani ndavar, the Lord (Muruga) of Palani.

Many rituals that center around the bathing (abhishekam) of an idol of Palani Andavar with many substances, including panchaamirtam consisting of five fruits and honey, were developed by him and continue to be followed to this day. The idol had to be created from a substance that would last throughout Kali Yuga. The most resilient of known substances, granite, was known to wear and crack after thousands of such rituals. So Bhoganthar fashioned it out of nine secret herbal and chemical ingredients, nava pashanam, which made it harder than granite. Eight of the ingredients were combined in a mold of the idol. The ninth, was added as a catalyst, to solidify it.

In recent times the scientists who attempted to determine the composition of a small sample of the material of the idol, were startled to find that it immediately sublimated when heated. Thus its composition remains a mystery to date. The traces of the substance are contained in the ritual offerings in which it is bathed. When these are returned and consumed by the devotee, their spiritual progress is enhanced.

Klangi Nthar decided to enter into samdhi in seclusion for 3,000 years. He summoned Bhoganthar telepathically from Tamil Nadu to China to take over his mission. Bhoganthar traveled by sea, following the trade route. In China, he was instructed by Klangi Nthar in all aspects of the Siddha sciences.

These included the preparation and use of the kaya kalpa herbal formulae to promote longevity.

After Klangi Nthar entered into trance, Bhoganthar assumed his teaching mission to the Chinese. To facilitate this, he transmigrated his vital body into the physical body of a deceased Chinese man, and thereafter went by the name Bo-Yang. Bo is a derivation of the word Bhogam which means bliss, material and spiritual.

This bliss, for which he was named Bo-Yang is experienced when the Kundalini shakti, the feminine primordial yin energy awakens, passes up to the crown of the head, the seat of Shiva, the masculine yang pole, in the Sahasra cakra at the summit of the head and unites with it.

The result of this integration of feminine and masculine parts of the being, or union (Yoga) of Shakti and Shiva, Yin and Yang, is Satchidananda: Absolute Existence-Consciousness-Bliss.

Bhoganthar decided to overcome the limitations of the Chinese body, with its degenerative tendencies, and prolong its life through the use of the kaya kalpa herbs long enough for the effect of Kriya Kundalini Pranayama and related yogic techniques to bring swarpa samdhi.

In his poem Bhogar Jna Sutra 8, verse number 4, he describes vividly what happened after carefully preparing a tablet using thirty five different herbs:

With great care and patience I made the (kaya kalpa) tablet and then swallowed it: Not waiting for fools and skeptics who would not appreciate its hidden meaning and importance. Steadily I lived in the land of the parangis (foreigners) For twelve thousand years, my fellow! I lived for a long time and fed on the vital ojas (sublimated spiritual energy) With the ojas vindhu I received the name, Bhogar: The body developed the golden color of the pill: Now I am living in a world of gold (based upon translation by Yogi S.A.A. Ramaiah, 1979, p. 40-42).

He chose three of his best disciples and his faithful dog, and took thorn to the top of a mountain. After first offering a tablet to the dog, the dog immediately fell over dead. He next offered it to his leading disciple, Yu, who also immediately fell over dead. After offering it to the two remaining disciples, who by this time were extremely nervous, and who promptly hid their tablets rather than swallow them, Bhoganthar swallowed the remaining tablets and also fell over unconscious. Crying with grief, the two remaining disciples went down the mountain to get material to bury the bodies. When the disciples returned to the spot where the bodies had been left lying, all that was found was a note, in Bhoganthars handwriting, which said:

The kaya kalpa tablets are working. After awakening from their trance I restored faithful Yu and the dog. You have missed your chance for immortality. (Ibid.)

This kaya kalpa enabled Bhoganthar to transform the Chinese body over a period of 12,000 years, during which time it developed a lustrous golden color. (The physiological transformation to the state of swarpa samdhi was, however, completed only later, at Palani in the final phases of Kriya Kundalini Yoga and related practices. These phases will be described in chapter 11. Bhoganthars own graphic description is recorded in the poem at the end of this chapter Initiation into Samdhi.)

In this poem Sutras of Wisdom 8. he sings prophetically of the taking up of the practice of pranayama in modern times by millions of persons who would otherwise have succumbed to drug abuse:

Will chant the unifying verse of the Vedanta. Glory to the holy feet of Uma (the Divine Mother of the Universe. Shakti), Will instruct you in the knowledge of the sciences, ranging from hypnotism to alchemy (kaya kalpa). Without the need for pills or tablets, the great scientific art of pranayama breathing, will be taught and recognized By millions of common people and chaste young women. Verse no. I (based upon translation by Yogi S.A.A. Ramaiah, 1982, p. 40).

After this incident with the Chinese disciples, Bo-Yang became also known as Lao-Tzu, and was accessible for nearly 200 years, and trained hundreds of Chinese disciples in Tantric Yoga practices, wherein semen and sexual energies are conserved and sublimated into spiritual energies. The advanced techniques which he taught involve raising the energies from the mladhra cakra corresponding to the perineum up to the sahasrara cakra during sexual intercourse with a spiritually minded partner, resulting in sublimated energy, tejas. manifesting throughout all the cells of the body.

In the fifth century B.C., Confucius met Lao-Tzu Bo-Yang and afterwards said of him:

I know a bird can fly, a fish can swim, and an animal can run. For that which runs, a net can be fashioned; for that which swims, a line can be strung. But the ascent of a Dragon on the wind into heaven is something which is beyond my knowledge. Today I have met Lao-Tzu, who is perhaps like a Dragon. Among the Chinese, particularly, the Taoists, the Dragon is the symbol of Kundalini Shakti, the primordial force.

At the end of his mission to China, about 400 BC, Bhoganthar, with his disciple Yu (whom he also gave the Indian name Pulipani) and other close disciples, left China by the land route. As recorded in the Taoist literature, at the request of the gatekeeper at the Han Ku mountain pass Lao-Tzu crystallized his teachings. He did so in two books, the Tao Ching, with 37 verses, and the Te Ching with 42 verses (MacKintosh, 1971).[3]

In book two he says Do good to him who has done you injury, which was also said by the contemporary Tamil Siddha, Tiruvalluvar in his Tirukkural (Tiruvalluvar, 1968). Taoist yoga traditions continue to seek physical immortality using techniques remarkably similar to those taught in Tamil Shiva Yoga Siddhnta.

Kriya Babaji, disciple of Bhogar

Bhogar Nath and his young disciple Babaji Nagaraj at Kataragama, illustration from Babaji and the 18 Siddha Kriya Yoga Tradition

Kriya Babaji shrine, Kataragama

Along their way, they visited several shrines in the Himalayas and Kmarpa, the famous Tantric Shakti shrine in Assam.[4] He composed his greatest work of 700,000 verses near Mt. Kailasa with the blessings of Lord Shiva. It was later abridged to 7,000 verses, and is known as Bhogar Sapta Kandam. He later visited Gaya, India and Arabia. Upon his return to Tamil Nadu he introduced the Chinese salts and chemistry, which he called Cna-cram and porcelain making. He submitted his 7,000 verse manuscript for evaluation to his guru, Agastyar at Courtrallam and to an academy of siddhas there. It was endorsed by all of them as a great work.

Following this, many siddhas, including Konkanavar, Karuvoorar, Nandeeswar, Kamala Muni, Satta Muni, Macchamuni, and Sundarandar became his disciples to study the sciences of kaya kalpa and yoga. He eventually turned over his teaching mission to Pulipani.

After performing tapas at Sathura Giri, and Shiva Gin, he went to Katirkamam in Sri Lanka to perform tapas and win the grace of Lord Muruga. Under inspiration from the Lord he established the famous Yantra shrine, representing the 1,008 petalled lotus cakra, which blossomed in Bhogar there.

Next he went to Palani where he attained swarpa samdhi. He retired to Katirkmam, where Babaji Nagaraj met him around 211 AD.

Later, after the period of the Six Dynasties (220 to 590 AD), Bhoganthar returned with some Tamil disciples to China. He left his mission in Tamil Nadu with Pulipani, the Chinese Siddha. During the construction of the Brihitswarar Shiva Temple in Tanjore, Tamil Nadu, around 900 AD. Bhoganthar advised its builders as to how to raise the eighty ton capstone to the top of the temple, more than 200 feet high. This was done through his disciple Karuvoorar and another Tamil disciple who acted as intermediaries and through messages tied to the legs of courier birds, like todays homing pigeons.

At Bhogars suggestion a gradient ramp five miles long was built, up which the stone was pulled to the top of the temple. This was one of the most remarkable engineering feats of all times. About this time he also advised the King of Tanjore to build a small shrine dedicated to one of his greatest disciples, Karuvoorar, behind the Bhrihiteeswarar Shiva Temple.

While Bhoganthar is reported to have left the physical plane at Palani, he continues to work on the astral plane, inspiring his disciples and devotees, and even in rare instances he transmigrates into anothers physical body for specific purposes.

Source: Babaji and the 18 Siddha Kriya Yoga Tradition, by M. Govindan (Kriya Yoga Publications, 1991), pp. 113-118.

The Tamil Siddars Vanaimoinen and Bhogar, Patanjali and Ramana Maharshi, Satchidananda and Satchidanand, and their Connection with Tolkien the Lord of the Rings and Energy Enhancement..

ENERGY ENHANCEMENT SATCHIDANAND

SATCHIDANAND IS A SERIOUS STUDENT OF ENLIGHTENMENT HAVING BEEN TAUGHT BY ZEN MASTER HOGEN OF JAPAN AND SWAMI SATCHIDANANDA OF VIRGINIA - YOGIRAJ AND STUDENT OF SWAMI SIVANANDA OF RISHIKESH. STUDENT OF SATHYA SAI BABA, FATHER BEDE GRIFFITHS, SRI YOGENDRA - NOW UNFORTUNATELY ALMOST ALL GONE!!

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THE TAMIL SIDDARS

Vanaimoinen and Bhogar, Patanjali and Ramana Maharshi, and their Connection with Tolkien and Energy Enhancement

THE TAMIL SIDDARS Vanaimoinen and Bhogar, Patanjali and Ramana Maharshi, and their Connection with Tolkien and Energy Enhancement

Vanaimoinen and Bhogar - Tamil Siddars

Tolkien's Connection with Energy Enhancement through Tamil Suddar Vanaimoinen and the Finnish Myth, The Kalevala of Lonnrot, Beowulf and Yggdrasil the World Tree and the Tamil Siddars

For 20,000 years - yes Tamil from Tamil Nadu in the South of India predates Sanskrit by thousands of years - Tamil Siddars have been at the Heart of Human Evolution. From Tamil Siddar Bhogar of Palani Hill Temple and his Spiritual and physical Alchemy to create Enlightenment and Immortality transmigrating into the body of Lao Tsu to create Taoism.

Tamil Siddar Bhogar - Siddar Alchemy is Taoist Alchemy- Bhogar Transmigrated - moved from Body to Body - into Lao Tsu - Swami Satchidananda, Master of satchidanand, was a Tamil Siddha - Satchidananda and Satchidanand at Palani Hill Temple - Bhogars temple - in 1995 - Patanjali was a Tamil Siddar!!

BHOGAR - The Tamil Siddar - Kundalini Yoga, Spiritual Alchemy Siddha Bhoganthar: An Oceanic Life Story

To Tamil Siddar Patanjali and his Yoga Sutras of Patanjali - "Here are complete instructions on Enlightenment!!" the Truth, the whole Truth with nothing left out - "Designed to Succeed!!"

Read the Energy Enhancement Commentary of the Yoga Sutras of Patanjali here!!

THE SUPER ADVANCED ENERGY ENHANCEMENT KUNDALINI KRIYAS OF ALCHEMIST TAMIL SIDDAR BHOGAR, AND HIS STUDENTS BABAJI, PATANJALI AND TAOIST LAO TSU

To Tamil Siddar Ramana Maharshi and his Ashram in Tamil Nadu, South India.

TAMIL SIDDAR SRI RAMANA MAHARSHI, GURU, ENLIGHTENED ILLUMINATED SPIRITUAL MASTER

Tamil Siddar SRI RAMANA MAHARSHI, GURU QUOTES, ENLIGHTENED ILLUMINATED SPIRITUAL MASTER

THE TAMIL SIDDARS Vanaimoinen and Bhogar, Patanjali and Ramana Maharshi, and their Connection with Tolkien and Energy Enhancement

ANGEL PSYCHIC POWERS THE ARCHANGEL SAINT MICHAEL'S BALLS AND HIS CONNECTION WITH SHIVA NATARAJ AND THE TAMIL SIDDARS, VANAIMOINEN, BHOGAR, LAO TSU AND THE TAOIST ORBITS, BABAJI, YOGANANDA AND THE KUNDALINI KRIYAS, PATANJALI AND THE YOGA SUTRAS OF PATANJALI, RAMANA MAHARSHI AND SWAMI SATCHIDANANDA

Tolkien, From the Tamil Siddars, From the Kalevala Saga, the Ancient sacred Texts he was studying, Tolkien absorbed, was Implanted with an Earth Protector Angel, a Good Psychic Program for the benefit of Humanity in order to defeat the Satanic Fascist Nazi Forces still, currently, ruling the World.

Everyone of the millions who read, "The Hobbit" or "The Lord of the Rings" was similarly implanted with this urge to defeat Sauron, or Lucifer creating an army of Earth Protectors still implacably opposed to the ultimate Evil.

"EVIL IS!!" from the poetry of Tolkien.

"ANGELS ARE" - Satchidanand

This implantation of Angels is, "Objective Art" as described by Gurdjieff, it is also one of the main methodologies of White Magic.

The creation of the pure steel of immaculate innocence by its courage in the face of implacable evil.

This is THE religious truth at the heart of all religions. I am a servant of the Secret Fire, wielder of the Flame of Anor. The dark fire (Luciferian Light) will not avail you, Flame of Udun! Go back to the shadow. "YOU SHALL NOT PASS!!" - GANDALF AND TOLKIEN

J.R.R. Tolkien identified in his 1936 lecture on the Saga "Beowulf: The Monsters and the Critics" a "Northern 'theory of courage'"

the heroic or "virtuous pagan" insistence to do the right thing even in the face of certain defeat without promise of reward or salvation:

"Enlightenment is the free will ONLY to do the right and good thing" - Satchidanand

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