視覚野においてT型Ca²⁺チャネル依存性長期増強を引き起こすためにはTNFαが必要である

Monocular deprivation produces depression and potentiation of visual responses evoked in visual cortical neurons by stimulation of deprived and nondeprived eyes, respectively, during the critical period of ocular dominance plasticity. Our previous studies suggested that T-type Ca²⁺ channel-dependent long-term potentiation (LTP), induced by 2 Hz stimulation, mediates the potentiation of visual responses. However, it was proposed that the experience-dependent response potentiation is mediated by tumor necrosis factor-α (TNFα)-dependent homeostatic synaptic scaling but not by Hebbian synaptic plasticity, because the potentiation was absent in TNFα knockout (TNFα-KO) mice. In this study, we investigated whether TNFα is required for LTP induced by 2 Hz stimulation using visual cortical slices prepared from critical period mice and rats. The production of LTP was prevented by pharmacological blockade of TNFα in rats and mice. LTP production was also prevented by an inhibitor of TNFα-converting enzyme that converts membrane-bound TNFα to soluble TNFα. In TNFα-KO mice, LTP did not occur and was rescued by exogenous soluble TNFα. Soluble TNFα was required for LTP production only during a restricted time window soon after 2 Hz stimulation. These results strengthen the view that T-type Ca²⁺ channel-dependent LTP contributes to the potentiation of nondeprived eye responses following monocular deprivation.博士（医学）・乙第1401号・平成29年6月28日Copyright © 2015 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved

Inhibitory effects of bisbenzylisoquinolines on synthesis of the inflammatory cytokines interleukin-1 and tumour necrosis factor-alpha

Synthesis of IL-1β and TNFα by human monocytesmacrophages was significantly inhibited by eleven bisbenzylisoquinolines and one half-molecule (benzylisoquinoline), with IC50 values in the μM range. The results indicate that these compounds may have value in the therapy of human diseases where these inflammatory cytokines have a central role in pathogenesis

Distribution of pCO2 and δ13C in the air and surface sea water in the Southern Ocean, south of Australia

Distribution of pCO_2 and δ^C in the air over the ocean and in the surface sea water of the Southern Ocean was determined during the cruise of BIOMASS (November 1983 to February 1984). In the study area, south of Australia, pCO_2 in the air was nearly constant (∿342ppm) throughout the cruise but pCO_2 in the surface sea water varied considerably ranging from 300 to 356ppm. In general, pCO_2 in the surface sea water tended to increase from north to south, and it was relatively higher than that in the air in higher latitudes. The average value in the south of 5°S was -7.97‰ for δ^C and 341.7ppm for pCO_2 of atmospheric CO_2. These results indicate that atmospheric CO_2 over the ocean is not isotopic equilibrium with the surface sea water and kinetic fractionation must be considered for understanding δ^C of atmospheric CO_2

The distribution of 85Kr in the air over the North and South Pacific Ocean

The north-south section of the atmospheric concentration of ^(Kr) over the Pacific is first reported. The most striking feature of the section is a large concentration difference at the geographical position of the intertropical convergence. The ^(Kr) concentration in the air over the North Pacific ranged from 22 to 23pCi m^ and in the South Pacific 16pCi m^. The concentration differences between two hemispheres is about 6pCi m^. Five year records from land stations in Japan indicate that the annual increase is about 1pCi m^y^. It seems that the amount of the southward transport of ^(Kr) from the northern hemisphere is nearly equilibrated with that of radioactive disintegration and/or dissolution of ^(Kr) into the ocean in the southern hemisphere