Former warmist Prof. Dr. Fritz Vahrenholt and geologist/paleontologist Dr. Sebastian Lüning have authored a book that is now no. 4 on the Amazon-Germany bestseller list under the category of environment and ecology……the book will not be available until February 6th……
As reported here, Fritz Vahrenholt, one of the fathers of the green movement, no longer trusts the forecasts of the IPCC….
NO missing heat found by these folks…..
Loeb, N.G., J.M. Lyman, G.C. Johnson, R.P. Allan, D.R. Doelling, T. Wong, B.J. Soden, and G.L. Stephens. Observed changes in top-of-the-atmosphere radiation and upper-ocean heating consistent within uncertainty,” Nature Geosciences, Jan 22, 2012, doi:10.1038/NGEO1375.
Global climate change results from a small yet persistent imbalance between the amount of sunlight absorbed by Earth and the thermal radiation emitted back to space. An apparent inconsistency has been diagnosed between interannual variations in the net radiation imbalance inferred from satellite measurements and upper-ocean heating rate from in situ measurements, and this inconsistency has been interpreted as ‘missing energy’ in the system. Here we present a revised analysis of net radiation at the top of the atmosphere from satellite data, and we estimate ocean heat content, based on three independent sources. We find that the difference between the heat balance at the top of the atmosphere and upper-ocean heat content change is not statistically significant when accounting for observational uncertainties in ocean measurements, given transitions in instrumentation and sampling. Furthermore, variability in Earth’s energy imbalance relating to El Niño-Southern Oscillation is found to be consistent within observational uncertainties among the satellite measurements, a reanalysis model simulation and one of the ocean heat content records. We combine satellite data with ocean measurements to depths of 1,800 m, and show that between January 2001 and December 2010, Earth has been steadily accumulating energy at a rate of 0.50±0.43 Wm−2 (uncertainties at the 90% confidence level). We conclude that energy storage is continuing to increase in the sub-surface ocean.
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Sharma, R., M. Tsuchiya, Z. Skobe, B.A., Tannous, and J.D. Bartlett. The acid test of fluoride: how pH modulates toxicity. PLoS One. 2010 May 28;5(5):e10895.
BACKGROUND: It is not known why the ameloblasts responsible for dental enamel formation are uniquely sensitive to fluoride (F(-)). Herein, we present a novel theory with supporting data to show that the low pH environment of maturating stage ameloblasts enhances their sensitivity to a given dose of F(-). Enamel formation is initiated in a neutral pH environment (secretory stage); however, the pH can fall to below 6.0 as most of the mineral precipitates (maturation stage). Low pH can facilitate entry of F(-) into cells. Here, we asked if F(-) was more toxic at low pH, as measured by increased cell stress and decreased cell function.
METHODOLOGY/PRINCIPAL FINDINGS: Treatment of ameloblast-derived LS8 cells with F(-) at low pH reduced the threshold dose of F(-) required to phosphorylate stress-related proteins, PERK, eIF2alpha, JNK and c-jun. To assess protein secretion, LS8 cells were stably transduced with a secreted reporter, Gaussia luciferase, and secretion was quantified as a function of F(-) dose and pH. Luciferase secretion significantly decreased within 2 hr of F(-) treatment at low pH versus neutral pH, indicating increased functional toxicity. Rats given 100 ppm F(-) in their drinking water exhibited increased stress-mediated phosphorylation of eIF2alpha in maturation stage ameloblasts (pH<6.0) as compared to secretory stage ameloblasts (pH approximately 7.2). Intriguingly, F(-)-treated rats demonstrated a striking decrease in transcripts expressed during the maturation stage of enamel development (Klk4 and Amtn). In contrast, the expression of secretory stage genes, AmelX, Ambn, Enam and Mmp20, was unaffected.
CONCLUSIONS: The low pH environment of maturation stage ameloblasts facilitates the uptake of F(-), causing increased cell stress that compromises ameloblast function, resulting in dental fluorosis.
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