Tesla_WTC_Solution
21st October 2013, 18:09
http://upload.wikimedia.org/wikipedia/commons/thumb/e/e1/Knockout_Mice5006-300.jpg/800px-Knockout_Mice5006-300.jpg
Useful links:
http://en.wikipedia.org/wiki/Recombineering
http://en.wikipedia.org/wiki/Knockout_mouse
http://en.wikipedia.org/wiki/Homologous_recombination
http://en.wikipedia.org/wiki/Anthrax_vaccines
http://openwetware.org/wiki/Recombineering/Lambda_red-mediated_gene_replacement
A Closer Look at Genetic Engineering and Its Modern Capabilities
Those of you who live in Washington state are well aware of the term "genetic engineering", and most of you probably have a clear understanding of the basic meaning of the phrase. We understand vaguely how invested companies crudely inject genetic material into plants -- in order to render them resistant to harsh herbicides that other plants cannot tolerate. There is little difference, in fact, between these herbicides used in the USA and the Agent Orange herbicides that were dumped on Vietnam.
However, where the public interest meets the most heinous neglect is in the realm of the shortcuts being taken by the ReCombineering industry. Recombineering is the use of a special type of bacteria (mostly E Coli) and viruses (many known Bacteriophages) to insert foreign DNA/RNA/Genes into an unsuspecting host.
Multi-stage vectors and catalysts, synthetic gene sequences and sequence tagging, are some of the terms you are unlikely to find written on any voter's ballot. But if you were to walk into a university lab that specializes in modern genetic engineering techniques, they are terms you would be likely to hear often.
Right on Wikipedia, you can see detailed information about how and why scientists are inserting foreign and synthetic genes into animals, and perhaps even human beings. Mice are a preferred model for the study of genetic changes on animals and humans.
The following text describes the process by which a human or animal gene may be disabled so that the effect on the organism may be studied:
KNOCKOUT MICE: How close to human?
A knockout mouse is a genetically engineered mouse in which researchers have inactivated, or "knocked out," an existing gene by replacing it or disrupting it with an artificial piece of DNA. The loss of gene activity often causes changes in a mouse's phenotype, which includes appearance, behavior and other observable physical and biochemical characteristics.
Knocking out a Gene
http://openwetware.org/wiki/Recombineering/Lambda_red-mediated_gene_replacement
Gene Knockout Overview
Overview
Single-gene knockouts using λ red system, adapted from Datsenko and Wanner paper. The goal of this protocol was to create an endA (endonuclease I) knockout, but obviously it can be adapted to any gene. The knocked-out gene is replaced with an antibiotic resistance gene, usually for kanamycin or chloramphenicol. In this example, the target strain was already kanamycin resistant, so the chloramphenicol resistance gene was used.
One of the genes which accounts for human speech and brain plasticity:
http://en.wikipedia.org/wiki/FOXP2
FOXP2 -- The Gene for Speech?
In humans, mutations of FOXP2 cause a severe speech and language disorder.[1][5] Versions of FOXP2 exist in similar forms in distantly related vertebrates; functional studies of the gene in mice[6] and in songbirds[7] indicate that it is important for modulating plasticity of neural circuits.[8] Outside the brain FOXP2 has also been implicated in development of other tissues such as the lung and gut.[9] FOXP2 directly regulates a large number of downstream target genes.[10][11]
One particular target that is directly downregulated by FOXP2 in human neurons is the CNTNAP2 gene, a member of the neurexin family; variants in this target gene have been associated with common forms of language impairment.[12] Two amino-acid substitutions distinguish the human FOXP2 protein from that found in chimpanzees,[13] but only one of these two changes is unique to humans.[14] Evidence from genetically manipulated mice[15] and human neuronal cell models[16] suggests that these changes affect the neural functions of FOXP2.
Selective elimination of genes is possible; knocking out genes which are specific to families and not necessarily the global population is possible:
http://www.ncbi.nlm.nih.gov/pubmed/15108192
Chinese Family Provides Strange Insight into the Link Between FOXP2 and Autism
Am J Med Genet B Neuropsychiatr Genet. 2004 May 15;127B(1):113-6.
Association between the FOXP2 gene and autistic disorder in Chinese population.
Gong X, Jia M, Ruan Y, Shuang M, Liu J, Wu S, Guo Y, Yang J, Ling Y, Yang X, Zhang D.
Source
Institute of Mental Health, Peking University, Beijing, China.
Abstract
Several genomewide screens indicated that chromosome 7q was linked to autistic disorder. FOXP2, located on 7q31, is a putative transcription factor containing a polyglutamine tract and a forkhead DNA binding domain. It is one member of the forkhead family who are known to be key regulators of embryogenesis. A point mutation at a highly conserved residue within the forkhead domain co-segregated with affected status in the KE family who was a unique three generation pedigree with a severe speech and language disorder and FOXP2 was directly disrupted by a translocation in an individual who had similar deficits as those of the KE family.
Several studies have investigated the role of FOXP2 polymorphisms in autism and none of them found positive association. We performed a family-based association study of three single nucleotide polymorphisms (SNPs) of FOXP2 in 181 Chinese Han trios using the analyses of transmission/disequilibrium test (TDT) and haplotype. We found a significant association between autistic disorder and one SNP, as well as with specific haplotypes formed by this SNP with two other SNPs we investigated. Our findings suggest that the FOXP2 gene may be involved in the pathogenesis of autism in Chinese population.
Copyright 2004 Wiley-Liss, Inc.
PMID: 15108192 [PubMed - indexed for MEDLINE]
FOXP2 the Master Gene for Regulating Autism?
http://sfari.org/news-and-opinion/news/2012/scientists-link-new-deficits-to-foxp2-mutations-in-mice
Scientists link new deficits to FOXP2 mutations in mice
E-mail Print Share This Alla Katsnelson
22 March 2012
Mice with mutations in a gene tied to language impairment and to autism have trouble learning to associate sounds with motor patterns, says a study published last week in PLoS ONE1.
The work lends further support to the idea that the gene, FOXP2, plays a crucial role in language learning. It also provides a new mouse model for investigating the genetic and molecular underpinnings of tasks that mirror a type of learning that likely takes place when humans acquire the ability to speak.
The study represents “an elegant use of mouse genetics to replicate known human mutations in a speech-related gene — but to investigate deficits appropriate to a mouse,” says Stephanie White, associate professor of integrative biology and physiology at the University of California, Los Angeles, who did not participate in the research.
Scientists first made the link between FOXP2 and language more than a decade ago, when the gene was discovered to underlie the severe pervasive language impairments that affected members of a London family dubbed KE2. Since then, studies have begun to identify its function in establishing neural connections during early stages of brain development, including those involved in motor coordination, acquisition of motor skills and the ability to integrate sensory and motor information.
No mutations in the gene-coding region of FOXP2 have been directly linked to autism, but the gene appears to regulate other genes, such as CNTNAP2 and MET, which have been associated with the disorder.
I will try to add to this later.
I got interrupted and lost my train of thought.
~TWTCS
p.s. It is possible to silence one or more genes simply by compromising the protein that enables their expression. I.e. stealth-muting.
_________________________________________
GMO plants and their potential effect on animal/human gene expression
Also looking at Transgenic Mammals
http://en.wikipedia.org/wiki/Genetically_modified_organism
Transgenic plants have been engineered for scientific research, to create new colours in plants, and to create different crops.
In research, plants are engineered to help discover the functions of certain genes. One way to do this is to knock out the gene of interest and see what phenotype develops. Another strategy is to attach the gene to a strong promoter and see what happens when it is over expressed. A common technique used to find out where the gene is expressed is to attach it to GUS or a similar reporter gene that allows visualisation of the location.[8]'
Genetically modified mammals are an important category of genetically modified organisms.[32] Ralph L. Brinster and Richard Palmiter developed the techniques responsible for transgenic mice, rats, rabbits, sheep, and pigs in the early 1980s, and established many of the first transgenic models of human disease, including the first carcinoma caused by a transgene. The process of genetically engineering animals is a slow, tedious, and expensive process. However, new technologies are making genetic modifications easier and more precise.[33]
The first transgenic (genetically modified) animal was produced by injecting DNA into mouse embryos then implanting the embryos in female mice.[34]
Genetically modified animals currently being developed can be placed into six different broad classes based on the intended purpose of the genetic modification:
to research human diseases (for example, to develop animal models for these diseases);
to produce industrial or consumer products (fibres for multiple uses);
to produce products intended for human therapeutic use (pharmaceutical products or tissue for implantation);
to enrich or enhance the animals' interactions with humans (hypo-allergenic pets);
to enhance production or food quality traits (faster growing fish, pigs that digest food more efficiently);
to improve animal health (disease resistance)[35]
____________________________
Transgenic animals are used as experimental models to perform phenotypic and for testing in biomedical research.[36]
Genetically modified (genetically engineered) animals are becoming more vital to the discovery and development of cures and treatments for many serious diseases. By altering the DNA or transferring DNA to an animal, we can develop certain proteins that may be used in medical treatment. Stable expressions of human proteins have been developed in many animals, including sheep, pigs, and rats. Human-alpha-1-antitrypsin,[37] which has been tested in sheep and is used in treating humans with this deficiency and transgenic pigs with human-histo-compatibility have been studied in the hopes that the organs will be suitable for transplant with less chances of rejection.
_____________________________________________________
Prophetic Novel by AutoDidact Scientist Clay Prince:
http://ecx.images-amazon.com/images/I/31Q77WYZYWL._SY344_BO1,204,203,200_.jpg
In a small laboratory located near downtown Dallas, a successful experiment has opened the door to a revolution in medicine. The pain of organ failure and replacement will soon be a thing of the past, as will a host of debilitating diseases. Thousands of miles away, amid the horror of war in Chechnya, a quantum leap in stem cell research has brought the promise of tissue generation therapy tantalizingly close to reality.
For many years, Doctors Clifford Roberts and Andre Baronovsky have quietly collaborated from a distance. At last, the time has come to combine their individual genius in a single, extraordinary result that will offer greater hope to mankind than anyone has ever dared to imagine.But a single germ of greed is all it takes to turn the expectation of a noble dream into the dread of a grisly nightmare. Technology has neither loyalty nor conscience. It honors no alliance and calls no one “Master.”
A dark, restive evil—perverse beyond measure—grows within the shelter and comfort of an unsuspecting womb. For many years, Patrick Donaldson has stood against the industry of human exploitation, often sacrificing his freedom in commitment to a divine ideal.
Unafraid of confrontation, he demands answers from Drs. Roberts and Baronovsky about the nature of their research. But nothing in his experience or imagination could possibly prepare him for the truth. And when it arrives, he may not be equipped to survive.In a world driven by pursuit of self-interest, history proves that murder, betrayal, and human depravity cannot be regarded as anomalous. They are tools, used like any other, as means to an end. Innocence is ultimately a victim of reality, and ignorance, sadly, is fleeting. Is there hope for humanity? Can the simple faith of Patrick Donaldson compete against the tangible power of human engineering?
It is said that all beginnings have an end. Yet pursuit of knowledge—so fundamental to the human experience—may be an exception to the rule. Who is qualified to judge between innocence and guilt in a moral quandary colored neither black nor white, but gray?
Time marches on, knowledge follows, and the victims lay silent.
The Sound of Silence
http://en.wikipedia.org/wiki/The_Sound_of_Silence
"The Sound of Silence" is a song by singer-songwriter duo Simon & Garfunkel. Written in February 1964 by Paul Simon in the aftermath of the 1963 assassination of John F. Kennedy,[1] the song propelled the group to mainstream popularity.
Paul Simon began working on the song some time after the Kennedy assassination. He had made progress on the music but had yet to write the lyrics. On February 19, 1964, the lyrics coalesced, as Simon recalled: "The main thing about playing the guitar, though, was that I was able to sit by myself and play and dream. And I was always happy doing that. I used to go off in the bathroom, because the bathroom had tiles, so it was a slight echo chamber. I'd turn on the faucet so that water would run (I like that sound, it's very soothing to me) and I'd play. In the dark. 'Hello darkness, my old friend / I've come to talk with you again'."[5]
4zLfCnGVeL4
1HFM0-2yMQg
Useful links:
http://en.wikipedia.org/wiki/Recombineering
http://en.wikipedia.org/wiki/Knockout_mouse
http://en.wikipedia.org/wiki/Homologous_recombination
http://en.wikipedia.org/wiki/Anthrax_vaccines
http://openwetware.org/wiki/Recombineering/Lambda_red-mediated_gene_replacement
A Closer Look at Genetic Engineering and Its Modern Capabilities
Those of you who live in Washington state are well aware of the term "genetic engineering", and most of you probably have a clear understanding of the basic meaning of the phrase. We understand vaguely how invested companies crudely inject genetic material into plants -- in order to render them resistant to harsh herbicides that other plants cannot tolerate. There is little difference, in fact, between these herbicides used in the USA and the Agent Orange herbicides that were dumped on Vietnam.
However, where the public interest meets the most heinous neglect is in the realm of the shortcuts being taken by the ReCombineering industry. Recombineering is the use of a special type of bacteria (mostly E Coli) and viruses (many known Bacteriophages) to insert foreign DNA/RNA/Genes into an unsuspecting host.
Multi-stage vectors and catalysts, synthetic gene sequences and sequence tagging, are some of the terms you are unlikely to find written on any voter's ballot. But if you were to walk into a university lab that specializes in modern genetic engineering techniques, they are terms you would be likely to hear often.
Right on Wikipedia, you can see detailed information about how and why scientists are inserting foreign and synthetic genes into animals, and perhaps even human beings. Mice are a preferred model for the study of genetic changes on animals and humans.
The following text describes the process by which a human or animal gene may be disabled so that the effect on the organism may be studied:
KNOCKOUT MICE: How close to human?
A knockout mouse is a genetically engineered mouse in which researchers have inactivated, or "knocked out," an existing gene by replacing it or disrupting it with an artificial piece of DNA. The loss of gene activity often causes changes in a mouse's phenotype, which includes appearance, behavior and other observable physical and biochemical characteristics.
Knocking out a Gene
http://openwetware.org/wiki/Recombineering/Lambda_red-mediated_gene_replacement
Gene Knockout Overview
Overview
Single-gene knockouts using λ red system, adapted from Datsenko and Wanner paper. The goal of this protocol was to create an endA (endonuclease I) knockout, but obviously it can be adapted to any gene. The knocked-out gene is replaced with an antibiotic resistance gene, usually for kanamycin or chloramphenicol. In this example, the target strain was already kanamycin resistant, so the chloramphenicol resistance gene was used.
One of the genes which accounts for human speech and brain plasticity:
http://en.wikipedia.org/wiki/FOXP2
FOXP2 -- The Gene for Speech?
In humans, mutations of FOXP2 cause a severe speech and language disorder.[1][5] Versions of FOXP2 exist in similar forms in distantly related vertebrates; functional studies of the gene in mice[6] and in songbirds[7] indicate that it is important for modulating plasticity of neural circuits.[8] Outside the brain FOXP2 has also been implicated in development of other tissues such as the lung and gut.[9] FOXP2 directly regulates a large number of downstream target genes.[10][11]
One particular target that is directly downregulated by FOXP2 in human neurons is the CNTNAP2 gene, a member of the neurexin family; variants in this target gene have been associated with common forms of language impairment.[12] Two amino-acid substitutions distinguish the human FOXP2 protein from that found in chimpanzees,[13] but only one of these two changes is unique to humans.[14] Evidence from genetically manipulated mice[15] and human neuronal cell models[16] suggests that these changes affect the neural functions of FOXP2.
Selective elimination of genes is possible; knocking out genes which are specific to families and not necessarily the global population is possible:
http://www.ncbi.nlm.nih.gov/pubmed/15108192
Chinese Family Provides Strange Insight into the Link Between FOXP2 and Autism
Am J Med Genet B Neuropsychiatr Genet. 2004 May 15;127B(1):113-6.
Association between the FOXP2 gene and autistic disorder in Chinese population.
Gong X, Jia M, Ruan Y, Shuang M, Liu J, Wu S, Guo Y, Yang J, Ling Y, Yang X, Zhang D.
Source
Institute of Mental Health, Peking University, Beijing, China.
Abstract
Several genomewide screens indicated that chromosome 7q was linked to autistic disorder. FOXP2, located on 7q31, is a putative transcription factor containing a polyglutamine tract and a forkhead DNA binding domain. It is one member of the forkhead family who are known to be key regulators of embryogenesis. A point mutation at a highly conserved residue within the forkhead domain co-segregated with affected status in the KE family who was a unique three generation pedigree with a severe speech and language disorder and FOXP2 was directly disrupted by a translocation in an individual who had similar deficits as those of the KE family.
Several studies have investigated the role of FOXP2 polymorphisms in autism and none of them found positive association. We performed a family-based association study of three single nucleotide polymorphisms (SNPs) of FOXP2 in 181 Chinese Han trios using the analyses of transmission/disequilibrium test (TDT) and haplotype. We found a significant association between autistic disorder and one SNP, as well as with specific haplotypes formed by this SNP with two other SNPs we investigated. Our findings suggest that the FOXP2 gene may be involved in the pathogenesis of autism in Chinese population.
Copyright 2004 Wiley-Liss, Inc.
PMID: 15108192 [PubMed - indexed for MEDLINE]
FOXP2 the Master Gene for Regulating Autism?
http://sfari.org/news-and-opinion/news/2012/scientists-link-new-deficits-to-foxp2-mutations-in-mice
Scientists link new deficits to FOXP2 mutations in mice
E-mail Print Share This Alla Katsnelson
22 March 2012
Mice with mutations in a gene tied to language impairment and to autism have trouble learning to associate sounds with motor patterns, says a study published last week in PLoS ONE1.
The work lends further support to the idea that the gene, FOXP2, plays a crucial role in language learning. It also provides a new mouse model for investigating the genetic and molecular underpinnings of tasks that mirror a type of learning that likely takes place when humans acquire the ability to speak.
The study represents “an elegant use of mouse genetics to replicate known human mutations in a speech-related gene — but to investigate deficits appropriate to a mouse,” says Stephanie White, associate professor of integrative biology and physiology at the University of California, Los Angeles, who did not participate in the research.
Scientists first made the link between FOXP2 and language more than a decade ago, when the gene was discovered to underlie the severe pervasive language impairments that affected members of a London family dubbed KE2. Since then, studies have begun to identify its function in establishing neural connections during early stages of brain development, including those involved in motor coordination, acquisition of motor skills and the ability to integrate sensory and motor information.
No mutations in the gene-coding region of FOXP2 have been directly linked to autism, but the gene appears to regulate other genes, such as CNTNAP2 and MET, which have been associated with the disorder.
I will try to add to this later.
I got interrupted and lost my train of thought.
~TWTCS
p.s. It is possible to silence one or more genes simply by compromising the protein that enables their expression. I.e. stealth-muting.
_________________________________________
GMO plants and their potential effect on animal/human gene expression
Also looking at Transgenic Mammals
http://en.wikipedia.org/wiki/Genetically_modified_organism
Transgenic plants have been engineered for scientific research, to create new colours in plants, and to create different crops.
In research, plants are engineered to help discover the functions of certain genes. One way to do this is to knock out the gene of interest and see what phenotype develops. Another strategy is to attach the gene to a strong promoter and see what happens when it is over expressed. A common technique used to find out where the gene is expressed is to attach it to GUS or a similar reporter gene that allows visualisation of the location.[8]'
Genetically modified mammals are an important category of genetically modified organisms.[32] Ralph L. Brinster and Richard Palmiter developed the techniques responsible for transgenic mice, rats, rabbits, sheep, and pigs in the early 1980s, and established many of the first transgenic models of human disease, including the first carcinoma caused by a transgene. The process of genetically engineering animals is a slow, tedious, and expensive process. However, new technologies are making genetic modifications easier and more precise.[33]
The first transgenic (genetically modified) animal was produced by injecting DNA into mouse embryos then implanting the embryos in female mice.[34]
Genetically modified animals currently being developed can be placed into six different broad classes based on the intended purpose of the genetic modification:
to research human diseases (for example, to develop animal models for these diseases);
to produce industrial or consumer products (fibres for multiple uses);
to produce products intended for human therapeutic use (pharmaceutical products or tissue for implantation);
to enrich or enhance the animals' interactions with humans (hypo-allergenic pets);
to enhance production or food quality traits (faster growing fish, pigs that digest food more efficiently);
to improve animal health (disease resistance)[35]
____________________________
Transgenic animals are used as experimental models to perform phenotypic and for testing in biomedical research.[36]
Genetically modified (genetically engineered) animals are becoming more vital to the discovery and development of cures and treatments for many serious diseases. By altering the DNA or transferring DNA to an animal, we can develop certain proteins that may be used in medical treatment. Stable expressions of human proteins have been developed in many animals, including sheep, pigs, and rats. Human-alpha-1-antitrypsin,[37] which has been tested in sheep and is used in treating humans with this deficiency and transgenic pigs with human-histo-compatibility have been studied in the hopes that the organs will be suitable for transplant with less chances of rejection.
_____________________________________________________
Prophetic Novel by AutoDidact Scientist Clay Prince:
http://ecx.images-amazon.com/images/I/31Q77WYZYWL._SY344_BO1,204,203,200_.jpg
In a small laboratory located near downtown Dallas, a successful experiment has opened the door to a revolution in medicine. The pain of organ failure and replacement will soon be a thing of the past, as will a host of debilitating diseases. Thousands of miles away, amid the horror of war in Chechnya, a quantum leap in stem cell research has brought the promise of tissue generation therapy tantalizingly close to reality.
For many years, Doctors Clifford Roberts and Andre Baronovsky have quietly collaborated from a distance. At last, the time has come to combine their individual genius in a single, extraordinary result that will offer greater hope to mankind than anyone has ever dared to imagine.But a single germ of greed is all it takes to turn the expectation of a noble dream into the dread of a grisly nightmare. Technology has neither loyalty nor conscience. It honors no alliance and calls no one “Master.”
A dark, restive evil—perverse beyond measure—grows within the shelter and comfort of an unsuspecting womb. For many years, Patrick Donaldson has stood against the industry of human exploitation, often sacrificing his freedom in commitment to a divine ideal.
Unafraid of confrontation, he demands answers from Drs. Roberts and Baronovsky about the nature of their research. But nothing in his experience or imagination could possibly prepare him for the truth. And when it arrives, he may not be equipped to survive.In a world driven by pursuit of self-interest, history proves that murder, betrayal, and human depravity cannot be regarded as anomalous. They are tools, used like any other, as means to an end. Innocence is ultimately a victim of reality, and ignorance, sadly, is fleeting. Is there hope for humanity? Can the simple faith of Patrick Donaldson compete against the tangible power of human engineering?
It is said that all beginnings have an end. Yet pursuit of knowledge—so fundamental to the human experience—may be an exception to the rule. Who is qualified to judge between innocence and guilt in a moral quandary colored neither black nor white, but gray?
Time marches on, knowledge follows, and the victims lay silent.
The Sound of Silence
http://en.wikipedia.org/wiki/The_Sound_of_Silence
"The Sound of Silence" is a song by singer-songwriter duo Simon & Garfunkel. Written in February 1964 by Paul Simon in the aftermath of the 1963 assassination of John F. Kennedy,[1] the song propelled the group to mainstream popularity.
Paul Simon began working on the song some time after the Kennedy assassination. He had made progress on the music but had yet to write the lyrics. On February 19, 1964, the lyrics coalesced, as Simon recalled: "The main thing about playing the guitar, though, was that I was able to sit by myself and play and dream. And I was always happy doing that. I used to go off in the bathroom, because the bathroom had tiles, so it was a slight echo chamber. I'd turn on the faucet so that water would run (I like that sound, it's very soothing to me) and I'd play. In the dark. 'Hello darkness, my old friend / I've come to talk with you again'."[5]
4zLfCnGVeL4
1HFM0-2yMQg