10 research outputs found

    Flocculation of Artemia induced by East Asian common Octopus octopus sinensis paralarvae under culture conditions

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    Artemia are potential food organisms for the mass culture of common octopus paralarvae but cause poor paralarval growth and mortality. To understand problems arising from Artemia use, we focused on Artemia flocculation in paralarval culture tanks; Artemia get caught up with each other, exhibit disrupted swimming, are deposited on the tank bottom and eventually die. To clarify whether paralarvae induce the flocculation of food organisms or not, we cultured newly hatched Artemia nauplii, 3-day-old metanauplii and decapod crustacean zoeae with or without paralarvae at different growth stages (weight). Flocculation occurred only when Artemia were cultured with paralarvae; metanauplii had a higher susceptibility for flocculation than nauplii. Flocculated Artemia proportion increased with increasing paralarval weight. Scanning electron microscopy revealed that flocculated metanauplii had deformed setules on their setae, with hook-shaped tips and adhesion of neighbouring tips, suggesting that flocculation may occur via a mechanism similar to the ‘hook-and-loop fastener’. As octopus paralarvae exhibit external digestion, digestive enzymes secreted by paralarvae may deform Artemia setules and result in flocculation. As flocculation did not occur when metanauplii were cultured in water in which paralarvae were cultured and then removed, causative enzymes were probably rapidly inactivated after secretion

    Favorable effects of burosumab on tumor-induced osteomalacia caused by an undetectable tumor A case report

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    Rationale: Tumor-induced osteomalacia (TIO) is curable by tumor resection, but detection of the tumor can be challenging. Overproduction of fibroblast growth factor 23 (FGF23) by the tumor causes hypophosphatemia and consequently induces inappropriate bone turnover. Conventionally oral phosphate supplementation was the only treatment for TIO, but had risks of hypercalciuria and nephrocalcinosis. Burosumab, a human monoclonal anti-FGF23 antibody, was recently post-marketed in Japan against for FGF23-related hypophosphatemia. Herein, we present a case of TIO with undetectable tumor that was successfully treated with burosumab. Patient concerns: A 47-year-old woman was forced to use a wheelchair because of pain in both feet. Diagnosis: Laboratory findings showed hypophosphatemia, elevated bone markers, and high serum FGF23 without renal tubular defects. Imaging studies revealed bone atrophy in the feet, decreased bone density, and multiple pseudofractures in the talar, sacral, and L5 vertebral regions. After excluding drug-induced and hereditary osteomalacia, we diagnosed her as TIO. Interventions: Comprehensive imaging studies and stepwise venous sampling failed to localize the tumor, and we started to administer subcutaneous burosumab. Outcomes: After administration of burosumab, her serum phosphate was normalized without phosphate supplementation within 2 months. Improvement of pseudofractures, relief of pain evaluated by a visual analog scale, and normalization of bone biomarkers were observed. The patient was able to stand by herself after 6 months administration of burosumab. Lessons: This is the first report in clinical practice to demonstrate favorable effects of burosumab, including not only normalization of serum phosphate but also improvements of pseudofractures and subjective pain, in a patient with TIO and undetectable tumor

    A role for IL-34 in osteolytic disease of multiple myeloma

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    Multiple myeloma (MM) is a hematological malignancy that grows in multiple sites of the axial skeleton and causes debilitating osteolytic disease. Interleukin-34 (IL-34) is a newly discovered cytokine that acts as a ligand of colony-stimulating factor-1 (CSF-1) receptor and can replace CSF-1 for osteoclast differentiation. In this study, we identify IL-34 as an osteoclastogenic cytokine that accelerates osteolytic disease in MM. IL-34 was found to be expressed in the murine MM cell line MOPC315.BM, and the expression of IL-34 was enhanced by stimulation with proinflammatory cytokines or by bone marrow (BM) stromal cells. MM-cell–derived IL-34 promoted osteoclast formation from mouse BM cells in vitro. Targeting Il34 by specific small interfering RNA impaired osteoclast formation in vitro and attenuated osteolytic disease in vivo. In BM aspirates from MM patients, the expression levels of IL-34 in CD138+ populations vary among patients from high to weak to absent. MM cell–derived IL-34 promoted osteoclast formation from human CD14+ monocytes, which was reduced by a neutralizing antibody against IL-34. Taken together, this study describes for the first time the expression of IL-34 in MM cells, indicating that it may enhance osteolysis and suggesting IL-34 as a potential therapeutic target to control pathological osteoclastogenesis in MM patients
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