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- Author or Editor: N. Satoh x
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Abstract
A simple method to determine 
-ray attenuation coefficients using Ba-133 -rays has been developed and applied to self-absorption correction in routine -ray spectrometry for environmental samples composed of unknown matrix elements. Experimental values of the mass attenuation coefficient obtained by the method agree well with calculated values for samples of known elemental composition which was determined by means of chemical analysis.
Abstract
Aomori Prefectural Govemment and Japan Nuclear Fuel Limited started environmental radiation monitoring around Nuclear Fuel Cycle Facilities in April 1989. External radiation is measured by NaI(TI) scintillator and Themoluminescence dosimeter. The level of external radiation is relatively low in the winter due to snow. We have collected terrestrial samples of drinking water, soil, agricultural products and marine samples of seawater, sea sediment, seafood, etc. periodically. We have measured many radionuclides and fluoride in these samples. In soil sample,239+240Pu ratio to137Cs was almost constant at all sampling points. A correlation was observed between salinity and concentration of tritium, uranium and fluoride in lake water of Lake Obuchinuma. The correlation between137Cs and239+240Pu in lake sediment was observed in each lake.
Abstract
Purpose
Acid-base transport in renal proximal tubules (PTs) is mainly sodium-dependent and conducted in coordination by the apical Na+/H+ exchanger (NHE3), vacuolar H+-adenosine triphosphatase (V-ATPase), and the basolateral Na+/HCO3 - cotransporter. V-ATPase on PTs is well-known to play an important role in proton excretion. Recently we reported a stimulatory effect of insulin on these transporters. However, it is unclear whether insulin is involved in acid-base balance in PTs. Thus, we assessed the role of insulin in acid-base balance in PTs.
Methods
V-ATPase activity was evaluated using freshly isolated PTs obtained from mice, and specific inhibitors were then used to assess the signaling pathways involved in the observed effects.
Results
V-ATPase activity in PTs was markedly enhanced by insulin, and its activation was completely inhibited by bafilomycin (a V-ATPase-specific inhibitor), Akt inhibitor VIII, and PP242 (an mTORC1/2 inhibitor), but not by rapamycin (an mTORC1 inhibitor). V-ATPase activity was stimulated by 1 nm insulin by approximately 20% above baseline, which was completely suppressed by Akt1/2 inhibitor VIII. PP242 completely suppressed the insulin-mediated V-ATPase stimulation in mouse PTs, whereas rapamycin failed to influence the effect of insulin. Insulin-induced Akt phosphorylation in the mouse renal cortex was completely suppressed by Akt1/2 inhibitor VIII and PP242, but not by rapamycin.
Conclusion
Our results indicate that stimulation of V-ATPase activity by insulin in PTs is mediated via the Akt2/mTORC2 pathway. These results reveal the mechanism underlying the complex signaling in PT acid-base balance, providing treatment targets for renal disease.
