Bill Clinton, "How Dare You" youtube

July 31, 2006 WTC lung loss
EXCERPT:
By Liz Szabo, USA TODAY
Working amid the rubble of the World Trade Center may have aged the lungs of firefighters and rescue workers by an average of 12 years, a new study shows.
"It's pretty shocking," says John Balmes, a professor of medicine at the University of California at San Francisco who reviewed the research, published today in the American Journal of Respiratory and Critical Care Medicine, but was not involved in writing it. "They got 12 years' worth of loss in one year."

Doctors have closely monitored the health of workers exposed to dust from the towers' collapse.

In other words, what the hell did the blown up towers (asbestos filled) do to the people of New York?
EXCERPT:
Mutat Res. 2004 Mar 14;558(1-2):81-92.

Effects of asbestos on initiation of DNA damage, induction of DNA-strand breaks, P53-expression and apoptosis in primary, SV40-transformed and malignant human mesothelial cells.
Burmeister B, Schwerdtle T, Poser I, Hoffmann E, Hartwig A, Müller WU, Rettenmeier AW, Seemayer NH, Dopp E.

Department of Biology, Institute of Cell Biology, University of Rostock, Rostock, Germany.

Abstract
Human mesothelial cells (HMC), the progenitor cells of asbestos-induced mesothelioma, are particularly sensitive to the genotoxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in HMC are not well known. The high susceptibility of HMC to simian virus 40 (SV40)-mediated transformation is assumed to play a causative role in the pathogenesis of mesothelioma. The aim of this study was to investigate the asbestos-induced DNA damage in cultured HMC and SV40-transformed HMC (MeT-5A) compared with their malignant counterparts, i.e. human mesothelioma cells (MSTO). The time-dependent initiation of DNA-strand breaks as well as the induction of oxidative DNA base modifications were key factors for investigation. HMC, MeT-5A and MSTO cells were exposed to chrysotile and crocidolite asbestos (3 microg/cm2) during different time periods (1-72 h). DNA damage was investigated by use of the Comet assay and alkaline unwinding, the latter in combination with the Fpg protein. The P53 level was analyzed by immunofluorescence, and measurement of apoptosis was conducted by flow cytometry. We found a significant induction of DNA damage in asbestos-treated HMC already after an exposure time of 1.5 h. This effect could not be observed in treated MeT-5A and MSTO cells. Also, a time-dependent significant increase in DNA-strand breaks was observed by alkaline unwinding in asbestos-treated HMC, but not in treated MeT-5A and MSTO cells. In none of the three cell lines we could detect oxidative DNA damage recognized by the Fpg protein (e.g. 8-oxo-guanine), up to 24 h after exposure to asbestos. In contrast to what was found in HMC, P53 was over-expressed in untreated MeT-5A and MSTO. The induction of apoptosis by asbestos fibers was suppressed in MeT-5A and MSTO cells. Crocidolite fibers induced the higher genotoxic effects and chrysotile the more pronounced apoptotic effects. We conclude that asbestos induces DNA damage in HMC already after a very short exposure time in the absence of 8-oxo-guanine formation. The presence of SV40-Tag in MeT-5A and MSTO cells results in an increased expression of P53, but not in additive genotoxic effects after exposure to asbestos. The deregulation of the apoptotic pathway may lead to proliferation of genomically damaged cells and finally to the development of mesothelioma.


Science Daily
EXCERPT:
Being able to sequence a human genome for $1,000 or less (which is the price most insurance companies are willing to pay) could open a new era in personal medicine, making it possible to precisely diagnose the cause of many diseases and tailor drugs and treatment procedures to the genetic make-up of an individual.

"Despite the tremendous interest in using nanopores for sequencing DNA, it was unclear how, exactly, nanopores could be used to read the DNA sequence," said U. of I. physics professor Aleksei Aksimentiev. "We now describe one such method."

Aksimentiev and collaborators describe the method in a paper accepted for publication in the journal Nano Letters, and posted on the journal's Web site.


Depleted Uranium, Mercury and Diabetes
EXCERPT:
DNA and Mitochondrial Time Bombs: Uranium, Mercury and Diabetes
By Mark Sircus

Forget Cancer, forget AIDS, Diabetes is fast becoming the king of all chronic disease which is decimating the human race.

The Centers of Disease Control (CDC) in Atlanta declares that 33% of the babies born this year will be diabetic by the year 2050. — Dr. Alan Cantwell

Diabetes, which is expanding almost exponentially in the world today, can in part be traced to the increasing radiation to which we are all being exposed. Every physician knows that radiation can lead to cancer, but making a connection between depleted uranium (DU) and diabetes seems ludicrous at first glance. Unfortunately it is not. Most medical doctors have never heard of this but neither have they paid attention to the fact that mercury and other toxic chemicals are also primary causes of diabetes. Even though there is little research into the connection between radiation poisoning and diabetes we should not remain blind, deaf and dumb about it.

Diabetes is a disease that affects a person’s every cell because it has to do with energy metabolism and the vastly important hormone insulin and its receptor sites.

Type two diabetes, which is fundamentally due to nutritional deficiencies (especially a lack of magnesium) colliding head on with a host of chemical poisons and heavy metals, is also being triggered by the heavy metal toxicity and radioactivity of uranium oxide and other radioactive isotopes that are circulating widely in the environment. Unfortunately, exposure levels are increasing dramatically with each ton of vaporized depleted uranium but that is not stopping the American and British governments from manufacturing, selling and using depleted uranium weaponry.

“Depleted (DU) uranium is highly toxic to humans, both chemically as a heavy metal and radiological as an alpha particle emitter, is very dangerous when taken internally,” writes Dr. Rosalie Bertell, Canadian Epidemiologist.i A new study, conducted by biochemist Dr. Diane Stearns at Northern Arizona University confirms that, separate from any radiation risks, cells exposed to uranium will bond with the metal chemically.ii Uranium and phosphate have a strong chemical affinity for each other and the DNA and Mitochondria are loaded with phosphate so uranium is a DNA and Mitochondria deep penetration bomb. The uranium is attacking on fundamental cellular levels while mercury offers a knock out punch by attacking the sulfur bonds besides being highly toxic to nerve cells. It’s totally crucial to medical practice in the 21st century to understand this convergence of toxicities. We can now clearly see what is being attacked and who are mortal enemies are. Invisible clouds of radiation are meeting up with what can only be called The Hun Hordes of Mercury. Mercury now sits across our planetary environment everywhere, an invisible chemical cloud whose density is only increasing.

Diabetes is often conceptualized as a severe imbalance of part of the endocrine system that destroys our ability to metabolize food. The imbalance results in elevated levels of insulin, a lack of insulin, or the cell insulin receptor sites becoming insensitive to insulin.


Fluoride and DNA damage
EXCERPT:
PO Box 2345, Beijing 100023, China World J Gastroenterol
2006 February 21; 12(7):1144-1148
www.wjgnet.com World Journal of Gastroenterology ISSN 1007-9327
wjg@wjgnet.com © 2006 The WJG Press. All rights reserved.
RAPID COMMUNICATION
DNA damage, apoptosis and cell cycle changes induced by
fluoride in rat oral mucosal cells and hepatocytes

Ling-Fei He, Jian-Gang Chen www.wjgnet.com
Ling-Fei He, Jian-Gang Chen,
Department of Dental Medicine,
Zhongnan Hospital,
Wuhan University, Wuhan 430071, Hubei
Province, China
Correspondence to: Ling-Fei,
Department of Dental Medicine,
Zhongnan Hospital,
Wuhan University, Wuhan 430071,
Hubei
Province, China.
helingfei.wh@163.com
Telephone: +86-27-67813132 Fax: +86-27-86819342
Received: 2005-08-02 Accepted:2005-12-31
Abstract
AIM: To study the effect of fluoride on oxidative stress, DNA damage
and apoptosis as well as cell cycle of ratoral mucosal cells and hepatocytes.

METHODS: Ten male SD rats weighing 80~120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in fluoride group had
free access to deionized water containing 150 mg/L sodium fluoride (NaF). The animals in control group were given distilled water.

Four weeks later, the animals were killed. Reactive oxygen species (ROS) in oral mucosa and liver were measured by Fenton reaction, lipid peroxidation
product, malondialdehyde (MDA), was detected by thiobarbituric acid (TBA) reaction, reduced glutathione (GSH) was assayed by dithionitrobenzoic acid (DTNB)
reaction. DNA damage in oral mucosal cells and hepatocytes was determined by single cell gel (SCG) electrophoresis or comet assay. Apoptosis and cell cycle in oral
mucosal cells and hepatocytes were detected by flow cytometry.

RESULTS: The contents of ROS and MDA in oral mucosa and liver tissue of fluoride group were significantly higher than those of control group ( P < 0.01), but the level of GSH was markedly decreased (P < 0.01). The contents of ROS, MDA and GSH were (134.73 ± 12.63) U/mg protein, (1.48 ± 0.13) mmol/mg protein and (76.38 ± 6.71) mmol/mg protein in oral mucosa respectively, and (143.45 ± 11.76) U/mg protein, (1.44 ± 0.12) mmol/mg protein and (78.83 ± 7.72) mmol/mg protein in liver tissue respectively.

The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higher than those in the control group ( P < 0.01). The apoptosis
rate in oral mucosal cells was (13.63 ± 1.81) % in fluoride group, and (12.76 ± 1.67) % in hepatocytes, higher than those in control group. Excess fl uoride could
differently lower the number of oral mucosal cells and hepatocytes at G0/G1 and S G2/M phases ( P < 0.05).

CONCLUSION: Excess fluoride can induce oxidative stress and DNA damage and lead to apoptosis and cell cycle change in rat oral mucosal cells and hepatocytes.
© 2006 The WJG Press. All rights reserved.

Key words: Fluoride; Oxidative stress; DNA damage; Apoptosis; Cell cycle
He LF, Chen JG. DNA damage, apoptosis and cell cycle changes induced by fl uoride in rat oral mucosal cells and hepatocytes. World J Gastroenterol; 2006; 12(7):1144-1148 http://www.wjgnet.com/1007-9327/12/1144.asp

INTRODUCTION
Fluoride is an essential trace element for human beings and animals.
Fluoride can prevent caries and enamel fluorosis. Caries is the demineralization of the enamel by acids produced by plaque bacteria, leading to cavitation.

Enamel fluorosis is a subsurface hypomineralization of the dental enamel caused by chronic ingestion of high fluoride concentration while the dentition is forming[1].
Other manifestations of fluoride toxic effects include skeletal fluorosis and damage to kidney, liver, parathyroid glands and brain[2-4]. Lipid peroxidation is implicated as an important mechanism of fluorosis. A close association between fluoride toxicity and oxidative stress has been reported in human beings[5], experimental animals[3] and cultured cells [2]. Studies have shown that excess fl uoride can cause DNA damage, trigger apoptosis and change cell cycle[2, 6].Wu M