Monthly Archives: October 2016

Government-Funded Research is Biased, Not-Repeatable?

A significant assertion indeed.

“Government funding is leading to scientific research that can’t be replicated, according to a new report detailing growing problems in the scientific community.” click here

Anti-Israel UN Resolutions should be Rejected

” “The denial of the historicity of the two Jerusalem Temples and the Temple Mount as recounted in both the Old and New Testaments is a terrible indictment of the international community when repeatedly adopted by a UN body,” he said. ” click here

NOAA Data Manipulation Changes Cooling to Warming

“NOAA thermometers show the south cooling over the last century, but by the magic of data tampering they turn the cooling into a strong warming trend. Equivalent to declaring the Cubs to be winners of last night’s game.” click here

Affordable Health Care Act Fraud

As a matter of conscience, President Obama promised to save you $2,500 per year on health care costs. He called it “The Affordable Health Care Act”

by the end of my first term as president that will cover every American and cut the cost of a typical family’s premiums by up to $2500 a year. That’s not simply a matter of policy or ideology – it’s a moral commitment.

  • Barack Obama

Click here for WUWT

Mr. John Podesta Emails Reveal Media Bias, Manipulation

“From the “say anything” department, comes this email where the League of Conservation Voters asks Hillary’s campaign manager John Podesta to “…help us pressure the evening news programs at CBS, NBC, and ABC to make climate science central to their extreme weather coverage this year?”. ” click here for WUWT

Greenland Ice Sheet Melting Rates Higher in the Past

“It should come as no surprise that the Greenland ice sheet gained so many billion tons of ice during the 50 years from 1942 to 1992. After all, the scientific literature has been replete with records of rapidly declining Greenland temperature trends between the 1940s and the 1990s, which followed a period of especially rapid warming during the 1920s and 1930s (that was greater in rapidity and magnitude when compared to the Greenland ice sheet warming trend in the last decade or two).” click here

Arsenic and Fluoride Toxicity to Human Umbilical Vein Cells

Ma Y, Ma Z, Yin S, Yan X, Wang J. Arsenic and fluoride induce apoptosis, inflammation and oxidative stress in cultured human umbilical vein endothelial cells. Chemosphere. 2016 Oct 14;167:454-461. doi: 10.1016/j.chemosphere.2016.10.025.

Excessive amount of inorganic arsenic (iAs) and fluoride (F) coexist in drinking water in many regions, which is associated with high risk of vascular diseases. However, the underlying mechanisms are not well studied. The present study was to evaluate the effects of iAs and F individual or combined exposure on endothelial activation and apoptosis in vitro. Primary human umbilical vein endothelial cells (HUVECs) were exposed to 5 μM As2O3 and/or 1 mM NaF. Changes in endothelial cell apoptosis, inflammation, oxidative stress and nitric oxide (NO) production were analyzed. The results showed that iAs and/or F induced significant increase in endothelial cell apoptosis and inflammation as indicated by the increase of mRNA and protein expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and pentraxin 3. Furthermore, iAs and/or F exposure induced intracellular reactive oxygen species and malondialdehyde generation. Results showed iAs and/or F exposure increased the activity of NADPH oxidase (NOX) and up-regulated the mRNA expression of NOX subunits p22phox. The results indicated that activation of NOX was related to oxidative stress induced by iAs and/or F. Also, iAs and/or F reduced NO production in HUVECs. The up-regulation of inflammation genes expression and oxidative stress in iAs and F co-exposed ECs were less pronounced as compared to single F-exposed cells, which showed an antagonistic effect between iAs and F. In conclusion, endothelial activation and apoptosis induced by iAs and/or F are potential mechanisms in their vascular toxicity. Oxidative stress and impaired NO production are involved in their pro-inflammatory and pro-apoptotic effects.