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Volcanism that occurs far from plate margins is di cult to explain with the current paradigm of plate tectonics. The Changbaishan volcanic complex, located on the border between China and North Korea, lies approximately 1,300 km away from the Japan Trench subduction zone and is unlikely to result from a mantle plume rising from a thermal boundary layer at the base of the mantle. Here we use seismic images and three-dimensional waveform modelling results obtained from the NECESSArray experiment to identify a slow, continuous seismic anomaly in the mantle beneath Changbaishan. The anomaly extends from just below 660 km depth to the surface beneath Changbaishan and occurs within a gap in the stagnant subducted Pacific Plate. We propose that the anomaly represents hot and buoyant sub-lithospheric mantle that has been entrained beneath the sinking lithosphere of the Pacific Plate and is now escaping through a gap in the subducting slab. We suggest that this subduction-induced upwelling process produces decompression melting that feeds the Changbaishan volcanoes. Subductioninduced upwelling may also explain back-arc volcanism observed at other subduction zones.

In ten patients with Prinzmetal's variant form of angina the effects of various drugs were assessed: subcutaneous injection of methacholine (10 mg), atropine (0.7 mg), and epinephrine (0.7 mg); intravenous infusion of isoproterenol (20-25 µg/min); and in the three of the above patients who were having recurrent spontaneous attacks at the time of the examination, oral administration of atropine (0.6-1.2 mg), propranolol (30-90 mg), and phenoxybenzamine (10 mg in one patient). Master's triple two-step test and selective coronary arteriography were done on all the patients. In the three patients who were having spontaneous attacks at the time of the examination, the administration of methacholine induced the attacks and that of atropine suppressed the attacks. Epinephrine induced the attacks in two patients and propranolol was without effect in suppressing the attacks. Phenoxybenzamine (in one patient) suppressed the attacks. Neither Master's triple two-step test nor isoproterenol infusion precipitated the attacks, though heart rate increased to more than 110 beats/min and 160 beats/min respectively in all the patients. Coronary arteriograms were normal in seven of the ten patients. It is concluded that enhanced activity of the parasympathetic nervous system, which occurs at rest, is involved in the initiation of the attack by stimulating the sympathetic nerve which in turn probably induces coronary arterial spasm by way of activating alpha (vasoconstrictor) receptors present in the large coronary arteries.

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ObjectiveTo evaluate cerebrospinal fluid (CSF) cytokine profiles in myelin oligodendrocyte glycoprotein IgG-positive (MOG-IgG+) disease in adult and paediatric patients.MethodsIn this cross-sectional study, we measured 27 cytokines in the CSF of MOG-IgG+ disease in acute phase before treatment (n=29). The data were directly compared with those in aquaporin-4 antibody-positive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) (n=20), multiple sclerosis (MS) (n=20) and non-inflammatory controls (n=14).ResultsIn MOG-IgG+ disease, there was no female preponderance and the ages were younger (mean 18 years, range 3–68; 15 were below 18 years) relative to AQP4-IgG+ NMOSD (41, 15–77) and MS (34, 17–48). CSF cell counts were higher and oligoclonal IgG bands were mostly negative in MOG-IgG+ disease and AQP4-IgG+ NMOSD compared with MS. MOG-IgG+ disease had significantly elevated levels of interleukin (IL)-6, IL-8, granulocyte-colony stimulating factor and granulocyte macrophage-colony stimulating factor, interferon-γ, IL-10, IL-1 receptor antagonist, monocyte chemotactic protein-1 and macrophage inflammatory protein-1α as compared with MS. No cytokine in MOG-IgG+ disease was significantly different from AQP4-IgG+ NMOSD. Moreover many elevated cytokines were correlated with each other in MOG-IgG+ disease and AQP4-IgG+ NMOSD but not in MS. No difference in the data was seen between adult and paediatric MOG-IgG+ cases.ConclusionsThe CSF cytokine profile in the acute phase of MOG-IgG+ disease is characterised by coordinated upregulation of T helper 17 (Th17) and other cytokines including some Th1-related and regulatory T cells-related ones in adults and children, which is similar to AQP4-IgG+ NMOSD but clearly different from MS. The results suggest that as with AQP4-IgG+ NMOSD, some disease-modifying drugs for MS may be ineffective in MOG-IgG+ disease while they may provide potential therapeutic targets.