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We demonstrate vector magnetometry using ensemble of the nitrogen-vacancy (NV) centers in diamond that are perfectly aligned along the [111] direction. By changing the direction and strength of the reference magnetic field, we perform three-dimensional vector measurement of the Oersted field generated by the current flowing in a nearby wire. We had a formula for evaluating the magnetic field sensitivity in the direction perpendicular to the NV axis. We demonstrate that the expected sensitivity is 1.2 times higher than that of the NV ensemble isotropically oriented on four equivalent crystal axes. Our precise method is suitable for time-varying magnetic signals.

ABSTRACT-Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 pM and enhanced by a 20 to 30-min treatment with thioperamide (H3-antagonist) at 3 pM with significance, but little affected by mepyramine (H,-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 106 mast cells/ml. At a low concentration of mast cells (104 mast cells/ml), (R)-a-methylhistamine (a-MH), an H3-agonist, at 0.9-90 pM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by a-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also a-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells. In the early 1980s, a third receptor of histamine was identified, which regulates the synthesis and release of histamine in the histaminergic nerve ends in the rat brain, and this was designated as the H3-receptor (1).Since then, the development of specific and selective agonists and antagonists of histamine receptor subtypes has revealed that H3-receptors exist in other tissues in cluding the ileum (2), airway (3, 4) and blood vessels (5); this was concluded from the observations that the neural stimulation-induced twitch responses of these tissues are inhibited by modulation of ACh, neuropeptides and other neurotransmitter release by H3-receptor stimula tion, in a similar manner to that of the rat cerebral cortex. Thus, the majority of the investigations on H3-receptors were initially focused on the modulation of neurotrans mitter release and/or histamine synthesis in the presynap tic ends of the brain or other tissues. In addition, there have recently been a number of reports on the roles of the receptor in effector organs: H3-receptor stimulation relaxed rabbit middle cerebral artery preconstricted with K+ by acceleration of nitric oxide and prostacyclin forma tion from the endothelium (6, 7); an H3-antagonist aggra vated experimental allergic asthma in the guinea pig (8); an H3-agonist and H3-antagonist inhibited and enhanced, respectively, the histamine release from isolated gastric glands (9), and H3-receptor stimulation specifically down regulated histamine synthesis in isolated fundic mucosal cells (10) in rabbits; an H3-receptor agonist reduced gas trin-induced vascular histamine release in the isolated rat stomach (11).In the present study, we obtained evidence indicating that isolated rat peritoneal mast cells have surface H3 re...

Two types of multimode fiber couplers made from plastic-clad fibers are described: (1) cross type couplers with coupling efficiencies from 30 dB to 50 dB depending on the crossover angle; and (2) parallel type couplers with low transmission loss and coupling efficiencies from 15 dB to 30 dB depending on the coupling length. These experimental results are in good agreement with theory.

ABSTRACT-Whether anaphylactic histamine release from rat peritoneal mast cells is influenced by betahistine, a histamine H1-receptor agonist/H3-antagonist, and dimaprit, an H2-agonist, was examined.Treatment with dimaprit at 6 and 60 uM for 20 min significantly inhibited the anaphylactic histamine release, whereas betahistine at up to 80 pM under the same conditions did not affect it. Treatment with dimaprit at 6 and 60 pM for 1 to 20 min and for 5 to 20 min, respectively, caused a time-dependent inhibi tion of the release, but up to 30 min treatment with 8 and 80 pM betahistine had no effect. The decreased histamine release induced by dimaprit was recovered by neither mepyramine nor cimetidine. However, thioperamide, an H3-selective antagonist, dose-dependently restored the diminished release. From these results, the inhibition of anaphylactic histamine release by dimaprit is not produced by the stimulation of H2receptors, but involves the stimulation of H3-like receptors or H3-subtype receptors, which are distinct from the H3-receptors located in brain, and suggests that the receptor plays an important role in the negative feed back regulation of histamine release.