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Kathy's pick, "Secret Fallout".

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Kathy

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My recommended reading for EVERYONE this new year, is a book by:

Dr. Ernest Sternglass called "SECRET FALLOUT"

While we work and worry about our own personal situations, (which is perfectly OK), this man has spent a half a century uncovering lies bigger and more sinister than the BSE fiasco.

This book can be read on-line at the link:

http://www.ratical.com/radiation/SecretFallout/SF.html#TOC

It is a biography of his research and investigation into the damaging effects of man-made ionizing radiation from, nuclear weapons testing, power plants, etc.

I am hoping that you will read this, and pass on the link and name to more people. The more we are aware of this problem, the better prepared we can be to manage our own health, and to stop any further "fallout". There are difinitive agriculture connections which demand our attention.

Since this book came to my knowledge, another study by the prominent chronic wasting disease scientist "Elizabeth Williams" (now deceased), has come to my attention. She must have been working on several research projects before her and her husbands tragic death last year, and they are still in the publishing processes, posthumously.

This CWD expert, had two papers published on ionizing radiation in 2005.

Radiat Res. 2005 Oct;164(4 Pt 2):497-504.

Suppression of DNA-PK by RNAi has different quantitative effects on telomere dysfunction and mutagenesis in human lymphoblasts treated with gamma rays or HZE particles.

Zhang Q, Williams ES, Askin KF, Peng Y, Bedford JS, Liber HL, Bailey SM.

Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523, USA.

Basic to virtually all relevant biological effects of ionizing radiation is the underlying damage produced in DNA and the subsequent cellular processing of such damage. The damage can be qualitatively different for different kinds of radiations, and the genetics of the biological systems exposed can greatly affect damage processing and ultimate outcome--the biological effect of concern. The accurate repair of DNA double-strand breaks (DSBs) is critical for the maintenance of genomic integrity and function. Incorrect repair of such lesions results in chromosomal rearrangements and mutations that can lead to cancer and heritable defects in the progeny of irradiated parents. We have focused on the consequent phenotypic effects of faulty repair by examining connections between cellular radiosensitivity phenotypes relevant for carcinogenesis after exposure to ionizing radiation, and deficiencies in various components of the non-homologous end-joining (NHEJ) system. Here we produced deficiencies of individual components of the DNA-dependent protein kinase (DNA-PK) holoenzyme (Ku86 and the catalytic subunit, DNA-PKcs), both singly and in combination, using RNA interference (RNAi) in human lymphoblastoid cell lines. Exposure of cells exhibiting reduced protein expression to either gamma rays or 1 GeV/nucleon iron particles demonstrated differential effects on telomere dysfunction and mutation frequency as well as differential effects between radiation qualities.


Cancer Res. 2005 Jul 1;65(13):5544-53.

NBS1 knockdown by small interfering RNA increases ionizing radiation mutagenesis and telomere association in human cells.

Zhang Y, Lim CU, Williams ES, Zhou J, Zhang Q, Fox MH, Bailey SM, Liber HL.

Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523, USA. [email protected]

Hypomorphic mutations which lead to decreased function of the NBS1 gene are responsible for Nijmegen breakage syndrome, a rare autosomal recessive hereditary disorder that imparts an increased predisposition to development of malignancy. The NBS1 protein is a component of the MRE11/RAD50/NBS1 complex that plays a critical role in cellular responses to DNA damage and the maintenance of chromosomal integrity. Using small interfering RNA transfection, we have knocked down NBS1 protein levels and analyzed relevant phenotypes in two closely related human lymphoblastoid cell lines with different p53 status, namely wild-type TK6 and mutated WTK1. Both TK6 and WTK1 cells showed an increased level of ionizing radiation-induced mutation at the TK and HPRT loci, impaired phosphorylation of H2AX (gamma-H2AX), and impaired activation of the cell cycle checkpoint regulating kinase, Chk2. In TK6 cells, ionizing radiation-induced accumulation of p53/p21 and apoptosis were reduced. There was a differential response to ionizing radiation-induced cell killing between TK6 and WTK1 cells after NBS1 knockdown; TK6 cells were more resistant to killing, whereas WTK1 cells were more sensitive. NBS1 deficiency also resulted in a significant increase in telomere association that was independent of radiation exposure and p53 status. Our results provide the first experimental evidence that NBS1 deficiency in human cells leads to hypermutability and telomere associations, phenotypes that may contribute to the cancer predisposition seen among patients with this disease.
 

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