Det kommer mer her om følgende nytt:

• Amish-folket i USA teller ca. tohundre tusen. Noen mener at dette folket har vaksinert seg mindre av religiøse grunner. De plages ikke i samme grad av de samme sykdommer som er vanlig hos oss.    Klikk her

• Det er en ny studie fra Nederland på vei. Vaksinerte og uvaksinert barn er sammenliknet - og uvaksinerte barn klarer seg bedre enn vaksinerte.

• Nye undersøkelser kommer fra tidligere Øst-Tyskland. Der ble man ikke vaksinert som i Vest og hadde lite luftveisplager til tross for mye bruk av kull og annen forurensing. Nå når barn har blitt vaksinert der etter Eurpeisk standard i snart 20 år, ser man også der en økning av lungesykdommer.

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Det er kjent at nyfødte barn av somaliske / afrikanske mødre i Sverige og USA, - og muligens Norge har større risiko for å utvikle autisme.
"Innvandrer barn"  får HepatitB vaksine like etter fødsel rutinemessig.
Studien her kan bidra til å forklare årsaksmekanismer.
I enkelte afrikanske land blir Autsme kalt for "den rike manns sjukdom", underforstått at det er dei som har råd til å kjøpe vaksiner som er utsatt for å få autisme hos sine barn.

Geir Flatabø



"We conclude that exposure of Hepa1-6 cells to a low dose of adjuvanted hepatitis B vaccine leads to loss of mitochondrial integrity, apoptosis induction, and cell death, apoptosis effect was observed also in C2C12 mouse myoblast cell line after treated with low dose of vaccine (0.3, 0.1, 0.05 μg/ml). In addition In vivo apoptotic effect of hepatitis B vaccine was observed in mouse liver." (1)

"Findings suggest that U.S. male neonates vaccinated with the hepatitis B vaccine prior to 1999 (from vaccination record) had a threefold higher risk for parental report of autism diagnosis compared to boys not vaccinated as neonates during that same time period. Nonwhite boys bore a greater risk." (2)

1. Hepatitis B vaccine induces apoptotic death in Hepa1-6 cells.
Hamza H, Cao J, Li X, Li C, Zhu M, Zhao S.
Apoptosis. 2012 Jan 17. [Epub ahead of print]

Vaccines can have adverse side-effects, and these are predominantly associated with the inclusion of chemical additives such as aluminum hydroxide adjuvant. The objective of this study was to establish an in vitro model system amenable to mechanistic investigations of cytotoxicity induced by hepatitis B vaccine, and to investigate the mechanisms of vaccine-induced cell death. The mouse liver hepatoma cell line Hepa1-6 was treated with two doses of adjuvanted (aluminium hydroxide) hepatitis B vaccine (0.5 and 1 μg protein per ml) and cell integrity was measured after 24, 48 and 72 h. Hepatitis B vaccine exposure increased cell apoptosis as detected by flow cytometry and TUNEL assay. Vaccine exposure was accompanied by significant increases in the levels of activated caspase 3, a key effector caspase in the apoptosis cascade. Early transcriptional events were detected by qRT-PCR. We report that hepatitis B vaccine exposure resulted in significant upregulation of the key genes encoding caspase 7, caspase 9, Inhibitor caspase-activated DNase (ICAD), Rho-associated coiled-coil containing protein kinase 1 (ROCK-1), and Apoptotic protease activating factor 1 (Apaf-1). Upregulation of cleaved caspase 3,7 were detected by western blot in addition to Apaf-1 and caspase 9 expressions argues that cell death takes place via the intrinsic apoptotic pathway in which release of cytochrome c from the mitochondria triggers the assembly of a caspase activation complex. We conclude that exposure of Hepa1-6 cells to a low dose of adjuvanted hepatitis B vaccine leads to loss of mitochondrial integrity, apoptosis induction, and cell death, apoptosis effect was observed also in C2C12 mouse myoblast cell line after treated with low dose of vaccine (0.3, 0.1, 0.05 μg/ml). In addition In vivo apoptotic effect of hepatitis B vaccine was observed in mouse liver.


2. Hepatitis B vaccination of male neonates and autism diagnosis, NHIS 1997-2002.
Gallagher CM, Goodman MS.
J Toxicol Environ Health A. 2010;73(24):1665-77.

Universal hepatitis B vaccination was recommended for U.S. newborns in 1991; however, safety findings are mixed. The association between hepatitis B vaccination of male neonates and parental report of autism diagnosis was determined. This cross-sectional study used weighted probability samples obtained from National Health Interview Survey 1997-2002 data sets. Vaccination status was determined from the vaccination record. Logistic regression was used to estimate the odds for autism diagnosis associated with neonatal hepatitis B vaccination among boys age 3-17 years, born before 1999, adjusted for race, maternal education, and two-parent household. Boys vaccinated as neonates had threefold greater odds for autism diagnosis compared to boys never vaccinated or vaccinated after the first month of life. Non-Hispanic white boys were 64% less likely to have autism diagnosis relative to nonwhite boys. Findings suggest that U.S. male neonates vaccinated with the hepatitis B vaccine prior to 1999 (from vaccination record) had a threefold higher risk for parental report of autism diagnosis compared to boys not vaccinated as neonates during that same time period. Nonwhite boys bore a greater risk.