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By comparing the focus of acupuncture standards, management modes of acupuncture in certain areas are summarized to provide a reference for institutions and regions when formulating suitable standards for local acupuncture services.

Inversin (Inv), a protein that contains ankyrin repeats, plays a key role in left-right determination during mammalian embryonic development, but its precise function remains unknown. Transgenic mice expressing an Inv and green fluorescent protein (GFP) fusion construct (Inv::GFP) were established to facilitate characterization of the subcellular localization of Inv. The Inv::GFP transgene rescued the laterality defects and polycystic kidney disease of Inv/Inv mice, indicating that the fusion protein is functional. In transgenic embryos, Inv::GFP protein was detected in the node monocilia. The fusion protein was also present in other 9+0 monocilia, including those of kidney epithelial cells and the pituitary gland, but it was not localized to 9+2 cilia. The N-terminal region of Inv (InvDeltaC) including the ankyrin repeats also localized to the node cilia and rescued the left-right defects of Inv/Inv mutants. Although no obvious abnormalities were detected in the node monocilia of Inv/Inv embryos, the laterality defects of such embryos were corrected by an artificial leftward flow of fluid in the node, suggesting that nodal flow is impaired by the Inv mutation. These results suggest that the Inv protein contributes to left-right determination as a component of monocilia in the node and is essential for the generation of normal nodal flow.

Komatsu: Novartis K.K: Speakers Bureau; Wako Pure Chemical Industries, Ltd.: Research Funding; Fuso Pharmaceutical Industries, Ltd.: Research Funding; Takeda Pharmaceutical Company Limited: Research Funding, Speakers Bureau; Pharma Essentia: Research Funding, Speakers Bureau.

【Introduction】 Although Ruxolitinib (Rux), a JAK1/2-inhibitor, is an effective treatment option for primary myelofibrosis, tumor cells become resistant to this drug in many MPN patients. Currently, Rux-resistance is a major problem and contributes to poor prognosis of MPN patients. Mechanisms of Rux-resistance in MPN cells with JAK2V617Fmutations have already been reported. On the other hand, MPN cells with CALRmutations resistant to Rux-treatment have not been fully characterized yet. In this study, we have clarified a mechanism of Rux-resistance in MPN tumor cells with CALRmutations in both cell lines and clinical samples.