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Pumice rafts that arrived at the Nansei Islands, Japan, provided a unique opportunity to investigate the Fukutoku‐Oka‐no‐Ba (FOB) eruption of August 2021. Despite drifting for 2 months for ~1300 km, the drift pumice raft had a large volume and contained a variety of pumice clasts, some of which were deposited during a high tide in a typhoon, while others were washed up on a sandy beach. Most of the drift pumice clasts are gray in color, vesicular, and have a groundmass containing black enclaves. Rare black pumice and the main gray pumice components have similar trachytic compositions, with SiO2 = 61–62 mass% and total alkalis = 8.6–10 mass% (on an anhydrous basis). Both pumice types contain clinopyroxene, plagioclase, and rare olivine phenocrysts. Thin‐section observations show that the gray pumice has more elongated vesicles as compared with the black pumice that has spherical vesicles, even where the two types of pumice are in the same clast. The glass in the black pumice is transparent and brown in color, while that in the gray pumice is colorless. No micro or nano‐crystals were observed during electron and optical microscopy. Raman spectra of the brown‐colored glass exhibit a clear magnetite peak, suggesting magnetite nanolites cause the brown color. High‐Mg olivine in the black pumice has an equilibrium temperature of c. 1200 °C and a rim diffusion profile indicative of re‐equilibration with the surrounding melt over a period of hours to days. The textural relationships between the gray and black pumice suggest that the black pumice had become black and viscous before the two types of pumice mixed. Therefore, crystallization of magnetite nanolites and a corresponding increase in melt viscosity were important in the eruption preparation process, which then resulted in a large‐scale Plinian eruption.

ETOC: The diverging contributions of the cytoskeletal linker proteins dystonin-a1 and dystonin-a2 to pathology in dystonia musculorum are largely unknown. Sensory neurodegeneration results primarily from the loss of the dystonin-a2 isoform, which is attributed a novel role in maintenance of organelle integrity.

Peripheral tissue inflammation can alter the properties of somatic sensory pathways, causing behavioral hypersensitivity and resulting in increased responses to pain caused by noxious stimulation (hyperalgesia) and normally innocuous stimulation (allodynia). These hypersensitivities for nociception are caused by changes in the excitability of trigeminal ganglion (TG) neurons. These changes alter sensory information processing in the neurons in the medullary trigeminal nucleus of caudalis. Increasing information is becoming available regarding trigeminal neuron-neuron/neuron-satellite glial cells (SGCs) communication. The activation of intraganglionic communication plays an important role in the creation and maintenance of trigeminal pathological pain. Therefore, in this review, we focus on the recent findings for sensory functions and pharmacological modulation of TG neurons and SGCs under normal and pathological conditions, and we discuss potential therapeutic targets in glia-neuronal interactions for the prevention of trigeminal neuropathic and inflammatory pain.

A newly identified lethal form of hereditary sensory and autonomic neuropathy (HSAN), designated HSAN-VI, is caused by a homozygous mutation in the bullous pemphigoid antigen 1 (BPAG1)/dystonin gene (DST). The HSAN-VI mutation impacts all major neuronal BPAG1/dystonin protein isoforms: dystonin-a1, -a2 and -a3. Homozygous mutations in the murine Dst gene cause a severe sensory neuropathy termed dystonia musculorum (dt). Phenotypically, dt mice are similar to HSAN-VI patients, manifesting progressive limb contractures, dystonia, dysautonomia and early postnatal death. To obtain a better molecular understanding of disease pathogenesis in HSAN-VI patients and the dt disorder, we generated transgenic mice expressing a myc-tagged dystonin-a2 protein under the regulation of the neuronal prion protein promoter on the dt(Tg4/Tg4) background, which is devoid of endogenous dystonin-a1 and -a2, but does express dystonin-a3. Restoring dystonin-a2 expression in the nervous system, particularly within sensory neurons, prevented the disorganization of organelle membranes and microtubule networks, attenuated the degeneration of sensory neuron subtypes and ameliorated the phenotype and increased life span in these mice. Despite these improvements, complete rescue was not observed likely because of inadequate expression of the transgene. Taken together, this study provides needed insight into the molecular basis of the dt disorder and other peripheral neuropathies including HSAN-VI.

Dystonia musculorum (dt) is a mouse inherited sensory neuropathy caused by mutations in the dystonin gene. While the primary pathology lies in the sensory neurons of dt mice, the overt movement disorder suggests motor neurons may also be affected. Here, we report on the contribution of motor neurons to the pathology in dt27J mice. Phenotypic dt27J mice display reduced alpha motor neuron cell number and eccentric alpha motor nuclei in the ventral horn of the lumbar L1 spinal cord region. A dramatic reduction in the total number of motor axons in the ventral root of postnatal day 15 dt27J mice was also evident. Moreover, analysis of the trigeminal nerve of the brainstem showed a 2.4 fold increase in number of degenerating neurons coupled with a decrease in motor neuron number relative to wild type. Aberrant phosphorylation of neurofilaments in the perikaryon region and axonal swellings within the pre-synaptic terminal region of motor neurons were observed. Furthermore, neuromuscular junction staining of dt27J mouse extensor digitorum longus and tibialis anterior muscle fibers showed immature endplates and a significant decrease in axon branching compared to wild type littermates. Muscle atrophy was also observed in dt27J muscle. Ultrastructure analysis revealed amyelinated motor axons in the ventral root of the spinal nerve, suggesting a possible defect in Schwann cells. Finally, behavioral analysis identified defective motor function in dt27J mice. This study reveals neuromuscular defects that likely contribute to the dt27J pathology and identifies a critical role for dystonin outside of sensory neurons.

The International Ocean Discovery Program Expedition 350 drilled between two Izu rear-arc seamount chains at Site U1437 and recovered the first complete succession of rear-arc rocks. The drilling reached 1806.5 m below seafloor. In situ hyaloclastites, which had erupted before the rear-arc seamounts came into existence at this site, were recovered in the deepest part of the hole (15-16 Ma). Here it is found that the composition of the oldest rocks recovered does not have rear-arc seamount chain geochemical signatures, but instead shows affinities with volcanic front or some of the extensional zone basalts between the present volcanic front and the rear-arc seamount chains. It is suggested that following the opening of the Shikoku back-arc Basin, Site U1437 was a volcanic front or a rifting zone just behind the volcanic front, and was followed at~9 Ma by the start of rear-arc seamount chains volcanism. This geochemical change records variations in the subduction components with time, which might have followed eastward moving of hot fingers in the mantle wedge and deepening of the subducting slab below Site U1437 after the cessation of Shikoku back-arc Basin opening.

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