Tesla_WTC_Solution
3rd May 2013, 16:44
http://www.newsinferno.com/?p=19310
Glaxo’s Infant Rotavirus Vaccine Tainted with Pig Virus, FDA Says
Posted on March 23, 2010 by Laurie Villanueva
http://www.cnn.com/2010/HEALTH/03/22/rotavirus.vaccine/index.html
Rotarix rotavirus vaccine contaminated, officials say
By Tom Watkins, CNN
March 22, 2010 4:22 p.m. EDT
(CNN) -- Federal health authorities recommended Monday that doctors suspend using Rotarix, one of two vaccines licensed in the United States against rotavirus, saying the vaccine is contaminated with material from a pig virus.
http://www.yourlawyer.com/articles/title/merck-vaccine-facility-cited-for-problems-by-fda
Merck Vaccine Facility Cited for Problems by FDA
tainted Hepatitis B vaccines, etc
http://rightteachings.wordpress.com/2006/04/07/fda-and-tainted-rubella-vaccine/
FDA and tainted rubella vaccine
Posted on April 7, 2006 by jamiebeu
Below is the letter sent to the FDA from Children of God for Life, requesting the import of the untainted Takahashi rubella vaccine (i.e., a rubella vaccine that does not use aborted fetal tissue as a substrate, like the one that Merck does) on behalf of nearly 2,000 children.
http://vactruth.com/2011/05/09/cow-fetuses-contaminated-vaccines-fda-did-nothing/
“Almost 2 years ago, scientists at the Bureau of Biologics of the Food and Drug Administration (FDA) reported that all live virus vaccines are grossly contaminated with phage (viruses that infect bacteria).” [emphasis mine]
http://forum.prisonplanet.com/index.php?topic=221822.0
Bacteriophages: A Sinister Synergy. How Viruses Enable Genetic Engineering!
« on: November 10, 2011, 01:19:33 PM »
global_fiefdom
Member Banned
Posts: 720
Through this thread, I wanted to bring this to the attention of all here who worry (and rightfully so!) about the safety of vaccines, the prevalence of bio- nano- and micro-warfare, and the idea that funding for innocuous programs like veterinary research could easily be redirected to weapons development programs and eugenics efforts.
The Lambda RED Delivery System:
http://www.ncbi.nlm.nih.gov/pubmed/11445160
FEMS Microbiol Lett. 2001 Jul 10;201(1):9-14.
What makes the bacteriophage lambda Red system useful for genetic engineering: molecular mechanism and biological function.
Through this thread, I wanted to bring this to the attention of all here who worry (and rightfully so!) about the safety of vaccines, the prevalence of bio- nano- and micro-warfare, and the idea that funding for innocuous programs like veterinary research could easily be redirected to weapons development programs and eugenics efforts.
The Lambda RED Delivery System:
http://www.ncbi.nlm.nih.gov/pubmed/11445160
FEMS Microbiol Lett. 2001 Jul 10;201(1):9-14.
What makes the bacteriophage lambda Red system useful for genetic engineering: molecular mechanism and biological function.
Poteete AR.
Source
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. anthony.poteete@umassmed.edu
Abstract
Recent studies have generated interest in the use of the homologous recombination system of bacteriophage lambda for genetic engineering. The system, called Red, consists primarily of three proteins: lambda exonuclease, which processively digests the 5'-ended strand of a dsDNA end; beta protein, which binds to ssDNA and promotes strand annealing; and gamma protein, which binds to the bacterial RecBCD enzyme and inhibits its activities. These proteins induce a 'hyper-rec' state in Escherichia coli and other bacteria, in which recombination events between DNA species with as little as 40 bp of shared sequence occur at high frequency. Red-mediated recombination in the hyper-rec bacterium proceeds via a number of different pathways, and with the involvement of different sets of bacterial proteins, depending in part on the nature of the recombining DNA species. The role of high-frequency double-strand break repair/recombination in the life cycle of the lambdoid phages is discussed.
_______________________________
http://en.wikipedia.org/wiki/SV40
SV40 is an abbreviation for Simian vacuolating virus 40 or Simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that has the potential to cause tumors, but most often persists as a latent infection.
SV40 became a highly controversial subject after it was revealed that millions were exposed to the virus after receiving a contaminated polio vaccine.[1]
The virus was first identified by Bernice E. Eddy (based on a work of her and Sarah Stewart about Polyoma viruses) in 1960 in cultures of rhesus monkey kidney cells that were being used to produce polio vaccine.[2][3] It was named for the effect it produced on infected green monkey cells, which developed an unusual number of vacuoles. This observation was repeated and confirmed by Hilleman and Sweet who were employed by Merck in their vaccine division. The complete viral genome was sequenced by Walter Fiers and his team at the University of Ghent (Belgium) in 1978.[4] The virus is dormant and is asymptomatic in Rhesus monkeys. The virus has been found in many macaque populations in the wild, where it rarely causes disease. However, in monkeys that are immunodeficient—due to, for example, infection with Simian immunodeficiency virus—SV40 acts much like the human JC and BK polyomaviruses, producing kidney disease and sometimes a demyelinating disease similar to PML. In other species, particularly hamsters, SV40 causes a variety of tumors, generally sarcomas. In rats, the oncogenic SV40 Large T-antigen was used to establish a brain tumor model for PNETs and medulloblastomas.[5]
_______________________________
http://en.wikipedia.org/wiki/Polyomaviridae
Polyomaviruses are DNA-based (double-stranded DNA, ~5000 base pairs, circular genome), small (40-50 nanometers in diameter), and icosahedral in shape, and do not have a lipoprotein envelope. Moreover, the genome possess early and late genes, contributing to its complex transcription program. They are potentially oncogenic (tumor-causing); they often persist as latent infections in a host without causing disease, but may produce tumors in a host of a different species, or a host with an ineffective immune system. The name polyoma refers to the viruses' ability to produce multiple (poly-) tumors (-oma).
_______________________________
https://en.wikipedia.org/wiki/Tuberous_sclerosis
Tuberous sclerosis or tuberous sclerosis complex (TSC) is a rare multi-system genetic disease that causes non-malignant tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. A combination of symptoms may include seizures, developmental delay, behavioral problems, skin abnormalities, lung and kidney disease. TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin respectively. These proteins act as tumor growth suppressors, agents that regulate cell proliferation and differentiation.[1]
The name, composed of the Latin tuber (swelling) and the Greek skleros (hard), refers to the pathological finding of thick, firm and pale gyri, called "tubers," in the brains of patients postmortem. These tubers were first described by Désiré-Magloire Bourneville in 1880; the cortical manifestations may sometimes still be known by the eponym Bourneville's disease.
_________________________________________________________
http://www.ncbi.nlm.nih.gov/pubmed/9813776
Performing your original search, autism tuberous sclerosis, in PubMed will retrieve 238 records.
J Autism Dev Disord. 1998 Oct;28(5):407-14.
Autism and tuberous sclerosis.
Smalley SL.
Source
Department of Psychiatry, University of California-Los Angeles-School of Medicine 90024, USA.
Abstract
Autism and pervasive developmental disorders (PDD) are common in tuberous sclerosis (TSC). The frequency of autism is about 25%, with 40-45% of TSC cases meeting criteria for autism or PDD. Among autistic populations, the frequency of TSC is 1-4% and perhaps as high as 8-14% among the subgroup of autistic individuals with a seizure disorder. Mental retardation (MR) and seizures, particularly infantile spasms, are significant risk factors in the development of autism/PDD in TSC; however, neither are sufficient or necessary for the development of these behaviors. The mechanism underlying the association of autism and TSC is as yet unclear but clinical features and neuroimaging investigations suggest that an abnormal TSC gene may directly influence the development of autism rather than it being a secondary effect of seizures or MR. The presence of autism/PDD may arise if the TSC gene mutations occur at critical stages of neural development in neural tissue of brain regions critical in the development of autism.
PMID: 9813776 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms
LinkOut - more resources
__________________________________________
http://www.ncbi.nlm.nih.gov/pubmed/20345322
J Neurovirol. 2010 Mar;16(2):141-9. doi: 10.3109/13550281003685839.
Association of autism with polyomavirus infection in postmortem brains.
Lintas C, Altieri L, Lombardi F, Sacco R, Persico AM.
Source
Laboratory of Molecular Psychiatry and Neurogenetics, University Campus Bio-Medico, Rome, Italy.
Abstract
Autism is a highly heritable behavioral disorder. Yet, two decades of genetic investigation have unveiled extremely few cases that can be solely explained on the basis of de novo mutations or cytogenetic abnormalities. Vertical viral transmission represents a nongenetic mechanism of disease compatible with high parent-to-offspring transmission and with low rates of disease-specific genetic abnormalities. Vertically transmitted viruses should be found more frequently in the affected tissues of autistic individuals compared to controls. Our initial step was thus to assess by nested polymerase chain reaction (PCR) and DNA sequence analysis the presence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV1), herpes simplex virus type 2 (HSV2), human herpes virus 6 (HHV6), BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) in genomic DNA extracted from postmortem temporocortical tissue (Brodmann areas 41/42) belonging to 15 autistic patients and 13 controls. BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P < .05). The majority of positives yielded archetypal sequences, whereas six patients and two controls unveiled single-base pair changes in two or more sequenced clones. No association is present with the remaining viruses, which are found in relatively few individuals (N <or= 3). Also polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P = .08). Follow-up studies exploring vertical viral transmission as a possible pathogenetic mechanism in autistic disorder should focus on, but not be limited to, the role of polyomaviruses.
Comment in
Polyomaviruses and autism: more than simple association? [J Neurovirol. 2010]
PMID: 20345322 [PubMed - indexed for MEDLINE]
Glaxo’s Infant Rotavirus Vaccine Tainted with Pig Virus, FDA Says
Posted on March 23, 2010 by Laurie Villanueva
http://www.cnn.com/2010/HEALTH/03/22/rotavirus.vaccine/index.html
Rotarix rotavirus vaccine contaminated, officials say
By Tom Watkins, CNN
March 22, 2010 4:22 p.m. EDT
(CNN) -- Federal health authorities recommended Monday that doctors suspend using Rotarix, one of two vaccines licensed in the United States against rotavirus, saying the vaccine is contaminated with material from a pig virus.
http://www.yourlawyer.com/articles/title/merck-vaccine-facility-cited-for-problems-by-fda
Merck Vaccine Facility Cited for Problems by FDA
tainted Hepatitis B vaccines, etc
http://rightteachings.wordpress.com/2006/04/07/fda-and-tainted-rubella-vaccine/
FDA and tainted rubella vaccine
Posted on April 7, 2006 by jamiebeu
Below is the letter sent to the FDA from Children of God for Life, requesting the import of the untainted Takahashi rubella vaccine (i.e., a rubella vaccine that does not use aborted fetal tissue as a substrate, like the one that Merck does) on behalf of nearly 2,000 children.
http://vactruth.com/2011/05/09/cow-fetuses-contaminated-vaccines-fda-did-nothing/
“Almost 2 years ago, scientists at the Bureau of Biologics of the Food and Drug Administration (FDA) reported that all live virus vaccines are grossly contaminated with phage (viruses that infect bacteria).” [emphasis mine]
http://forum.prisonplanet.com/index.php?topic=221822.0
Bacteriophages: A Sinister Synergy. How Viruses Enable Genetic Engineering!
« on: November 10, 2011, 01:19:33 PM »
global_fiefdom
Member Banned
Posts: 720
Through this thread, I wanted to bring this to the attention of all here who worry (and rightfully so!) about the safety of vaccines, the prevalence of bio- nano- and micro-warfare, and the idea that funding for innocuous programs like veterinary research could easily be redirected to weapons development programs and eugenics efforts.
The Lambda RED Delivery System:
http://www.ncbi.nlm.nih.gov/pubmed/11445160
FEMS Microbiol Lett. 2001 Jul 10;201(1):9-14.
What makes the bacteriophage lambda Red system useful for genetic engineering: molecular mechanism and biological function.
Through this thread, I wanted to bring this to the attention of all here who worry (and rightfully so!) about the safety of vaccines, the prevalence of bio- nano- and micro-warfare, and the idea that funding for innocuous programs like veterinary research could easily be redirected to weapons development programs and eugenics efforts.
The Lambda RED Delivery System:
http://www.ncbi.nlm.nih.gov/pubmed/11445160
FEMS Microbiol Lett. 2001 Jul 10;201(1):9-14.
What makes the bacteriophage lambda Red system useful for genetic engineering: molecular mechanism and biological function.
Poteete AR.
Source
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. anthony.poteete@umassmed.edu
Abstract
Recent studies have generated interest in the use of the homologous recombination system of bacteriophage lambda for genetic engineering. The system, called Red, consists primarily of three proteins: lambda exonuclease, which processively digests the 5'-ended strand of a dsDNA end; beta protein, which binds to ssDNA and promotes strand annealing; and gamma protein, which binds to the bacterial RecBCD enzyme and inhibits its activities. These proteins induce a 'hyper-rec' state in Escherichia coli and other bacteria, in which recombination events between DNA species with as little as 40 bp of shared sequence occur at high frequency. Red-mediated recombination in the hyper-rec bacterium proceeds via a number of different pathways, and with the involvement of different sets of bacterial proteins, depending in part on the nature of the recombining DNA species. The role of high-frequency double-strand break repair/recombination in the life cycle of the lambdoid phages is discussed.
_______________________________
http://en.wikipedia.org/wiki/SV40
SV40 is an abbreviation for Simian vacuolating virus 40 or Simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that has the potential to cause tumors, but most often persists as a latent infection.
SV40 became a highly controversial subject after it was revealed that millions were exposed to the virus after receiving a contaminated polio vaccine.[1]
The virus was first identified by Bernice E. Eddy (based on a work of her and Sarah Stewart about Polyoma viruses) in 1960 in cultures of rhesus monkey kidney cells that were being used to produce polio vaccine.[2][3] It was named for the effect it produced on infected green monkey cells, which developed an unusual number of vacuoles. This observation was repeated and confirmed by Hilleman and Sweet who were employed by Merck in their vaccine division. The complete viral genome was sequenced by Walter Fiers and his team at the University of Ghent (Belgium) in 1978.[4] The virus is dormant and is asymptomatic in Rhesus monkeys. The virus has been found in many macaque populations in the wild, where it rarely causes disease. However, in monkeys that are immunodeficient—due to, for example, infection with Simian immunodeficiency virus—SV40 acts much like the human JC and BK polyomaviruses, producing kidney disease and sometimes a demyelinating disease similar to PML. In other species, particularly hamsters, SV40 causes a variety of tumors, generally sarcomas. In rats, the oncogenic SV40 Large T-antigen was used to establish a brain tumor model for PNETs and medulloblastomas.[5]
_______________________________
http://en.wikipedia.org/wiki/Polyomaviridae
Polyomaviruses are DNA-based (double-stranded DNA, ~5000 base pairs, circular genome), small (40-50 nanometers in diameter), and icosahedral in shape, and do not have a lipoprotein envelope. Moreover, the genome possess early and late genes, contributing to its complex transcription program. They are potentially oncogenic (tumor-causing); they often persist as latent infections in a host without causing disease, but may produce tumors in a host of a different species, or a host with an ineffective immune system. The name polyoma refers to the viruses' ability to produce multiple (poly-) tumors (-oma).
_______________________________
https://en.wikipedia.org/wiki/Tuberous_sclerosis
Tuberous sclerosis or tuberous sclerosis complex (TSC) is a rare multi-system genetic disease that causes non-malignant tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. A combination of symptoms may include seizures, developmental delay, behavioral problems, skin abnormalities, lung and kidney disease. TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin respectively. These proteins act as tumor growth suppressors, agents that regulate cell proliferation and differentiation.[1]
The name, composed of the Latin tuber (swelling) and the Greek skleros (hard), refers to the pathological finding of thick, firm and pale gyri, called "tubers," in the brains of patients postmortem. These tubers were first described by Désiré-Magloire Bourneville in 1880; the cortical manifestations may sometimes still be known by the eponym Bourneville's disease.
_________________________________________________________
http://www.ncbi.nlm.nih.gov/pubmed/9813776
Performing your original search, autism tuberous sclerosis, in PubMed will retrieve 238 records.
J Autism Dev Disord. 1998 Oct;28(5):407-14.
Autism and tuberous sclerosis.
Smalley SL.
Source
Department of Psychiatry, University of California-Los Angeles-School of Medicine 90024, USA.
Abstract
Autism and pervasive developmental disorders (PDD) are common in tuberous sclerosis (TSC). The frequency of autism is about 25%, with 40-45% of TSC cases meeting criteria for autism or PDD. Among autistic populations, the frequency of TSC is 1-4% and perhaps as high as 8-14% among the subgroup of autistic individuals with a seizure disorder. Mental retardation (MR) and seizures, particularly infantile spasms, are significant risk factors in the development of autism/PDD in TSC; however, neither are sufficient or necessary for the development of these behaviors. The mechanism underlying the association of autism and TSC is as yet unclear but clinical features and neuroimaging investigations suggest that an abnormal TSC gene may directly influence the development of autism rather than it being a secondary effect of seizures or MR. The presence of autism/PDD may arise if the TSC gene mutations occur at critical stages of neural development in neural tissue of brain regions critical in the development of autism.
PMID: 9813776 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms
LinkOut - more resources
__________________________________________
http://www.ncbi.nlm.nih.gov/pubmed/20345322
J Neurovirol. 2010 Mar;16(2):141-9. doi: 10.3109/13550281003685839.
Association of autism with polyomavirus infection in postmortem brains.
Lintas C, Altieri L, Lombardi F, Sacco R, Persico AM.
Source
Laboratory of Molecular Psychiatry and Neurogenetics, University Campus Bio-Medico, Rome, Italy.
Abstract
Autism is a highly heritable behavioral disorder. Yet, two decades of genetic investigation have unveiled extremely few cases that can be solely explained on the basis of de novo mutations or cytogenetic abnormalities. Vertical viral transmission represents a nongenetic mechanism of disease compatible with high parent-to-offspring transmission and with low rates of disease-specific genetic abnormalities. Vertically transmitted viruses should be found more frequently in the affected tissues of autistic individuals compared to controls. Our initial step was thus to assess by nested polymerase chain reaction (PCR) and DNA sequence analysis the presence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV1), herpes simplex virus type 2 (HSV2), human herpes virus 6 (HHV6), BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) in genomic DNA extracted from postmortem temporocortical tissue (Brodmann areas 41/42) belonging to 15 autistic patients and 13 controls. BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P < .05). The majority of positives yielded archetypal sequences, whereas six patients and two controls unveiled single-base pair changes in two or more sequenced clones. No association is present with the remaining viruses, which are found in relatively few individuals (N <or= 3). Also polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P = .08). Follow-up studies exploring vertical viral transmission as a possible pathogenetic mechanism in autistic disorder should focus on, but not be limited to, the role of polyomaviruses.
Comment in
Polyomaviruses and autism: more than simple association? [J Neurovirol. 2010]
PMID: 20345322 [PubMed - indexed for MEDLINE]