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Humans are biological weapons, The bacteria and viruses we are exposed to make us unique on Earth.
page: 2share:
www.sciencedaily.com...
from sciencedaily (which i love )
Blood Mystery Solved: Two New Blood Types Identified
Feb. 23, 2012 — You probably know your blood type: A, B, AB or O. You may even know if you're Rhesus positive or negative. But how about the Langereis blood type? Or the Junior blood type? Positive or negative? Most people have never even heard of these.
Yet this knowledge could be "a matter of life and death," says University of Vermont biologist Bryan Ballif.
While blood transfusion problems due to Langereis and Junior blood types are rare worldwide, several ethnic populations are at risk, Ballif notes. "More than 50,000 Japanese are thought to be Junior negative and may encounter blood transfusion problems or mother-fetus incompatibility," he writes.
But the molecular basis of these two blood types has remained a mystery -- until now.
In the February issue of Nature Genetics, Ballif and his colleagues report on their discovery of two proteins on red blood cells responsible for these lesser-known blood types.
Ballif identified the two molecules as specialized transport proteins named ABCB6 and ABCG2.
"Only 30 proteins have previously been identified as responsible for a basic blood type," Ballif notes, "but the count now reaches 32."
The last new blood group proteins to be discovered were nearly a decade ago, Ballif says, "so it's pretty remarkable to have two identified this year."
Both of the newly identified proteins are also associated with anticancer drug resistance, so the findings may also have implications for improved treatment of breast and other cancers.
As part of the international effort, Ballif, assistant professor in the biology department, used a mass spectrometer at UVM funded by the Vermont Genetics Network. With this machine, he analyzed proteins purified by his longtime collaborator, Lionel Arnaud at the French National Institute for Blood Transfusion in Paris, France.
Ballif and Arnaud, in turn, relied on antibodies to Langereis and Junior blood antigens developed by Yoshihiko Tani at the Japanese Red Cross Osaka Blood Center and Toru Miyasaki at the Japanese Red Cross Hokkaido Blood Center.
After the protein identification in Vermont, the work returned to France. There Arnaud and his team conducted cellular and genetic tests confirming that these proteins were responsible for the Langereis and Junior blood types. "He was able to test the gene sequence," Ballif says, "and, sure enough, we found mutations in this particular gene for all the people in our sample who have these problems."
Transfusion troubles
Beyond the ABO blood type and the Rhesus (Rh) blood type, the International Blood Transfusion Society recognizes twenty-eight additional blood types with names like Duffy, Kidd, Diego and Lutheran. But Langereis and Junior have not been on this list. Although the antigens for the Junior and Langereis (or Lan) blood types were identified decades ago in pregnant women having difficulties carrying babies with incompatible blood types, the genetic basis of these antigens has been unknown until now.
Therefore, "very few people learn if they are Langereis or Junior positive or negative," Ballif says.
"Transfusion support of individuals with an anti-Lan antibody is highly challenging," the research team wrote in Nature Genetics, "partly because of the scarcity of compatible blood donors but mainly because of the lack of reliable reagents for blood screening." And Junior-negative blood donors are extremely rare too. That may soon change.
With the findings from this new research, health care professionals will now be able to more rapidly and confidently screen for these novel blood group proteins, Ballif wrote in a recent news article. "This will leave them better prepared to have blood ready when blood transfusions or other tissue donations are required," he notes.
"Now that we know these proteins, it will become a routine test," he says.
A better match
This science may be especially important to organ transplant patients. "As we get better and better at transplants, we do everything we can to make a good match," Ballif says. But sometimes a tissue or organ transplant, that looked like a good match, doesn't work -- and the donated tissue is rejected, which can lead to many problems or death.
"We don't always know why there is rejection," Ballif says, "but it may have to do with these proteins."
The rejection of donated tissue or blood is caused by the way the immune system distinguishes self from not-self. "If our own blood cells don't have these proteins, they're not familiar to our immune system," Ballif says, so the new blood doesn't "look like self" to the complex cellular defenses of the immune system. "They'll develop antibodies against it," Ballif says, and try to kill off the perceived invaders. In short, the body starts to attack itself.
"Then you may be out of luck," says Ballif, who
from sciencedaily (which i love )
Blood Mystery Solved: Two New Blood Types Identified
Feb. 23, 2012 — You probably know your blood type: A, B, AB or O. You may even know if you're Rhesus positive or negative. But how about the Langereis blood type? Or the Junior blood type? Positive or negative? Most people have never even heard of these.
Yet this knowledge could be "a matter of life and death," says University of Vermont biologist Bryan Ballif.
While blood transfusion problems due to Langereis and Junior blood types are rare worldwide, several ethnic populations are at risk, Ballif notes. "More than 50,000 Japanese are thought to be Junior negative and may encounter blood transfusion problems or mother-fetus incompatibility," he writes.
But the molecular basis of these two blood types has remained a mystery -- until now.
In the February issue of Nature Genetics, Ballif and his colleagues report on their discovery of two proteins on red blood cells responsible for these lesser-known blood types.
Ballif identified the two molecules as specialized transport proteins named ABCB6 and ABCG2.
"Only 30 proteins have previously been identified as responsible for a basic blood type," Ballif notes, "but the count now reaches 32."
The last new blood group proteins to be discovered were nearly a decade ago, Ballif says, "so it's pretty remarkable to have two identified this year."
Both of the newly identified proteins are also associated with anticancer drug resistance, so the findings may also have implications for improved treatment of breast and other cancers.
As part of the international effort, Ballif, assistant professor in the biology department, used a mass spectrometer at UVM funded by the Vermont Genetics Network. With this machine, he analyzed proteins purified by his longtime collaborator, Lionel Arnaud at the French National Institute for Blood Transfusion in Paris, France.
Ballif and Arnaud, in turn, relied on antibodies to Langereis and Junior blood antigens developed by Yoshihiko Tani at the Japanese Red Cross Osaka Blood Center and Toru Miyasaki at the Japanese Red Cross Hokkaido Blood Center.
After the protein identification in Vermont, the work returned to France. There Arnaud and his team conducted cellular and genetic tests confirming that these proteins were responsible for the Langereis and Junior blood types. "He was able to test the gene sequence," Ballif says, "and, sure enough, we found mutations in this particular gene for all the people in our sample who have these problems."
Transfusion troubles
Beyond the ABO blood type and the Rhesus (Rh) blood type, the International Blood Transfusion Society recognizes twenty-eight additional blood types with names like Duffy, Kidd, Diego and Lutheran. But Langereis and Junior have not been on this list. Although the antigens for the Junior and Langereis (or Lan) blood types were identified decades ago in pregnant women having difficulties carrying babies with incompatible blood types, the genetic basis of these antigens has been unknown until now.
Therefore, "very few people learn if they are Langereis or Junior positive or negative," Ballif says.
"Transfusion support of individuals with an anti-Lan antibody is highly challenging," the research team wrote in Nature Genetics, "partly because of the scarcity of compatible blood donors but mainly because of the lack of reliable reagents for blood screening." And Junior-negative blood donors are extremely rare too. That may soon change.
With the findings from this new research, health care professionals will now be able to more rapidly and confidently screen for these novel blood group proteins, Ballif wrote in a recent news article. "This will leave them better prepared to have blood ready when blood transfusions or other tissue donations are required," he notes.
"Now that we know these proteins, it will become a routine test," he says.
A better match
This science may be especially important to organ transplant patients. "As we get better and better at transplants, we do everything we can to make a good match," Ballif says. But sometimes a tissue or organ transplant, that looked like a good match, doesn't work -- and the donated tissue is rejected, which can lead to many problems or death.
"We don't always know why there is rejection," Ballif says, "but it may have to do with these proteins."
The rejection of donated tissue or blood is caused by the way the immune system distinguishes self from not-self. "If our own blood cells don't have these proteins, they're not familiar to our immune system," Ballif says, so the new blood doesn't "look like self" to the complex cellular defenses of the immune system. "They'll develop antibodies against it," Ballif says, and try to kill off the perceived invaders. In short, the body starts to attack itself.
"Then you may be out of luck," says Ballif, who
edit on 16-2-2013 by CrypticSouthpaw because: (no reason given)
-continued) notes that in addition to certain Japanese populations, European Gypsies are also at higher risk for not carrying the Langereis and Junior
blood type proteins.
"There are people in the United States who have these challenges too," he says, "but it's more rare."
Other proteins
Ballif and his international colleagues are not done with their search. "We're following up on more unknown blood types," he says. "There are probably on the order of 10 to 15 more of these unknown blood type systems -- where we know there is a problem but we don't know what the protein is that is causing the problem."
Although these other blood systems are very rare, "if you're that one individual, and you need a transfusion," Ballif says, "there's nothing more important for you to know."
www.sciencedaily.com...
AB Blood Type Strong Risk Factor for Venous Blood Clots
Feb. 4, 2013 — The non-O ABO blood type is the most important risk factor for venous thromboembolism (blood clots in veins), making up 20% of attributable risk for the condition, according to a new study in CMAJ (Canadian Medical Association Journal).
This finding has implications for genetic screening for thrombophilia, a genetic predisposition to abnormal blood clotting.
Danish researchers looked at data on 66,001 people who had been followed for 33 years from 1977 through 2010 to determine whether ABO blood type is associated with an increased risk of venous blood clots in the general population. They found that the risk increased when ABO blood type was combined with factor V Leiden R506Q or prothrombin G20210A, genetic mutations associated with an increased risk of venous thromboembolisms. This finding confirms the conclusion of other studies. The researchers also found an 11-fold increased risk of venous thromboembolism for people with the prothrombin G20210A mutation in double dose, something other smaller trials did not pick up.
"We found an additive effect of ABO blood type on risk of venous thromboembolism when combined with factor V Leiden R506Q and prothrombin G20210A; ABO blood type was the most important risk factor for venous thromboembolism in the general population.," writes Dr. Børge G. Nordestgaard, Herlev Hospital, Copenhagen University Hospital with coauthors. "This suggests that ABO blood type should be included in genetic screening for thrombophilia."
The study was large, followed participants over a long period and follow up was 100% complete for participants. Although the study cohort was genetically homogenous compared with populations with ethnic diversity, the ABO blood type, factor V Leiden R506Q and prothrombin G20210A are found in all ethnicities.
"There are people in the United States who have these challenges too," he says, "but it's more rare."
Other proteins
Ballif and his international colleagues are not done with their search. "We're following up on more unknown blood types," he says. "There are probably on the order of 10 to 15 more of these unknown blood type systems -- where we know there is a problem but we don't know what the protein is that is causing the problem."
Although these other blood systems are very rare, "if you're that one individual, and you need a transfusion," Ballif says, "there's nothing more important for you to know."
www.sciencedaily.com...
AB Blood Type Strong Risk Factor for Venous Blood Clots
Feb. 4, 2013 — The non-O ABO blood type is the most important risk factor for venous thromboembolism (blood clots in veins), making up 20% of attributable risk for the condition, according to a new study in CMAJ (Canadian Medical Association Journal).
This finding has implications for genetic screening for thrombophilia, a genetic predisposition to abnormal blood clotting.
Danish researchers looked at data on 66,001 people who had been followed for 33 years from 1977 through 2010 to determine whether ABO blood type is associated with an increased risk of venous blood clots in the general population. They found that the risk increased when ABO blood type was combined with factor V Leiden R506Q or prothrombin G20210A, genetic mutations associated with an increased risk of venous thromboembolisms. This finding confirms the conclusion of other studies. The researchers also found an 11-fold increased risk of venous thromboembolism for people with the prothrombin G20210A mutation in double dose, something other smaller trials did not pick up.
"We found an additive effect of ABO blood type on risk of venous thromboembolism when combined with factor V Leiden R506Q and prothrombin G20210A; ABO blood type was the most important risk factor for venous thromboembolism in the general population.," writes Dr. Børge G. Nordestgaard, Herlev Hospital, Copenhagen University Hospital with coauthors. "This suggests that ABO blood type should be included in genetic screening for thrombophilia."
The study was large, followed participants over a long period and follow up was 100% complete for participants. Although the study cohort was genetically homogenous compared with populations with ethnic diversity, the ABO blood type, factor V Leiden R506Q and prothrombin G20210A are found in all ethnicities.
edit on 16-2-2013 by CrypticSouthpaw because: (no reason given)
edit on 16-2-2013 by CrypticSouthpaw because: (no reason
given)
edit on 16-2-2013 by CrypticSouthpaw because: (no reason given)
www.sciencedaily.com...
Humans and Chimps Share Genetic Strategy in Battle Against Pathogens
Feb. 14, 2013 — A genome-wide analysis searching for evidence of long-lived balancing selection -- where the evolutionary process acts not to select the single best adaptation but to maintain genetic variation in a population -- has uncovered at least six regions of the genome where humans and chimpanzees share the same combination of genetic variants.
The finding, to be published Feb. 14 in the journal Science, suggests that in these regions, human genetic variation dates back to a common ancestor with chimpanzees millions of years ago, before the species split. It also highlights the importance of the dynamic co-evolution of human hosts and their pathogens in maintaining genetic variation.
Balancing selection allows evolution to keep all hereditary options open. The classic human example is the persistence of two versions of the hemoglobin gene: a normal version and hemoglobin S., a mutation that distorts the shape and function of red blood cells. Those who inherit two normal hemoglobin genes are at high risk for malaria, a parasitic disease that infects more than 200 million people each year. Those who inherit one normal gene and one hemoglobin S. gene are partially protected from malaria -- a potentially life-saving benefit. Those with two copies of the gene suffer from sickle-cell anemia, a serious and lifelong circulatory disease.
"When we looked for genetic clues pointing to other, more ancient, examples of balancing selection, we found strong evidence for at least six such regions and weaker evidence for another 119 -- many more than we expected," said study author Molly Przeworski, PhD, professor of human genetics and of ecology and evolution at the University of Chicago.
"We don't yet know what their functions are," she said. None of the six regions codes for a protein. There are clues that they are involved in host-pathogen interactions, "but which pathogens, what immune processes," she said, "we don't know."
The researchers used genetic data from 10 chimpanzees from Western Africa and 59 humans from sub-Saharan Africa who were part of the 1,000 Genomes Project.
The scientists looked for cases in which genetic variations that arose in the ancestor of humans and chimpanzees have been maintained through both lines. The fact that variation in these regions of the genome has persisted for so long argues that they "must have been functionally important over evolutionary time," said Ellen Leffler, a graduate student in Przeworski's laboratory and first author of the study.
The researchers, from the University of Chicago and Oxford University, designed the study to be very conservative. "We wanted to find the cases we believed the most, rather than the most cases," Przeworski said.
Computers sorted snippets of the genetic data from humans and chimps into clusters depending on how similar the subjects were to each other. For almost every snippet, they found a cluster of humans and a separate cluster of chimpanzees, as expected. But there were a few segments of the genomes in which each cluster included both chimpanzees and humans; in those regions, some humans were more closely related to some chimpanzees than to other humans.
Humans and Chimps Share Genetic Strategy in Battle Against Pathogens
Feb. 14, 2013 — A genome-wide analysis searching for evidence of long-lived balancing selection -- where the evolutionary process acts not to select the single best adaptation but to maintain genetic variation in a population -- has uncovered at least six regions of the genome where humans and chimpanzees share the same combination of genetic variants.
The finding, to be published Feb. 14 in the journal Science, suggests that in these regions, human genetic variation dates back to a common ancestor with chimpanzees millions of years ago, before the species split. It also highlights the importance of the dynamic co-evolution of human hosts and their pathogens in maintaining genetic variation.
Balancing selection allows evolution to keep all hereditary options open. The classic human example is the persistence of two versions of the hemoglobin gene: a normal version and hemoglobin S., a mutation that distorts the shape and function of red blood cells. Those who inherit two normal hemoglobin genes are at high risk for malaria, a parasitic disease that infects more than 200 million people each year. Those who inherit one normal gene and one hemoglobin S. gene are partially protected from malaria -- a potentially life-saving benefit. Those with two copies of the gene suffer from sickle-cell anemia, a serious and lifelong circulatory disease.
"When we looked for genetic clues pointing to other, more ancient, examples of balancing selection, we found strong evidence for at least six such regions and weaker evidence for another 119 -- many more than we expected," said study author Molly Przeworski, PhD, professor of human genetics and of ecology and evolution at the University of Chicago.
"We don't yet know what their functions are," she said. None of the six regions codes for a protein. There are clues that they are involved in host-pathogen interactions, "but which pathogens, what immune processes," she said, "we don't know."
The researchers used genetic data from 10 chimpanzees from Western Africa and 59 humans from sub-Saharan Africa who were part of the 1,000 Genomes Project.
The scientists looked for cases in which genetic variations that arose in the ancestor of humans and chimpanzees have been maintained through both lines. The fact that variation in these regions of the genome has persisted for so long argues that they "must have been functionally important over evolutionary time," said Ellen Leffler, a graduate student in Przeworski's laboratory and first author of the study.
The researchers, from the University of Chicago and Oxford University, designed the study to be very conservative. "We wanted to find the cases we believed the most, rather than the most cases," Przeworski said.
Computers sorted snippets of the genetic data from humans and chimps into clusters depending on how similar the subjects were to each other. For almost every snippet, they found a cluster of humans and a separate cluster of chimpanzees, as expected. But there were a few segments of the genomes in which each cluster included both chimpanzees and humans; in those regions, some humans were more closely related to some chimpanzees than to other humans.
edit on 16-2-2013 by CrypticSouthpaw because: (no reason given)
"Instances in which natural selection maintains genetic variation in a population over millions of years are thought to be extremely rare," the
authors wrote. The oldest and best known example of balanced polymorphism shared between humans and chimpanzees is the major histocompatibility
complex (MHC), a group of genes that help the immune system distinguish between the body and potential invaders, such as bacteria or viruses.
Last year, a team led by Przeworski found that humans and gibbons shared genetic variation related to the ABO blood-group system from a common ancestor.
The six new examples of balanced selection described in this study appear to play a role, like the MHC, in fending off infectious disease. This requires a variety of evolutionary tools, including balancing selection. When a population moves to a new environment -- for example the exodus out of Africa to northern Europe -- they face many one-time adjustments, such as adapting to less intense sunlight and decreased ultraviolet radiation. Over many generations, their offspring manage to decrease melanin production -- a static adaptation for a static environment.
Fighting off pathogens is more dynamic, a constant arms race. Balancing selection may have enabled humans and chimps to retain multiple lines of defense that can be called on when a pathogen evolves new weapons.
"Our results imply that dynamic co-evolution of human hosts and their pathogens has played an important role in shaping human variation," Przeworski said. "This highlights the importance of a different kind of selection pressure in human evolution."
The National Institutes of Health, The Royal Society, the Wellcome Trust and the Howard Hughes Medical Institute funded this study. Additional authors include Ziyue Gao, Laure Segurel and Guy Sella from the University of Chicago; Susanne Pfeifer, Adam Auton, Oliver Venn, Rory Bowden, Peter Donnelly and Gilean McVean from Oxford University; Ronald Bonstrop from the Biomedical Primate Research Centre in the Netherlands; and Jeffrey Wall from the University of California at San Francisco.
Last year, a team led by Przeworski found that humans and gibbons shared genetic variation related to the ABO blood-group system from a common ancestor.
The six new examples of balanced selection described in this study appear to play a role, like the MHC, in fending off infectious disease. This requires a variety of evolutionary tools, including balancing selection. When a population moves to a new environment -- for example the exodus out of Africa to northern Europe -- they face many one-time adjustments, such as adapting to less intense sunlight and decreased ultraviolet radiation. Over many generations, their offspring manage to decrease melanin production -- a static adaptation for a static environment.
Fighting off pathogens is more dynamic, a constant arms race. Balancing selection may have enabled humans and chimps to retain multiple lines of defense that can be called on when a pathogen evolves new weapons.
"Our results imply that dynamic co-evolution of human hosts and their pathogens has played an important role in shaping human variation," Przeworski said. "This highlights the importance of a different kind of selection pressure in human evolution."
The National Institutes of Health, The Royal Society, the Wellcome Trust and the Howard Hughes Medical Institute funded this study. Additional authors include Ziyue Gao, Laure Segurel and Guy Sella from the University of Chicago; Susanne Pfeifer, Adam Auton, Oliver Venn, Rory Bowden, Peter Donnelly and Gilean McVean from Oxford University; Ronald Bonstrop from the Biomedical Primate Research Centre in the Netherlands; and Jeffrey Wall from the University of California at San Francisco.
www.sciencedaily.com...
Insights Into Primate Diversity: Lessons from the Rhesus Macaque
Humans and rhesus macaques shared a common ancestor approximately 25 million years ago. Although there are now over seven billion humans on the planet only 100,000 years ago the human population was as low as one million. The effective human population, the number of people required to explain current genetic variation rate, was until recently less than 8,000.
The population size of rhesus macaques is in the millions and is exceeded only by humans (among primates). However there are 13 subspecies which have evolved to exploit environments as diverse as savannah and forests, and across a range of climate zones.
A team of researchers led by Christina Barr and David Goldman from the NIH determined that the effective population size for these primates was 80,000, ten times that of humans. Analysis of genetic variation, using single nucleotide polymorphisms (SNPs), showed that the macaque genome had three times higher genetic variation than humans. Most of these SNP were previously unknown and were disproportionally found in functionally important regions of DNA and each known gene had at least one SNP.
Dr. Goldman explained, "Although macaques have more variation than humans in the protein coding regions of genes, the ratio of variation in these regions compared to non-coding regions is significantly lower. Additionally the macaque variation is less likely to alter protein function. This brings down the amount of damaging variation to a level close to what was actually seen in humans."
Dr Barr continued "Our comparative approach across primate species (human and macaques) gives us a genomic view of evolutionary selection and reaffirms the effects of population history on genetic variation. Not very long ago, on an evolutionary timescale, there were more macaques than people, and the genomes of both species are a legacy of those times past."
The Rhesus monkey can carry many pathogens yet population density is not effected. Much like humans. We have our plagues, but we are as diverse as the Rhesus. If anything had to use a template for a viral being, One that can mutate and evolve in synchronicity with viruses we could see new genetic variations everyday when a pathogen enters a suitable host, the host makes use of that pathogen in rare cases. Those rare cases are what surge Evolution forward. Now the GMO crops. Now the fear campaigns, Now the need to deficient the population. Does this not reach conclusions that we are being denied humane ethics? With something like to dollar backing up a project by those who care not for dollars. They want to isolate these rare blood types. Extract genomes and virally infect themselves. As well as soldiers with a strength and intelligence *syrum*. Those people will house a number of deadly pathogens, conquered by science. Now if this is possible with humans. This is not out of the realm of possibility. That aliens could be harvesting the rare blood types for this specific reason. It is hybridization. Imagine an energy race so powerful, That they have been piggy backing off of us their genetic experiments. To create hybrids and rna codes so that they evolve rapidly. Make the people sick, collect the mutated specimens. Extract mutated rna sequences and inject new genomes into themselves.
We literally are the perfect species for doing this you know? And the scary part is. This would be enough motive. For any government without morals. This would suffice for a species playing god. After all, Who else in the galaxy is going to keep up with your technology and evolution? Any peace loving planet would be overwhelmed... by locus.
Insights Into Primate Diversity: Lessons from the Rhesus Macaque
June 28, 2012 — New research published in BMC Genetics shows that the rhesus macaque has three times as much genetic variation as humans. However despite much of this extra variation within genes, protein function is not affected. Consequently damaging variations are at similar levels in macaques and humans -- indicating a strong selection pressure to maintain gene function regardless of mutation rate or population size.
Humans and rhesus macaques shared a common ancestor approximately 25 million years ago. Although there are now over seven billion humans on the planet only 100,000 years ago the human population was as low as one million. The effective human population, the number of people required to explain current genetic variation rate, was until recently less than 8,000.
The population size of rhesus macaques is in the millions and is exceeded only by humans (among primates). However there are 13 subspecies which have evolved to exploit environments as diverse as savannah and forests, and across a range of climate zones.
A team of researchers led by Christina Barr and David Goldman from the NIH determined that the effective population size for these primates was 80,000, ten times that of humans. Analysis of genetic variation, using single nucleotide polymorphisms (SNPs), showed that the macaque genome had three times higher genetic variation than humans. Most of these SNP were previously unknown and were disproportionally found in functionally important regions of DNA and each known gene had at least one SNP.
Dr. Goldman explained, "Although macaques have more variation than humans in the protein coding regions of genes, the ratio of variation in these regions compared to non-coding regions is significantly lower. Additionally the macaque variation is less likely to alter protein function. This brings down the amount of damaging variation to a level close to what was actually seen in humans."
Dr Barr continued "Our comparative approach across primate species (human and macaques) gives us a genomic view of evolutionary selection and reaffirms the effects of population history on genetic variation. Not very long ago, on an evolutionary timescale, there were more macaques than people, and the genomes of both species are a legacy of those times past."
The Rhesus monkey can carry many pathogens yet population density is not effected. Much like humans. We have our plagues, but we are as diverse as the Rhesus. If anything had to use a template for a viral being, One that can mutate and evolve in synchronicity with viruses we could see new genetic variations everyday when a pathogen enters a suitable host, the host makes use of that pathogen in rare cases. Those rare cases are what surge Evolution forward. Now the GMO crops. Now the fear campaigns, Now the need to deficient the population. Does this not reach conclusions that we are being denied humane ethics? With something like to dollar backing up a project by those who care not for dollars. They want to isolate these rare blood types. Extract genomes and virally infect themselves. As well as soldiers with a strength and intelligence *syrum*. Those people will house a number of deadly pathogens, conquered by science. Now if this is possible with humans. This is not out of the realm of possibility. That aliens could be harvesting the rare blood types for this specific reason. It is hybridization. Imagine an energy race so powerful, That they have been piggy backing off of us their genetic experiments. To create hybrids and rna codes so that they evolve rapidly. Make the people sick, collect the mutated specimens. Extract mutated rna sequences and inject new genomes into themselves.
We literally are the perfect species for doing this you know? And the scary part is. This would be enough motive. For any government without morals. This would suffice for a species playing god. After all, Who else in the galaxy is going to keep up with your technology and evolution? Any peace loving planet would be overwhelmed... by locus.
edit on 16-2-2013 by CrypticSouthpaw because: (no reason given)
reply to post by CrypticSouthpaw
This got me thinking that maybe scientists can look to find an answer to the ailing antibiotics immunity problem in something like the Rhesus monkey's genetics.
This got me thinking that maybe scientists can look to find an answer to the ailing antibiotics immunity problem in something like the Rhesus monkey's genetics.
reply to post by beautyofperil
www.ncbi.nlm.nih.gov...
These are tests back in 2008, pretty much exactly what you just stated about the MRSA outbreak this year thats becoming a pandemic.
They have found monkeys with isolated mutations and i believe they are working on *syrum* from its genomes to create a new anti body that you will see them market. I don't think that they will vaccinate people with this until they have a syrum to control an outbreak. But i believe they will be gathering extensive human subjects for the varying super mutated diseases coming out with the cultivation of GMO crops and Chemicals as well as drugs that provide certain reactions within people, blood type and pathogen relationship related. New pain killers and such could be used to create an unset of deficiencies and cultivation of certain instances that would be otherwise to rare in nature. Occur on grand scale. Through an intricate web of disinformation and continued funding for genetic research. Little do people know they could be funding the machine making them sick. With the government and companies hiring chemists and biologists to further research on these topics.
Would you like ultra hearing? Heat vision. God knows what they can accomplish with viral gene therapy.
www.ncbi.nlm.nih.gov...
Methicillin-resistant Staphylococcus non-aureus Infection in an Irradiated Rhesus Macaque (Macaca mulatta)
J Am Assoc Lab Anim Sci. 2008 May; 47(3): 64–67. Published online 2008 May. Abstract We describe a case of methicillin-resistant Staphylococcus non-aureus infection in a rhesus macaque (Macaca mulatta). The nonhuman primate described was part of a research project that involved whole-body gamma irradiation and subsequently developed acute generalized dermatitis with skin dryness, peeling, and erythema around the eyes. After initial evaluation, which included microbiologic culture and 6 d of medical treatment, the animal was euthanized due to concern regarding a possible outbreak of infectious or zoonotic disease. On the basis of skin culture, diagnosis of methicillin-resistant Staphylococcus non-aureus was confirmed. This report underscores the importance of the occupational risk of methicillin-resistant Staphylococcus non-aureus to research and animal care staff in a research animal facility setting. Abbreviation: MRSA, methicillin-resistant Staphylococcus aureus
Methicillin-resistant Staphylococcus aureus (MRSA) infection and colonization has occurred in various domestic animals, including horses, dogs, cats, birds, and cattle.3 Transmission of infection from animals to humans and from humans to animals has been reported.2,8,10,15,17,19 MRSA is more common in humans with severe illness, comorbid conditions, and immunosuppression.1 MRSA infection in a rhesus macaque in a research animal facility setting and showing signs of respiratory distress has been reported.13 Similar to MRSA, methicillin-resistant Staphylococcus non-aureus appears to be an emerging pathogen in veterinary medicine. Methicillin-resistant Staphylococcus non-aureus species such as S. epidermidis are seen commonly in the human hospital setting and are sometimes even more resistant than and displace the growth of MRSA.7,11,16 This report describes an acute case of methicillin-resistant Staphylococcus non-aureus in an immunosuppressed rhesus macaque whose infection was characterized by skin dryness, dermatitis, hyperkeratosis, and erythema in the facial area.
These are tests back in 2008, pretty much exactly what you just stated about the MRSA outbreak this year thats becoming a pandemic.
They have found monkeys with isolated mutations and i believe they are working on *syrum* from its genomes to create a new anti body that you will see them market. I don't think that they will vaccinate people with this until they have a syrum to control an outbreak. But i believe they will be gathering extensive human subjects for the varying super mutated diseases coming out with the cultivation of GMO crops and Chemicals as well as drugs that provide certain reactions within people, blood type and pathogen relationship related. New pain killers and such could be used to create an unset of deficiencies and cultivation of certain instances that would be otherwise to rare in nature. Occur on grand scale. Through an intricate web of disinformation and continued funding for genetic research. Little do people know they could be funding the machine making them sick. With the government and companies hiring chemists and biologists to further research on these topics.
Would you like ultra hearing? Heat vision. God knows what they can accomplish with viral gene therapy.
reply to post by CrypticSouthpaw
I actually set on becoming a brain in a cyborg's body but super powers are good too.
I actually set on becoming a brain in a cyborg's body but super powers are good too.
Public release date: 14-Feb-2013
www.eurekalert.org...
Oh look. More evidence. So they are not making super bugs in labs? Infecting people and what not so polyploid humans become noticeable. Get blood samples from doctors and create syrums. A virus can merge with a hosts body in unison for benefits. Scientists try to isolate these people to extract their dna to make these processes much quicker and efficient.
Discovery in HIV may solve efficiency problems for gene therapy
www.eurekalert.org...
Case Western Reserve researchers pinpoint RNA element missing from viral vectors A research team from Case Western Reserve University School of Medicine has discovered an approach that could make gene therapy dramatically more effective for patients. Led by professor Eric Arts, PhD, the scientists discovered that the process of gene therapy is missing essential elements thereby reducing the effectiveness of this treatment. Re-introducing this element into their model system suggests that improvements for gene therapy areon the horizon. The findings are detailed in the article, "A new genomic RNA packaging element in retroviruses and the interplay with ribosomal frameshifting," published today in the journal Cell Host & Microbe. Advances in gene therapy offer promising treatment for genetic abnormalities, tumors and resistance to toxic chemotherapies. Such therapy has been used to treat cystic fibrosis, hemophilia, muscular dystrophy and sickle cell anemia. But a failure to distribute enough modified genetic information to the patient's body has prohibited gene therapy from being more widely used. Gene therapy relies mainly on viruses—which transport genomes inside the cells they infect—to deliver genetic material into a patient's cells. The virus-driven delivery tools are called "viral vectors." Unfortunately, the success rate of viral vectors is uneven. For instance, adenoviruses, a cause for the common cold, and lentiviruses, such as HIV-1, are routinely converted into viral vectors. But adenovirus vectors don't last long, so therapy must be frequently re-administered. And lentiviral vectors, while stable, fail to deliver genetic material to enough defective human cells. Arts, a professor of medicine in the Division of Infectious Diseases and HIV Medicine, learned that lentiviral carriers lack sufficient genetic material necessary for treatment. HIV-1, when converted from virus to lentiviral vector, loses a specific RNA element required to pack its "container" with its own genetic material to be effective. After identifying the problem, researchers introduced the element into a lentiviral vector, successfully and significantly improving the quality and quantity of the gene therapy. Arts and colleagues named the genetic element, Genomic RNA Packaging Enhancer element (or GRPE). During virus production, GRPE coordinates the production and filling of the container with the genetic material of HIV-1, or the desired human gene. Delivery and success of gene therapy for human cells has the potential of increasing five to ten times with the introduction of the GRPE into the lentiviral vector. "Using lentivirus for gene transfer appears to be a safe option," said Stanton L. Gerson, MD, director of the Case Comprehensive Cancer Center and the Asa and Patricia Shiverick- Jane Shiverick (Tripp) Professor of Hematological Oncology at Case Western Reserve School of Medicine and director of the Seidman Cancer Center at University Hospitals Case Medical Center, who is not involved in the study. "This discovery could greatly advance the recent successes ongoing in cancer and childhood congenital diseases. Improvements in the technology of gene delivery identified by Arts and his colleagues could lead to many more effective studies that help patients with many different diseases, including cancer. Its impact could be felt in a few short years." Ultimately, introducing GRPE elements into viral vectors could enhance the ease and effectiveness of gene therapy, which typically uses transplanted human stem cells. Enhanced gene therapy and other improvements in targeted cell delivery might eliminate the need for stem cells and allow cells to be administered directly into patients. ### About Case Western Reserve University School of Medicine Founded in 1843, Case Western Reserve University School of Medicine is the largest medical research institution in Ohio and is among the nation's top medical schools for research funding from the National Institutes of Health. The School of Medicine is recognized throughout the international medical community for outstanding achievements in teaching. The School's innovative and pioneering Western Reserve2 curriculum interweaves four themes--research and scholarship, clinical mastery, leadership, and civic professionalism--to prepare students for the practice of evidence-based medicine in the rapidly changing health care environment of the 21st century. Nine Nobel Laureates have been affiliated with the School of Medicine. Annually, the School of Medicine trains more than 800 MD and MD/PhD students and ranks in the top 25 among U.S. research-oriented medical schools as designated by U.S. News & World Report's "Guide to Graduate Education."
Oh look. More evidence. So they are not making super bugs in labs? Infecting people and what not so polyploid humans become noticeable. Get blood samples from doctors and create syrums. A virus can merge with a hosts body in unison for benefits. Scientists try to isolate these people to extract their dna to make these processes much quicker and efficient.
edit on 17-2-2013 by CrypticSouthpaw because: (no reason given)
interested in Viral gene therapy?
www.genetherapynet.com...
taken from this website. The quote would mess it up but here it is.
"
28 - 30 January 2013
Phacilitate 9th Annual Cell & Gene Therapy Forum 2013
Washington DC, MD
13 - 15 February 2013
Gene Transfer Technologies into Multicellular Eukaryotes
Vienna, Austria
28 February - 2 March 2013
19th Annual Meeting German Society for Gene Therapy (DG-GT e.V.)
Munich, Germany
15 - 16 March 2013
Spring Symposium of the Netherlands Society of Gene & Cell Therapy (NVGCT)
Lunteren, The Netherlands
22 March 2013
French Society of Cell and Gene Therapy (SFTCG) Annual Congress 2013
Paris, France
17 - 19 April 2013
Annual conference of the British Society for Gene Therapy (BSGT)
London, UK
22 April 2013
8th Annual Conference of The Israeli Society of Gene Therapy (ISGCT)
Jerusalem, Israel
22 - 25 April 2013
International Society for Cellular Therapy (ISCT) 19th Annual Meeting
Auckland, New Zealand
5 - 10 May 2013
Gordon Research Conference: Virusses & Cells
Lucca (Barga), Italy
8 – 10 May 2013
8th Australasian Gene Therapy Society Meeting (AGTS)
Sydney, Australia
15 – 18 May 2013
American Society of Gene and Cell Therapy (ASGCT) 16th Annual Meeting
Salt Lake City, Utah
4 – 6 July 2013
The 19th Annual Meeting of the Japan Society of Gene Therapy (JSGT)
Okayama, Japan
12 – 14 August 2013
International Conference on Genetic Engineering & Genetically Modified Organisms
Raleigh, North Carolina
23 – 25 October 2013
2nd International Conference and Exhibition on Cell & Gene Therapy
Orlanda, Florida
24 – 28 October 2013
VII Congress of the Spanish Society of Gene (SETGyC) and Cell Therapy, and XXI Congress of the European Society of Gene and Cell Therapy (ESGCT)
Madrid, Spain
20 – 22 November 2013
12th Annual Gene Therapy Symposium for Heart, Lung, and Blood Diseases"
Sonoma, California
www.genetherapynet.com...
taken from this website. The quote would mess it up but here it is.
"
28 - 30 January 2013
Phacilitate 9th Annual Cell & Gene Therapy Forum 2013
Washington DC, MD
13 - 15 February 2013
Gene Transfer Technologies into Multicellular Eukaryotes
Vienna, Austria
28 February - 2 March 2013
19th Annual Meeting German Society for Gene Therapy (DG-GT e.V.)
Munich, Germany
15 - 16 March 2013
Spring Symposium of the Netherlands Society of Gene & Cell Therapy (NVGCT)
Lunteren, The Netherlands
22 March 2013
French Society of Cell and Gene Therapy (SFTCG) Annual Congress 2013
Paris, France
17 - 19 April 2013
Annual conference of the British Society for Gene Therapy (BSGT)
London, UK
22 April 2013
8th Annual Conference of The Israeli Society of Gene Therapy (ISGCT)
Jerusalem, Israel
22 - 25 April 2013
International Society for Cellular Therapy (ISCT) 19th Annual Meeting
Auckland, New Zealand
5 - 10 May 2013
Gordon Research Conference: Virusses & Cells
Lucca (Barga), Italy
8 – 10 May 2013
8th Australasian Gene Therapy Society Meeting (AGTS)
Sydney, Australia
15 – 18 May 2013
American Society of Gene and Cell Therapy (ASGCT) 16th Annual Meeting
Salt Lake City, Utah
4 – 6 July 2013
The 19th Annual Meeting of the Japan Society of Gene Therapy (JSGT)
Okayama, Japan
12 – 14 August 2013
International Conference on Genetic Engineering & Genetically Modified Organisms
Raleigh, North Carolina
23 – 25 October 2013
2nd International Conference and Exhibition on Cell & Gene Therapy
Orlanda, Florida
24 – 28 October 2013
VII Congress of the Spanish Society of Gene (SETGyC) and Cell Therapy, and XXI Congress of the European Society of Gene and Cell Therapy (ESGCT)
Madrid, Spain
20 – 22 November 2013
12th Annual Gene Therapy Symposium for Heart, Lung, and Blood Diseases"
Sonoma, California
pheromones.com...
Human pheromones and the viruses that make us We Are Viral From the Beginning
June 14th, 2012 1:42 PM by Carl Zimmer in A Planet of Viruses, Evolution, Medicine, Top posts | Excerpt: “On rare occasion, a retrovirus may infect an egg. Now something odd may happen. If the egg becomes fertilized and gives rise to a whole adult individual, all the cells in its body will carry that virus. And if that individual has offspring, the virus gets carried down to the next generation.” My Comment I’m struck by the parallels with The Viruses That Make Us: A Role For Endogenous Retrovirus In The Evolution Of Placental Species by Luis P. Villarreal, which was brought to my attention by Greg Bear. Among his other excellent works, Bear wrote two science fiction novels that incorporated ERV-driven adaptive evolution, and pheromonal communication, which is as essential to communication in a new species of humans as it is in microbes. Pheromones, as we now know, are the chemicals that control nutrient chemical-dependent reproduction in all species. It seems likely that ERVs, including human ERVs (HERVs) cause the changes in intracellular signaling and stochastic gene expression that allow us to use olfaction and odor receptors in the clear evolutionary trail that can be followed from unicellular organisms to insects to humans. The HERVs, for example, need only alter a cell’s ability to metabolize nutrient chemicals (food) to cause downstream effects on every cell of any organism. The metabolism of the nutrient chemicals to pheromones does the rest in the context of adaptive evolution. For those who question whether there is sufficient evidence across species for transgenerational epigenetic inheritance, one need only examine the trail that begins with the nutrient-dependent ecological niche of organisms. The metabolism of the nutrients to pheromones establishes a social niche. In multicellular organisms with a nervous system, ecological and social niche construction contribute equally to the construction of a neurogenic niche (a group of nerve cells) that enables brain development, which facilitates construction of our cognitive niche. My cognitive niche, for example, allows me to recognize patterns, like the design in biology that is apparent in the adaptive evolution that results from ecological, social, neurogenic, and cognitive niche construction.
www.ncbi.nlm.nih.gov...
J Insect Sci. 2005;5:6.
Department of Entomology, University of Massachusetts-Amherst, Amherst, Massachusetts 01003, USA
www.sciencedirect.com...
J Insect Sci. 2005;5:6.
Infection with the insect virus Hz-2v alters mating behavior and pheromone production in female Helicoverpa zea moths.
Department of Entomology, University of Massachusetts-Amherst, Amherst, Massachusetts 01003, USA
Abstract The effect of Hz-2V virus infection on the reproductive physiology and behavior of infected Helicoverpa zea female moths was examined. In the absence of males, infected females exhibited calling behavior and called as often but for shorter periods on average than control females. As expected, control females mated with males for extend periods when they were present and did not call after mating, while virus-infected females made many frequent contacts with males and continued to call even after these contacts. Virus-infected females were found to produce five to seven times more pheromone than control females and attracted twice as many males as did control females in flight tunnel experiments. The ability of Hz-2V to alter the physiology and behavior of infected females observed here may serve to facilitate the transmission of virus in insect populations.
www.sciencedirect.com...
Integration of early virus treatment with a pheromone detection system to control Douglas-fir tussock moth, Orgyia pseudotsugata (Lepidoptera: Lymantriidae), populations at pre-outbreak levels
Abstract A naturally occurring virus often leads to the development of an epizootic late in the outbreak cycle of the Douglas-fir tussock moth, but not before significant damage occurs to the trees. This virulent virus can be mass-produced in the laboratory and, when applied early in the outbreak cycle, can prevent severe defoliation. This, however, requires that an early-warning system be integrated with a virus treatment. The development and integration of a pheromone monitoring system with a virus treatment is described. Stands susceptible to Douglas-fir tussock-moth outbreaks are defined by overlying maps of past outbreaks, forest and habitat types, and climatic zones. Pheromone-baited traps are placed and monitored annually at permanent locations in the susceptible areas. Measuring annual trends of moth density indicates the time and location of the next outbreak. Trap-catch data provide an early warning of impending outbreaks. This is confirmed by ground reconnaissance. Insect density and defoliation is predicted from egg-mass and larval sampling. The virus then can be applied from the air or from the ground into threatened stands to initiate an epizootic to prevent the development of an outbreak and to minimize tree damage. The virus appears to spread, and field tests with reduced dosages indicate that that small amount of virus applied can still decimate larval populations and prevent tree mortality, at considerably reduced cost.
edit on 17-2-2013 by CrypticSouthpaw because: (no reason given)
check out the US page for agriculture lol.
Just look at this gov page after reading everything iv provided and what does it looks like.
www.ars.usda.gov...
Beneficial insects
Insect pheromones, attractants, & repellents
Pest-killing viruses & microbes
Genetically engineered plants & other molecular approaches
So all of this will have effect on society. And as we are virally impressionable what traits we genetically alter within all of our experiments have vast impacts on our genetics. It would be wise for a government to utilize these techniques well the possibilities are viable. If they can keep people dumb and ignorant of what they are doing. All the power to them. Current events aren't the only thing we should be worrying about.
but we have nothing to worry about right? And this plan isn't being carried out? Wrong.
Just look at this gov page after reading everything iv provided and what does it looks like.
www.ars.usda.gov...
WELCOME TO THE Invasive Insect Biocontrol and Behavior Laboratory
he Invasive Insect Biocontrol and Behavior Laboratory was formed in 2007 from the former Insect Biocontrol & Chemicals Affecting Insect Behavior Laboratories. Our mission is to develop new, cost-effective and sustainable strategies for controlling native insect pests and newly-introduced invasive species. Our laboratory uses a multidisciplinary approach to develop and evaluate a wide range of methods and tools for pest control, including...he Invasive Insect Biocontrol and Behavior Laboratory was formed in 2007 from the former Insect Biocontrol & Chemicals Affecting Insect Behavior Laboratories. Our mission is to develop new, cost-effective and sustainable strategies for controlling native insect pests and newly-introduced invasive species. Our laboratory uses a multidisciplinary approach to develop and evaluate a wide range of methods and tools for pest control, including...
Beneficial insects
Insect pheromones, attractants, & repellents
Pest-killing viruses & microbes
Genetically engineered plants & other molecular approaches
So all of this will have effect on society. And as we are virally impressionable what traits we genetically alter within all of our experiments have vast impacts on our genetics. It would be wise for a government to utilize these techniques well the possibilities are viable. If they can keep people dumb and ignorant of what they are doing. All the power to them. Current events aren't the only thing we should be worrying about.
but we have nothing to worry about right? And this plan isn't being carried out? Wrong.
edit on 17-2-2013 by CrypticSouthpaw because: (no reason given)
discovermagazine.com...
An unknown number of women may perceive millions of colors invisible to the rest of us. One British scientist is trying to track them down and understand their extraordinary power of sight.
The Humans With Super Human Vision
An unknown number of women may perceive millions of colors invisible to the rest of us. One British scientist is trying to track them down and understand their extraordinary power of sight.
An average human, utterly unremarkable in every way, can perceive a million different colors. Vermilion, puce, cerulean, periwinkle, chartreuse—we have thousands of words for them, but mere language can never capture our extraordinary range of hues. Our powers of color vision derive from cells in our eyes called cones, three types in all, each triggered by different wavelengths of light. Every moment our eyes are open, those three flavors of cone fire off messages to the brain. The brain then combines the signals to produce the sensation we call color. Vision is complex, but the calculus of color is strangely simple: Each cone confers the ability to distinguish around a hundred shades, so the total number of combinations is at least 1003, or a million. Take one cone away—go from being what scientists call a trichromat to a dichromat—and the number of possible combinations drops a factor of 100, to 10,000. Almost all other mammals, including dogs and New World monkeys, are dichromats. The richness of the world we see is rivaled only by that of birds and some insects, which also perceive the ultraviolet part of the spectrum. Researchers suspect, though, that some people see even more. Living among us are people with four cones, who might experience a range of colors invisible to the rest. It’s possible these so-called tetrachromats see a hundred million colors, with each familiar hue fracturing into a hundred more subtle shades for which there are no names, no paint swatches. And because perceiving color is a personal experience, they would have no way of knowing they see far beyond what we consider the limits of human vision. Over the course of two decades, Newcastle University neuroscientist Gabriele Jordan and her colleagues have been searching for people endowed with this super-vision. Two years ago, Jordan finally found one. A doctor living in northern England, referred to only as cDa29 in the literature, is the first tetrachromat known to science. She is almost surely not the last. The first hint that tetrachromats might exist came in a 1948 paper on color blindness. Dutch scientist HL de Vries was studying the eyes of color-blind men, who, along with two normal cones, possess a mutant cone that is less sensitive to either green or red, making it difficult for them to distinguish the two colors. He tested their vision by having them perform a basic matching task. Twiddling the dials on a lab instrument back and forth, the men had to mix red and green light so that the result, to their eyes, matched a standard shade of yellow. To compensate for their difficulty in discerning hues, color-blind men need to add more green or red than normal trichromats to make a match. Out of curiosity, De Vries tested the daughters of one subject and observed that even though they were not color-blind—they seemed to distinguish red and green as well as anyone—they needed more red in their test light than normal people to make the match precise. If the women weren’t color-blind, what was going on? Pondering the situation, De Vries thought he saw an explanation. Color blindness ran in families, affecting men but not women. While color-blind men had two normal cones and one mutant cone, De Vries knew that the mothers and daughters of color-blind men had the mutant cone and three normal cones—a total of four separate cones in their eyes. He suspected the extra cone could be why the women perceived color differently—not because they saw less than most people but because they saw more. He speculated that such women might be using the fourth cone to distinguish more colors than a trichromat, but he buried this insight on the last page of the paper. De Vries never wrote about four-coned women again.
In the 1980s neuroscientist John Mollon of Cambridge University, then Jordan’s adviser there, was studying color vision in monkeys and became interested in De Vries’s note on tetrachromacy. Mollon and Jordan realized that since color blindness is common, four-coned women must be as well. Jordan estimates they make up as many as 12 percent of women. To find if tetrachromats were hidden in this group, the researchers sought out the mothers of color-blind sons and had them take matching tests similar to the one used by De Vries, but with a twist. If they were true tetrachromats, they would never be able to make a satisfactory match, because they would be able to sense color gradations beyond those available on the test. No luck: Mollon and Jordan found that women with four cones could consistently make a match on the tests. Jordan began to have doubts. Perhaps the fourth cone was not active. Perhaps super-vision was not real. In 2007 Jordan, now at Newcastle, returned to testing using a new method. Sitting in a dark room, peering into a lab device, women saw three colored circles flash before their eyes. To a trichromat, they all looked the same. To a tetrachromat, though, one would stand out. That circle was not a pure color but a subtle mixture of red and green light randomly generated by a computer. Only a tetrachromat would be able to perceive the difference, thanks to the extra shades made visible by her fourth cone. Jordan gave the test to 25 women who all had a fourth cone. One woman, code named cDa29, got every single question correct. “I was jumping up and down,” Jordan says. She had finally found her tetrachromat. What would it be like to see through cDa29’s eyes? Unfortunately, she cannot describe how her color vision compares with ours, any more than we can describe to a dichromatic person what red looks like. “This private perception is what everybody is curious about,” Jordan says. “I would love to see that.” Jordan’s next challenge is discovering why cDa29 is different from the other women she tested. “We now know tetrachromacy exists,” Jordan says. “But we don’t know what allows someone to become functionally tetrachromatic, when most four-coned women aren’t.” Jay Neitz, a vision researcher at the University of Washington, thinks that potential tetrachromats may need practice to awaken their abilities. “Most of the things that we see as colored are manufactured by people who are trying to make colors that work for trichromats,” he says. “It could be that our whole world is tuned to the world of the trichromat.” He also suspects the natural world may not have enough variation in color for the brain to learn to use a fourth cone. Tetrachromats might never need to draw on their full capacity. They may be trapped in a world tailored to creatures with lesser powers. Perhaps if these women regularly visited a lab where they had to learn—really learn—to tell extremely subtle shades apart, they would awaken in themselves the latent abilities of their fourth cone. Then they could begin to see things they had never tried to see before, a kaleidoscope of colors beyond our imagining.
www.xrite.com...
here is a color test ! try it yourself! see if you are a tetrachromat.
www.perceptionweb.com...
ECVP 2004 Abstract
a movie about a tetrachromat.
I'm thinking we track one down, kidnap em and do a series of viral tests > Joking. But they are working on viral gene therapy by finding these individuals and isolating the virus that is causing this effect. Take some cells cultivate then inject them into test subject B to see if we have a tretrachromatic effect. Beyond that. This is not all that is going on. There are numerous other genetic traits scientists are trying to track down brought on by the synchronicity of bonding virus proteins, it is in the best interest of biologists and scientists to isolate genomes created by RNA for the *benefit* of mankind.
www.dnalc.org... Check out this website.
here is a color test ! try it yourself! see if you are a tetrachromat.
www.perceptionweb.com...
ECVP 2004 Abstract
Detecting tetrachromacy in human subjects Z Jakab, K Wenzel Human tetrachromacy is a rare condition in which the retina contains four different types of wavelength-selective photoreceptors (cones). There exist reports of both L-cone tetrachromacy, and M-cone tetrachromacy (two subtypes of the long-wave-sensitive or the middle-wave-sensitive cones in the same retina). We developed two psychophysical procedures, one for identifying L-cone tetrachromacy, and another to test for M-cone tetrachromacy. First we presented to subjects 720 nm and 760 nm monochromatic lights in the two halves of a vertically split circular field viewed through the aperture of a Pulfrich spectrophotometer. Subjects were asked to adjust the intensity of the 720 nm light to achieve a perfect match; we expected that L-cone tetrachromats would always sense a residual hue difference between the two lights. In testing for M-cone tetrachromacy, we looked for a peak of discriminability (corresponding to the sensitivity crossover of two slightly different M-cone subtypes) in the middle portion of the spectrum while the subjects' L-cones and M-cones were desensitised by a mixture of 380 nm and 720 nm lights. Eighty colour-normal subjects were examined; one L-cone tetrachromat and one M-cone tetrachromat were identified. Further examination of these subjects is in progress.
a movie about a tetrachromat.
I'm thinking we track one down, kidnap em and do a series of viral tests > Joking. But they are working on viral gene therapy by finding these individuals and isolating the virus that is causing this effect. Take some cells cultivate then inject them into test subject B to see if we have a tretrachromatic effect. Beyond that. This is not all that is going on. There are numerous other genetic traits scientists are trying to track down brought on by the synchronicity of bonding virus proteins, it is in the best interest of biologists and scientists to isolate genomes created by RNA for the *benefit* of mankind.
www.dnalc.org... Check out this website.
edit on 17-2-2013 by CrypticSouthpaw because: (no reason given)
www.health-matrix.net...
www.health-matrix.net...
Should read this. Talks a lot about what i'm mentioning here.
Viral “Junk” DNA The greatest shock of genomic science was to find that the human genome contains more viral than “human” genes. That is, the human genome is made from thousands of viruses that infected our distant ancestors. They got there by infecting eggs or sperm, inserting their own DNA into ours.
Viruses are peculiar things that at a zoomed-in level may look very pretty or downright creepy depending on the virus. A virus may have DNA or RNA and the type of genetic material depends on the function and nature of the virus. Some are very infectious, others allowed us be alive since the gene that encodes for a protein that allows for babies to fuse to their mothers during pregnancy, is a virus gene.[2] Most of the genetic diversity can be found in virus genes. Scientists agree that there are some 1,000,000,000,000,000,000,000,000,000,000 viruses in the ocean and it matches almost nothing to any gene from any microbe, animal, plant or other organism, even from any other known virus. All living things have hundreds or thousands of genes imported by viruses. There are a group of viral species known as retroviruses which insert their genetic material into the host cell’s DNA. When the host cell divides, it copies the virus’s DNA along with its own. Retroviruses have “on switches” that prompt their host cell to make proteins out of nearby genes. Sometimes their switches turn on host genes that ought to be kept shut off, and cancer can result. This is precisely what our junk DNA –ncRNA- seems to be doing “next” to genes that have to do with stem cells and cancer cells. What is known as endogenous retrovirus – endogenous meaning generated within, are the viruses that lurk in the genomes of just about every major group of vertebrates, from fish to reptiles to mammals. Virologists have found retrovirus-like segments in our human genome and they were able to track its genetic code down to an original functioning virus. The virus was called Phoenix, for the mythical bird that rose from its own ashes. It is known that part of our junk DNA, the retrotransposable elements, are viral in its origin. It includes the endogenous retroviruses. But it is now argued that ncRNA (non coding RNA) might be viral in its origin as well.[3] This has interesting implications in the sense that epigenetic control of gene expression involves this junk DNA – ncRNAs.[4] It would mean that our entire junk DNA (98%) might well be very functional epigenetically speaking (more info on epigenetics below), and active in the induction of regulatory genes that code for stem cells, or for reprogramming o modulating genes known to response to oxidative stress, DNA damage and p53 – a protein that regulates the cell cycle and is implicated in about half of all human cancers. You might be wondering why we are reviewing all this viral genome potential. As it happens, the damage done by evil lectins – antinutrients – in our diet is through a lock and key mechanism, that is, a circulating lectin serves as a key that unlocks the cell to within it attaches. Evil lectins can initiate a cascade of events once they attach to the cell “mem-brain” that may lead to attraction of the immune system, cell death, production of chemicals, multiplication of the cell and so forth. It depends. And it might well depend on the adaptation response from the viral-like properties inside the cell, our “junk” DNA. Harmful lectins – such as the ones found in gluten, soy, dairy, corn – cause inflammation and damage without a defense/immune response which end up being secondary to the initial damage. Some response in quite a drastic way (i.e. autoimmune diseases) others respond in a milder way, constituting thus the wide nature of symptoms among people. Moreover, wheat’s evil lectin (WGA) and viruses share similar properties. For instance, when the influenza virus incorporates its own genetic material into our cells, the defense/immune system must attack its own virally transformed cell in order to fight the infection. WGA has access to our bodies and to our cells’ “mem-brain’s” through viral ports. Then they influence gene expression and trigger autoimmune attacks like viruses do. As John B. Symes, D.V.M. pointed
www.health-matrix.net...
Should read this. Talks a lot about what i'm mentioning here.
edit on 17-2-2013 by CrypticSouthpaw because: (no reason given)
endoftheamericandream.com...
oh look. Does not surprise me that this exactly whats going on. Whats the military up to with viral gene therapy? Lets see.
"So how is this possible?
How would you genetically modify a human to be able to have these abilities?
A different Daily Mail article recently explained how this basically works…."
U.S. Super Soldiers Of The Future Will Be Genetically Modified Transhumans Capable Of Superhuman Feats
oh look. Does not surprise me that this exactly whats going on. Whats the military up to with viral gene therapy? Lets see.
The future of war is going to look really, really weird. The “super soldier” research that DARPA (the Defense Advanced Research Projects Agency) is working on right now is unlike anything we have ever seen before. If DARPA is successful, and if the American people don’t object, the soldiers of the future will be genetically modified transhumans capable of superhuman feats. Do you want a soldier that can run faster than Usain Bolt? DARPA is working on that. Do you want a soldier that won’t need food or sleep for days? DARPA is working on that? Do you want a soldier that can regrow lost limbs? DARPA is working on that. Do you want a soldier that can outlift Olympic weightlifters and that can communicate telepathically? DARPA is working on that. Americans flock to movies about superheroes and mutants, and soon they may actually have real life “superheroes” and “mutants” fighting their wars for them. But at what cost? A recent Daily Mail article detailed many of the strange research projects that DARPA is working on right now. The fact that DARPA has actually allowed these projects to be revealed in the mainstream media probably means that the development stage is nearly over and they are ready to try to convince a wary public to accept them….
Tomorrow’s soldiers could be able to run at Olympic speeds and will be able to go for days without food or sleep, if new research into gene manipulation is successful. According to the U.S. Army’s plans for the future, their soldiers will be able to carry huge weights, live off their fat stores for extended periods and even regrow limbs blown apart by bombs. The plans were revealed by novelist Simon Conway, who was granted behind-the-scenes access to the Pentagon’s high-tech Defence Advanced Research Projects Agency.
"So how is this possible?
How would you genetically modify a human to be able to have these abilities?
A different Daily Mail article recently explained how this basically works…."
Most gene modification techniques involve placing genetically modified DNA inside a virus and injecting it into the human body. The virus then enters human cells, and its modified DNA attaches itself to the human DNA inside those cells.
When you really stop and think about this kind of technology, the implications are staggering. Could viruses be used to genetically modify humanity on a large scale? How would the rest of humanity respond to a “super race” of mutants that are clearly “superior” to the rest of us in a bunch of different ways? When you start messing with creation, it opens up Pandora’s Box. The possibilities are endless, but so are the potential problems. Just because we can do something does not mean that we should. There may be consequences decades down the road that we cannot even conceive of right now. Other “super soldier” research projects that DARPA is working on at the moment involve advanced technology and robotics rather than genetic modification. For example, DARPA is developing helmets that would allow our soldiers to communicate telepathically….
More recently, DARPA’s Silent Talk programme has been exploring mind-reading technology with devices that can pick up the electrical signals inside soldiers’ brains and send them over the internet. With these implants, entire armies will be able to talk without radios. Orders will leap instantly into soldiers’ heads and commanders’ wishes will become the wishes of their men.
I don’t know about you, but I would not want anyone reading my thoughts or beaming orders directly into my brain. DARPA is also working on “exoskeletons” that will enable soldiers to lift incredible weights without tiring and perform other physical tasks that normal soldiers simply could not do. You can see video of this kind of exoskeleton being demonstrated right here. DARPA is also hoping to one day implant microchips into our soldiers that will constantly monitor the health and physical condition of our boys and girls in the field. For many, these new technologies are very exciting. For others, they cross the line. Merging men with machines or messing with the very fabric of life is the kind of thing that science fiction movies are made of. Unfortunately, if we make a very serious mistake we just can’t get up and turn off the movie. Any mistakes that we make could stay with us indefinitely. But at this point it looks like there is very little standing in the way of these kinds of technology becoming mainstream. Tests on rats have already shown what is possible….
In 2005, Ronald Evans, a hormone expert working at the Salk Institute of Biological Studies in La Jolla, California, showed how genetic modification can increase the athletic power of mice. Evans produced a group of genetically modified mice with an increased amount of slow-twitch muscle fibre. This type of fibre is associated with strong cardiovascular muscles and boosts an athlete’s endurance. Evans’s mice could run for an hour longer than normal mice, were resistant to weight gain no matter what they were fed on, and remained at peak fitness even when they took no exercise.
How much do you think people would pay to be able to remain at peak fitness without doing any exercise at all? When the general public realizes what is possible there will be an overwhelming demand for these technologies. So just how far can all of this go? Well, futurist Ray Kurzeil believes that we are only about 20 years away from actually achieving immortality….
Ray Kurzweil, a world-renowned scientist and author of The Singularity is Near, thinks the world as we know it will be unrecognizable in 20 years. One of the changes he thinks are possible: Scientists may finally crack immortality. “I and many other scientists now believe that in around 20 years we will have the means to reprogramme our bodies’ stone-age software so we can halt, then reverse, aging,” he writes in The Sun. “Then nanotechnology will let us live for ever. Ultimately, nanobots will replace blood cells and do their work thousands of times more effectively.”
Eternal life? I wouldn’t count on the human body being able to live forever. But without a doubt we are going to see a whole lot of humans attempting to “merge with technology” and “reprogram themselves” through genetic modification in future years. The wars of the future will look nothing like the wars of the past. The genetically modified soldiers of the future will be supported by robots on the ground and by “swarms of drones” in the sky. In fact, the “swarms of drones” are already here. The following is from a recent CBS News article….
According to a Boeing press release, the researchers and engineers conducted the test flights in Oregon in June using two ScanEagle drones which performed like a “swarm of insects.” The flight operator was able to connect with the autonomous drones using only a laptop and a military radio. Boeing engineers said the drones were able to complete tasks more efficiently by communicating with each other. “This swarm technology may one day enable warfighters in battle to request and receive time-critical intelligence, surveillance and reconnaissance information directly from airborne (unmanned aerial vehicles) much sooner than they can from ground control stations today,” Gabriel Santander, program director of Advanced Autonomous Networks for Boeing Phantom Works, said in the press release.
Technology is advancing at such a rapid pace that it is really hard to keep track of it all. But where is it taking us? Recently I wrote about the nightmarish high tech Big Brother surveillance grid that is going up all around us. Our lives are becoming completely dominated by technology, and that is a very dangerous thing. We like to think that all of these new technologies will always be used for good and will never fall into the hands of tyrannical madmen, but history tells us that liberty and freedom are very rare phenomenons. Throughout most of human history, most people have lived under some form of tyranny. And today liberty and freedom are already rapidly disappearing all over the globe. Technology has progressed to the point where it would definitely be possible for a “scientific dictatorship” to completely and totally dominate humanity unlike anything we have ever seen before. So we should be very careful about what we create. We might be creating our own living hell.
So there you have it. We are taking sickness and technology to new levels. The predictions about us reaching a peak of enlightenment speaks of this. When we come to terms with what we are and what we can do. We are abusing it to our fullest extent and as far as the researchers, and the men behind the curtain. This is priority number one. Not the comfort of the people. Not the health of the people. Not the freedom we want. The whole big brother campaign is to accelerate procedures. To actively seek in multiple studies in pandemics and bio technological advancements. We will carry our disease and technology with us to the heavens. Like a mighty plague, we will devour this universe and all that come in contact. We are moving towards a total state of war that will last for eternity. The war that is evolution.
No doubt other planets are watching our atrocities and are fearing the steps into godhood we are taking. We are quickly becoming a race that will be revered by all. Wither we are enslaved we persevere as viruses. You cannot suppress a virus, And that was their mistake for trying. The mistake is done. And the future is locked. Behold the future of humanity. The locus of space.
Some very interesting info in this video i think people should check out.
like i was saying. the interstellar beings of this galaxy have all their eyes on us. And we may be siding with a species for war. If those are space stations. Why are they orbiting earth in close proximity? Is there something they are afraid of?
edit on 18-2-2013 by CrypticSouthpaw because:
(no reason given)
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