Tokushima University / Educator and Researcher Directory --- Oura, Masahiro

Field of Study

Subject of Study

Book / Paper

Book:

1.	Kumiko Kagawa, 前田悠作, Masahiro Oura, Kimiko Sogabe, 藤野ひかる, 髙橋真美子, 丸橋朋子, 岩佐昌美, 宇高憲吾, Takeshi Harada, Takayuki Ise, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shusuke Yagi, Kyoko Takeuchi, Shuji Ozaki, Masahiro Abe and 藤野ひかる : Analysis of long-term survivors with cardiac AL amyloidosis, The Japanese Society of Hematology, Oct. 2017. (Summary) <p>Cardiac AL amyloidosis (CA) is generally known as a severe disease with very poor prognosis. Here we retrospectively examined seven patients with CA in our cohort who achieved long-term survival. All six patients who underwent high-dose melphalan and autologous stem cell transplantation (ASCT) survived for >3 years, whereas four patients survived for >5 years. Patients who underwent ASCT had prompt hematological responses, and five patients showed organ responses. ASCT helps to achieve a quick and deep hematological response required for long-term survival in patients with CA. New agents have been implemented for the treatment of CA. However, the risks and benefits of each treatment modality should be considered according to patient condition, thus making the best use of ASCT in combination with new agents for the treatment of CA.</p> (Keyword) Cardiac AL amyloidosis / Autologous hematopoietic stem cell transplantation / Long-term survival (Link to Publication Site) ● Publication site (DOI): 10.11406/rinketsu.58.2197 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680011466240 ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.58.2197 (DOI: 10.11406/rinketsu.58.2197, CiNii: 1390282680011466240)

Academic Paper (Judged Full Paper):

1.	Mamiko Takahashi, Shin Kondo, Kumiko Kagawa, Masafumi Nakamura, Yusaku Maeda, Ryohei Sumitani, Hikaru Yagi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Itsuro Endo, Masahiro Abe and Shingen Nakamura : Skeletal muscle mass during chemotherapy for haematological malignancies: a retrospective study., BMJ Supportive & Palliative Care, Vol.14, No.2, 195-199, 2024. (Summary) This study investigated whether baseline or alteration in muscle mass affects complications during chemotherapy or overall survival (OS) in haematological malignancies. Skeletal Muscle Index (SMI) was evaluated by bioimpedance analysis before and after chemotherapy in patients with haematological malignancies, and the association between muscle mass and clinical data was retrospectively analysed. Exactly 104 patients were enrolled, with a mean age of 62.2 years. SMI was 7.85 and 6.08 in male and female patients under 65 years and 7.10 and 5.92 over 65 years, before chemotherapy, respectively. Lower baseline SMI was not correlated with worse OS in total patients (p=0.915). After a median measurement interval of 30 days after chemotherapy (n=67), body weight and SMI decreased by 2.73% and 2.87% (mean), respectively. The decrease in body weight correlated with the loss of trunk muscle mass (R=0.2107) but was more strongly associated with the loss of lower limbs muscle mass (R=0.3985). The muscle mass of lower limbs significantly decreased in lymphoma patients who experienced febrile neutropenia (-0.42% vs -6.04%, p=0.040). OS significantly decreased in lymphoma patients with loss of lower limbs muscle ≥2.8% (p=0.0327). Muscle loss occurred following anticancer treatments, significantly contributing to worse outcomes. Body composition assessment and relevant multimodal prevention of muscle loss may be vital for patients receiving chemotherapy for haematological malignancies. (Keyword) Humans / Male / Female / Retrospective Studies / Middle Aged / Hematologic Neoplasms / Muscle, Skeletal / Aged / Adult / Antineoplastic Agents / Aged, 80 and over / Body Composition / Sarcopenia (Tokushima University Institutional Repository) ● Metadata: 119635 (Link to Publication Site) ● Publication site (DOI): 10.1136/spcare-2024-004870 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38569748 ● Search Scopus @ Elsevier (PMID): 38569748 ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-004870 (Tokushima University Institutional Repository: 119635, DOI: 10.1136/spcare-2024-004870, PubMed: 38569748)
2.	Shingen Nakamura, Keijiro Hara, Tomoko Kobayashi, Ryohei Sumitani, Masahiro Oura, Yusaku Maeda, Kimiko Sogabe, Hikaru Yagi, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Yoshimi Bando, Masahiro Abe and Hirokazu Miki : Tl uptake and retention mimicking malignant lymphoma in a patient with human immunodeficiency virus infection., Parasitology International, Vol.101, 102895, 2024. (Summary) Various opportunistic infections develop during immunodeficiency due to human immunodeficiency virus (HIV) infection. The treatment options for malignant lymphoma (ML) and toxoplasmic encephalitis (TE) are completely different; therefore, their discrimination is critical. A 25-year-old female of foreign nationality had been experiencing headaches for several weeks and suddenly developed convulsions. Brain computed tomography revealed multiple intracranial lesions; therefore, the patient was referred to the neurosurgery department. Brain magnetic resonance imaging (MRI) revealed multiple masses with surrounding edema, accompanied by enhanced contrast. The largest mass (2 cm) in the left occipital lobe exhibited ringed contrast enhancement. Her blood test results showed a CD4 count of 40/μL, positive HIV Ag/Ab, HIV-RNA level of 56 × 10 copies/mL, positive anti-Toxoplasma IgG (63 IU/mL), and negative anti-Toxoplasma IgM. Tl- single photon emission computed tomography (Tl-SPECT) revealed abnormal accumulation only in the tumor in the left occipital lobe (early T/N ratio, 3.034; delayed T/N ratio, 2.738; retention index, 0.9), which was suspected to be a ML. Both tumors, with or without high accumulation of Tl, were subjected to craniotomy biopsy. Pathological examination revealed infiltration of small lymphocytes with a necrotic background. The patient was diagnosed with TE based on a positive result of a tissue polymerase chain reaction test for Toxoplasma gondii. Two weeks after sulfamethoxazole and trimethoprim combination therapy, MRI imaging showed dramatic improvement in multiple brain tumors. This case is atypical because ML was ruled out despite high Tl-SPECT uptake and retention. Careful diagnosis through pathological examination and DNA testing is important. (Keyword) Humans / Female / Adult / Toxoplasmosis, Cerebral / Lymphoma / HIV Infections / Magnetic Resonance Imaging / Diagnosis, Differential / Tomography, Emission-Computed, Single-Photon / Toxoplasma (Tokushima University Institutional Repository) ● Metadata: 119634 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.parint.2024.102895 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38614255 ● Search Scopus @ Elsevier (PMID): 38614255 ● Search Scopus @ Elsevier (DOI): 10.1016/j.parint.2024.102895 (Tokushima University Institutional Repository: 119634, DOI: 10.1016/j.parint.2024.102895, PubMed: 38614255)
3.	Tomoko Maruhashi, Hirokazu Miki, Kimiko Sogabe, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Acute suppression of translation by hyperthermia enhances anti-myeloma activity of carfilzomib, International Journal of Hematology, Vol.119, No.3, 291-302, 2024. (Summary) Hyperthermia is a unique treatment option for cancers. Multiple myeloma (MM) remains incurable and innovative therapeutic options are needed. We investigated the efficacy of hyperthermia and carfilzomib in combination against MM cells. Although MM cell lines exhibited different susceptibilities to pulsatile carfilzomib treatment, mild hyperthermia at 43℃ induced MM cell death in all cell lines in a time-dependent manner. Hyperthermia and carfilzomib cooperatively induced MM cell death even under suboptimal conditions. The pro-survival mediators PIM2 and NRF2 accumulated in MM cells due to inhibition of their proteasomal degradation by carfilzomib; however, hyperthermia acutely suppressed translation in parallel with phosphorylation of eIF2α to reduce these proteins in MM cells. Recovery of β5 subunit enzymatic activity from its immediate inhibition by carfilzomib was observed at 24 h in carfilzomib-insusceptible KMS-11, OPM-2, and RPMI8226 cells, but not in carfilzomib-sensitive MM.1S cells. However, heat treatment suppressed the recovery of β5 subunit activity in these carfilzomib-insusceptible cells. Therefore, hyperthermia re-sensitized MM cells to carfilzomib. Our results support the treatment of MM with hyperthermia in combination with carfilzomib. Further research is warranted on hyperthermia for drug-resistant extramedullary plasmacytoma. (Keyword) Humans / Multiple Myeloma / Oligopeptides / Hyperthermia, Induced (Tokushima University Institutional Repository) ● Metadata: 119321 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03706-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38252236 ● Search Scopus @ Elsevier (PMID): 38252236 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03706-8 (Tokushima University Institutional Repository: 119321, DOI: 10.1007/s12185-023-03706-8, PubMed: 38252236)
4.	Kimiko Sogabe, Shingen Nakamura, Yoshiki Higa, Hirokazu Miki, Asuka Oda, Tomoko Maruhashi, Ryohei Sumitani, Masahiro Oura, Mamiko Takahashi, Masafumi Nakamura, Yusaku Maeda, Tomoyo Hara, Hiroki Yamagami, Shiroh Fujii, Kumiko Kagawa, Shuji Ozaki, Kiyoe Kurahashi, Itsuro Endo, Ken-ichi Aihara, Emiko Nakaue, Masahiro Hiasa, Jumpei Teramachi, Takeshi Harada and Masahiro Abe : Acute accumulation of PIM2 and NRF2 and recovery of β5 subunit activity mitigate multiple myeloma cell susceptibility to proteasome inhibitors., International Journal of Hematology, Vol.119, No.3, 303-315, 2024. (Summary) Resistance to proteasome inhibitors (PIs) has emerged as an important clinical issue. We investigated the mechanisms underlying multiple myeloma (MM) cell resistance to PIs. To mimic their pharmacokinetic/pharmacodynamic (PK/PD) profiles, MM cells were treated with bortezomib and carfilzomib for 1 h at concentrations up to 400 and 1,000 nM, respectively. Susceptibility to these PIs markedly varied among MM cell lines. Pulsatile treatments with PIs suppressed translation, as demonstrated by incorporation of puromycin at 24 h in PI-susceptible MM.1S cells, but not PI-resistant KMS-11 cells. Inhibition of β5 subunit activity decreased at 24 h in KMS-11 cells, even with the irreversible PI carfilzomib, but not under suppression of protein synthesis with cycloheximide. Furthermore, the proteasome-degradable pro-survival factors PIM2 and NRF2 acutely accumulated in MM cells subjected to pulsatile PI treatments. Accumulated NRF2 was trans-localized into the nucleus to induce the expression of its target gene, HMOX1, in MM cells. PIM and Akt inhibition restored the anti-MM effects of PIs, even against PI-resistant KMS-11 cells. Collectively, these results suggest that increased synthesis of β5 proteasome subunit and acute accumulation of PIM2 and NRF2 reduce the anti-MM effects of PIs. (Keyword) Humans / Proteasome Inhibitors / NF-E2-Related Factor 2 / Multiple Myeloma / Proteasome Endopeptidase Complex / Drug Resistance, Neoplasm / Cell Line, Tumor / Bortezomib / Antineoplastic Agents / Proto-Oncogene Proteins / Protein Serine-Threonine Kinases (Tokushima University Institutional Repository) ● Metadata: 119384 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03705-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38245883 ● Search Scopus @ Elsevier (PMID): 38245883 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03705-9 (Tokushima University Institutional Repository: 119384, DOI: 10.1007/s12185-023-03705-9, PubMed: 38245883)
5.	Masahiro Oura, Takeshi Harada, Asuka Oda, Jumpei Teramachi, Atsushi Nakayama, Ryohei Sumitani, Yusuke Inoue, Yusaku Maeda, Kimiko Sogabe, Maruhashi Tomoko, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Shingen Nakamura, Tomoyo Hara, Hiroki Yamagami, Kiyoe Kurahashi, Itsuro Endo, Hiroo Hasegawa, Hiroshi Fujiwara and Masahiro Abe : Therapeutic efficacy of the resorcylic acid lactone LL-Z1640-2 for adult T-cell leukaemia/lymphoma, eJHaem, Vol.4, No.3, 667-678, 2023. (Summary) Adult T-cell leukaemia/lymphoma (ATL) remains incurable. The NF-κB and interferon regulatory factor 4 (IRF4) signalling pathways are among the critical survival pathways for the progression of ATL. TGF-β-activated kinase 1 (TAK1), an IκB kinase-activating kinase, triggers the activation of NF-κB. The resorcylic acid lactone LL-Z1640-2 is a potent irreversible inhibitor of TAK1/extracellular signal-regulated kinase 2 (ERK2). We herein examined the therapeutic efficacy of LL-Z1640-2 against ATL. LL-Z1640-2 effectively suppressed the in vivo growth of ATL cells. It induced in vitro apoptosis and inhibited the nuclear translocation of p65/RelA in ATL cells. The knockdown of strongly induced ATL cell death while downregulating MYC. LL-Z1640-2 as well as the NF-κB inhibitor BAY11-7082 decreased the expression of IRF4 and MYC at the protein and mRNA levels, indicating the suppression of the NF-κB-IRF4-MYC axis. The treatment with LL-Z1640-2 also mitigated the phosphorylation of p38 MAPK along with the expression of CC chemokine receptor 4. Furthermore, the inhibition of STAT3/5 potentiated the cytotoxic activity of LL-Z1640-2 against IL-2-responsive ATL cells in the presence of IL-2. Therefore, LL-Z1640-2 appears to be an effective treatment for ATL. Further studies are needed to develop more potent compounds that retain the active motifs of LL-Z1640-2. (Link to Publication Site) ● Publication site (DOI): 10.1002/jha2.758 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37601887 ● Search Scopus @ Elsevier (PMID): 37601887 ● Search Scopus @ Elsevier (DOI): 10.1002/jha2.758 (DOI: 10.1002/jha2.758, PubMed: 37601887)
6.	Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, Sou Shimizu, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Eiji Tanaka and Masahiro Abe : Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors., International Journal of Hematology, 2023. (Summary) Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders. (Tokushima University Institutional Repository) ● Metadata: 118380 (Link to Publication Site) ● Publication site (DOI): 10.1007/s12185-023-03601-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37039914 ● Search Scopus @ Elsevier (PMID): 37039914 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03601-2 (Tokushima University Institutional Repository: 118380, DOI: 10.1007/s12185-023-03601-2, PubMed: 37039914)
7.	Takeshi Harada, Hiroto Ohguchi, Asuka Oda, Michiyasu Nakao, Jumpei Teramachi, Masahiro Hiasa, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Shigeki Sano, Teru Hideshima and Masahiro Abe : Novel antimyeloma therapeutic option with inhibition of the HDAC1-IRF4 axis and PIM kinase, Blood Advances, Vol.7, No.6, 1019-1032, 2023. (Summary) Multiple myeloma (MM) preferentially expands and acquires drug resistance in the bone marrow (BM). We herein examined the role of histone deacetylase 1 (HDAC1) in the constitutive activation of the master transcription factor IRF4 and the prosurvival mediator PIM2 kinase in MM cells. The knockdown or inhibition of HDAC1 by the class I HDAC inhibitor MS-275 reduced the basal expression of IRF4 and PIM2 in MM cells. Mechanistically, the inhibition of HDAC1 decreased IRF4 transcription through histone hyperacetylation and inhibiting the recruitment of RNA polymerase II at the IRF4 locus, thereby reducing IRF4-targeting genes, including PIM2. In addition to the transcriptional regulation of PIM2 by the HDAC1-IRF4 axis, PIM2 was markedly upregulated by external stimuli from BM stromal cells and interleukin-6 (IL-6). Upregulated PIM2 contributed to the attenuation of the cytotoxic effects of MS-275. Class I HDAC and PIM kinase inhibitors cooperatively suppressed MM cell growth in the presence of IL-6 and in vivo. Therefore, the present results demonstrate the potential of the simultaneous targeting of the intrinsic HDAC1-IRF4 axis plus externally activated PIM2 as an efficient therapeutic option for MM fostered in the BM. (Keyword) Histone Deacetylase 1 / Interleukin-6 / Benzamides / Pyridines (Tokushima University Institutional Repository) ● Metadata: 118211 (Link to Publication Site) ● Publication site (DOI): 10.1182/bloodadvances.2022007155 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36129197 ● Search Scopus @ Elsevier (PMID): 36129197 ● Search Scopus @ Elsevier (DOI): 10.1182/bloodadvances.2022007155 (Tokushima University Institutional Repository: 118211, DOI: 10.1182/bloodadvances.2022007155, PubMed: 36129197)
8.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, Mariko Tanaka, Sooha Kim, Motosumi Nakagawa, Sou Shimizu, Kotaro Tanimoto, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : The Xanthine Oxidase Inhibitor Febuxostat Suppresses Adipogenesis and Activates Nrf2., Antioxidants, Vol.12, No.1, 2023. (Summary) Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine catabolism that acts as a novel regulator of adipogenesis. In pathological states, xanthine oxidoreductase activity increases to produce excess reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical inducer of antioxidants, which is bound and repressed by a kelch-like ECH-associated protein 1 (Keap1) in the cytoplasm. The Keap1-Nrf2 axis appears to be a major mechanism for robust inducible antioxidant defenses. Here, we demonstrate that febuxostat, a xanthine oxidase inhibitor, alleviates the increase in adipose tissue mass in obese mouse models with a high-fat diet or ovariectomy. Febuxostat disrupts in vitro adipocytic differentiation in adipogenic media. Adipocytes appeared at day 7 in absence or presence of febuxostat were 160.8 ± 21.2 vs. 52.5 ± 12.7 (p < 0.01) in 3T3L1 cells, and 126.0 ± 18.7 vs. 55.3 ± 13.4 (p < 0.01) in 10T1/2 cells, respectively. Adipocyte differentiation was further enhanced by the addition of hydrogen peroxide, which was also suppressed by febuxostat. Interestingly, febuxostat, but not allopurinol (another xanthine oxidase inhibitor), rapidly induced the nuclear translocation of Nrf2 and facilitated the degradation of Keap1, similar to the electrophilic Nrf2 activator omaveloxolone. These results suggest that febuxostat alleviates adipogenesis under oxidative conditions, at least in part by suppressing ROS production and Nrf2 activation. Regulation of adipocytic differentiation by febuxostat is expected to inhibit obesity due to menopause or overeating. (Tokushima University Institutional Repository) ● Metadata: 118313 (Link to Publication Site) ● Publication site (DOI): 10.3390/antiox12010133 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36670994 ● Search Scopus @ Elsevier (PMID): 36670994 ● Search Scopus @ Elsevier (DOI): 10.3390/antiox12010133 (Tokushima University Institutional Repository: 118313, DOI: 10.3390/antiox12010133, PubMed: 36670994)
9.	高原由実子, Hirokazu Miki, Shingen Nakamura, 林成樹, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 富永誠記, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, 大坂朱美, Takeshi Harada, Shiroh Fujii, Toshiyuki Suge, Keiko Aota, Shuji Ozaki and Masahiro Abe : 徳島県におけるHIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題, Shikoku Acta Medica, Vol.78, No.5-6, 193-198, 2022. (Summary) 【Introduction】The survival rate in patients with HIV infection and acquired immunodeficiency syndrome (AIDS) has been improved dramatically due to the advances in anti-HIV drug therapy, while aging-associated complications become a critical issue. The incidence of sudden occurrence of AIDS without prior detection of HIV infection, so called ``Ikinari AIDS'', still remains high. 【Objective】We retrospectively analyzed the incidence and clinical characteristics of HIV/AIDS patients in both Tokushima University Hospital and Tokushima Prefectural Central Hospital. 【Results】Eighty four patients (74 males and 10 females) with a median age of 39 years old (range 16 - 85) were enrolled. Thirty-four patients (40.5%) were diagnosed with ``Ikinari AIDS'' from 2001 to 2020. All 4 patients were diagnosed with ``Ikinari AIDS'' after 2020. AIDS-defining illnesses were diagnosed as follows ; pneumocystis pneumonia in 21 cases, CMV infection in 8 cases and candidiasis in 6 cases. All patients over 60 years old were suffered from AIDS. Other complications included syphilis in 17 cases, hepatitis B infection in 12 and herpes zoster in 7. 【Discussion/Conclusion】In Tokushima, the incidence rate of ``Ikinari AIDS'' appeared to be higher than that of national average. COVID - 19 pandemic hampered the public health care services of awareness-raising activity for HIV infection and telephone consultations about HIV, which may become more lease asymptomatic HIV patients without diagnosis. For early diagnosis of HIV/AIDS, it is becoming more important to share information to make early screening of HIV infection among medical staffs, such as medical doctors, dentists, nurses, pharmacists and MSWs. (Keyword) HIV / AIDS / Ikinari AIDS (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520013962706680448 (CiNii: 1520013962706680448)
10.	Shin Kondo, Tatsuro Inoue, Takashi Saito, Yuka Kawamura, Ayane Katayama, Masafumi Nakamura, Ryohei Sumitani, Mamiko Takahashi, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh : Allogeneic haematopoietic stem cell transplantation and patient falls: impact of lower extremity muscle strength., BMJ Supportive & Palliative Care, 2022. (Summary) Pretransplant LEMS was a significant predictor of post-transplant falls. The results of this study may help to prevent falls in patients undergoing allo-HSCT. (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjspcare-2022-003582 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35534187 ● Search Scopus @ Elsevier (PMID): 35534187 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2022-003582 (DOI: 10.1136/bmjspcare-2022-003582, PubMed: 35534187)
11.	Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression., Clinical & translational immunology, Vol.11, No.1, 2022. (Summary) TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA. (Tokushima University Institutional Repository) ● Metadata: 117260 (Link to Publication Site) ● Publication site (DOI): 10.1002/cti2.1371 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379 ● Search Scopus @ Elsevier (PMID): 35079379 ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371 (Tokushima University Institutional Repository: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379)
12.	Shin Kondo, Kumiko Kagawa, Takashi Saito, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Nori Sato, Rei Ono, Masahiro Abe and Shinsuke Katoh : Allogeneic haematopoietic stem cell transplantation-clinical outcomes: impact of leg muscle strength., BMJ Supportive & Palliative Care, 2021. (Summary) Pre-transplant LEMS was a significant factor in predicting OS and NRM. (Link to Publication Site) ● Publication site (DOI): 10.1136/bmjspcare-2021-003256 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34949601 ● Search Scopus @ Elsevier (PMID): 34949601 ● Search Scopus @ Elsevier (DOI): 10.1136/bmjspcare-2021-003256 (DOI: 10.1136/bmjspcare-2021-003256, PubMed: 34949601)
13.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Asuka Oda, Ariunzaya Bat-Erdene, Takeshi Harada, Shingen Nakamura, Mohannad Ashtar, Sou Shimizu, Masami Iwasa, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma, Haematologica, Vol.106, No.5, 1401-1413, 2021. (Summary) Along with the tumor progression, the bone marrow microenvironment is skewed in multiple myeloma (MM), which underlies the unique pathophysiology of MM and confers aggressiveness and drug resistance in MM cells. TGF-β-activated kinase-1 (TAK1) mediates a wide range of intracellular signaling pathways. We demonstrate here that TAK1 is constitutively overexpressed and phosphorylated in MM cells, and that TAK1 inhibition suppresses the activation of NF-κB, p38MAPK, ERK and STAT3 to decrease the expression of critical mediators for MM growth and survival, including PIM2, MYC, Mcl-1, IRF4, and Sp1, along with a substantial reduction in the angiogenic factor VEGF in MM cells. Intriguingly, TAK1 phosphorylation was also induced along with upregulation of vascular cell adhesion molecule-1 (VCAM-1) in bone marrow stromal cells (BMSCs) in cocultures with MM cells, which facilitated MM cell-BMSC adhesion while inducing IL-6 production and receptor activator of nuclear factor κ-Β ligand (RANKL) expression by BMSCs. TAK1 inhibition effectively impaired MM cell adhesion to BMSCs to disrupt the support of MM cell growth and survival by BMSCs. Furthermore, TAK1 inhibition suppressed osteoclastogenesis enhanced by RANKL in cocultures of bone marrow cells with MM cells, and restored osteoblastic differentiation suppressed by MM cells or inhibitory factors for osteoblastogenesis overproduced in MM. Finally, treatment with the TAK1 inhibitor LLZ1640-2 markedly suppressed MM tumor growth and prevented bone destruction and loss in mouse MM models. Therefore, TAK1 inhibition may be a promising therapeutic option targeting not only MM cells but also the skewed bone marrow microenvironment in MM. (Keyword) Animals / Bone Marrow Cells / MAP Kinase Kinase Kinases / Mice / Multiple Myeloma / NF-kappa B / Osteoclasts / Osteolysis / RANK Ligand / Tumor Microenvironment (Tokushima University Institutional Repository) ● Metadata: 116529 (Link to Publication Site) ● Publication site (DOI): 10.3324/haematol.2019.234476 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32273474 ● Search Scopus @ Elsevier (PMID): 32273474 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2019.234476 (Tokushima University Institutional Repository: 116529, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474)
14.	Motoki SUGASAKI, Naoki TOKUNAGA, Akishige IKEGAME, Takayuki NAKAO, Masahiro Oura, Hirokazu Miki, Kojiro Nagai and Tetsuji Takayama : A case of congenital prekallikrein deficiency discovered by preoperative screening, Japanese Journal of Medical Technology, Vol.70, No.1, 132-137, 2021. (Keyword) プレカリクレイン / 接触因子 / 先天性プレカリクレイン欠乏症 / クロスミキシングテスト / prekallikrein / contact factor / congenital prekallikrein deficiency / cross-mixing test (Link to Publication Site) ● Publication site (DOI): 10.14932/jamt.20-5 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1391694356262403200 ● Search Scopus @ Elsevier (DOI): 10.14932/jamt.20-5 (DOI: 10.14932/jamt.20-5, CiNii: 1391694356262403200)
15.	Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis., Internal Medicine, Vol.60, No.11, 1753-1757, 2021. (Summary) A 33-year-old man was admitted to our hospital for fever and abdominal pain. A blood analysis revealed pancytopenia and increased serum pancreatic enzymes with disseminated intravascular coagulation. A detailed examination revealed acute pancreatitis, with diffuse swelling of the pancreas and diffuse beaded dilatation of the main pancreatic duct, which mimicked autoimmune pancreatitis complicated by acute myeloid leukemia. Systemic cytotoxic chemotherapy led to the remission of leukemia and pancreatitis. We hypothesized that the etiology of acute pancreatitis was invasion of leukemia cells. Acute pancreatitis is rare as a symptom of leukemia; however, we should consider the possibility of leukemia during the differential diagnosis of acute pancreatitis. (Keyword) Acute Disease / Adult / Autoimmune Diseases / Autoimmune Pancreatitis / Humans / Leukemia, Myeloid, Acute / Male / Pancreatitis (Tokushima University Institutional Repository) ● Metadata: 116536 (Link to Publication Site) ● Publication site (DOI): 10.2169/internalmedicine.4916-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33456032 ● Search Scopus @ Elsevier (PMID): 33456032 ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.4916-20 (Tokushima University Institutional Repository: 116536, DOI: 10.2169/internalmedicine.4916-20, PubMed: 33456032)
16.	Mamiko Takahashi, Ryohei Sumitani, Taiki Hori, Jumpei Murai, Shiyori Kawata, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Intravenous busulfan-based conditioning with autologous stem cell transplantation for refractory B-cell lymphoma with central nervous system involvement., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 196-201, 2021. (Summary) The prognosis of relapsed or refractory lymphoma with central nervous system (CNS) involvement remains poor because of the lack of anticancer drugs with sufficient CNS penetration. [Case 1] A 65-year-old man was diagnosed with Stage IV mantle cell lymphoma. After two courses of chemotherapy and autologous hematopoietic stem cell (HSC) collection, urinary retention with fever developed. Cerebrospinal fluid analysis revealed leptomeningeal involvement, which was refractory to high-dose methotrexate therapy. Autologous peripheral blood stem cell transplantation (ASCT) was performed, followed by intravenous busulfan (ivBU), cyclophosphamide, and etoposide ; thereafter, no relapse has been detected for over six years. [Case 2] A 40-year-old woman with right lower hemiplegia was diagnosed with primary CNS lymphoma. Although four courses of high-dose methotrexate therapy were administered, the cerebral tumor increased in size. HSCs were collected after methotrexate therapy, and ASCT was performed in addition to conditioning using ivBU, cyclophosphamide, and etoposide, followed by whole-brain and local boost irradiation. She achieved complete remission, but relapsed two years after ASCT. High-dose ivBU-containing conditioning regimens with ASCT may be useful for refractory B-cell lymphoma with CNS involvement. J. Med. Invest. 68 : 196-201, February, 2021. (Tokushima University Institutional Repository) ● Metadata: 116021 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.196 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994471 ● Search Scopus @ Elsevier (PMID): 33994471 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.196 (Tokushima University Institutional Repository: 116021, DOI: 10.2152/jmi.68.196, PubMed: 33994471)
17.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Ryohei Sumitani, Hirokazu Miki, Kengo Udaka, Mamiko Takahashi, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat., Cancers, Vol.12, No.4, 2020. (Summary) Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox's anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage. (Tokushima University Institutional Repository) ● Metadata: 115041 (Link to Publication Site) ● Publication site (DOI): 10.3390/cancers12040929 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32283857 ● Search Scopus @ Elsevier (PMID): 32283857 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers12040929 (Tokushima University Institutional Repository: 115041, DOI: 10.3390/cancers12040929, PubMed: 32283857)
18.	Kengo Udaka, Shingen Nakamura, Shiroh Fujii, Ryosuke Miyamoto, Naoko Matsui, Shiyori Kawata, Taiki Hori, Junpei Murai, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Takeshi Harada, Kumiko Kagawa, Yuishin Izumi, Masahiro Abe and Hirokazu Miki : Successful treatment of progressive multifocal leukoencephalopathy with mirtazapine and mefloquine in refractory myeloma, International Journal of Myeloma, Vol.10, No.1, 8-12, 2020.
19.	Masami Iwasa, Takeshi Harada, Asuka Oda, Ariunzaya Bat-Erdene, Jumpei Teramachi, Hirofumi Tenshin, Mohannad Ashtar, Masahiro Oura, Kimiko Sogabe, Kengo Udaka, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki and Masahiro Abe : PD-L1 upregulation in myeloma cells by panobinostat in combination with interferon-γ., Oncotarget, Vol.10, No.20, 1903-1917, 2019. (Summary) gene silencing abolished the PD-L1 upregulation by panobinostat and IFN-γ in combination, indicating a critical role for STAT1. These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-γ-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-γ. PD-L1 upregulation should be taken into account when combining immunotherapies with panobinostat. (Tokushima University Institutional Repository) ● Metadata: 113359 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.26726 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30956773 ● Summary page in Scopus @ Elsevier: 2-s2.0-85062760316 (Tokushima University Institutional Repository: 113359, DOI: 10.18632/oncotarget.26726, PubMed: 30956773, Elsevier: Scopus)
20.	Yuko Miyakami, Shingen Nakamura, Masahiro Oura, Yasunobu Okamoto, 高橋真美子, Kimiko Sogabe, 岩佐昌美, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Hisanori Uehara and Masahiro Abe : De novo CD 20-negative diffuse large B-cell lymphoma developed with sustained fever and markedly high C-reactive protein level, Shikoku Acta Medica, Vol.74, No.5-6, 193-200, 2018. (Summary) A 68-year-old woman presented with sustained fever for more than 1 month and admitted due to hematemesis and systemic edema. Computed tomography scan revealed swelling of the cervical, paraaortic lymph nodes. Blood test results showed severe anemia, elevation of white blood cell count, elevation of liver enzyme and coagulopathy with high C-reactive protein. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells with necrosis and hemorrhage, which are positive for CD79α, CD30, MUM-1, and bcl-6 and negative for CD20, CD5, CD10, ALK, CD38, CD138, and EBER. Gene rearrangement of immunoglobulin heavy chain was detected in tumor cells. Bone marrow aspiration showed tumor involvement. The patient was diagnosed with de novo CD20-negative diffuse large B-cell lymphoma(DLBCL)stage IV B. Reduced CHOP therapy was performed under artificial respiration due to pulmonary edema and takotsubo cardiomyopathy. Although her general condition and high CRP levels temporarily improved, she died 47 days after admission due to rapid relapse. De novo CD20-negative DLBCL was rare and presented with high CRP levels and rapid progression, and was thought to be clinically different from the existing DLBCL. It is imperative to elucidate molecular pathophysiology and establish new treatment strategy for de novo CD20-negative DLBCL. (Keyword) CD20 / fever of unknown origin / diffuse large B-cell lymphoma / CRP (Tokushima University Institutional Repository) ● Metadata: 112987 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050583647829887360 (Tokushima University Institutional Repository: 112987, CiNii: 1050583647829887360)
21.	Ariunzaya Bat-Erdene, Shingen Nakamura, Asuka Oda, Masami Iwasa, Jumpei Teramachi, Mohannad Ashtar, Takeshi Harada, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Shiroh Fujii, Kimiko Sogabe, Masahiro Oura, Kengo Udaka, Kumiko Kagawa, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Itsuro Endo and Masahiro Abe : Class 1 HDAC and HDAC6 inhibition inversely regulates CD38 induction in myeloma cells via interferon-α and ATRA., British Journal of Haematology, 2018. (Tokushima University Institutional Repository) ● Metadata: 113393 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15673 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30474853 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057280798 (Tokushima University Institutional Repository: 113393, DOI: 10.1111/bjh.15673, PubMed: 30474853, Elsevier: Scopus)
22.	Shiroh Fujii, Shingen Nakamura, Asuka Oda, Hirokazu Miki, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Itsuro Endo, Sumiko Yoshida, Ken-ichi Aihara, Kiyoe Kurahashi, Takeshi Harada, Kumiko Kagawa, Michiyasu Nakao, Shigeki Sano and Masahiro Abe : Unique anti-myeloma activity by thiazolidine-2,4-dione compounds with Pim inhibiting activity., British Journal of Haematology, Vol.180, No.2, 246-258, 2018. (Summary) Proviral Integrations of Moloney virus 2 (PIM2) is overexpressed in multiple myeloma (MM) cells, and regarded as an important therapeutic target. Here, we aimed to validate the therapeutic efficacy of different types of PIM inhibitors against MM cells for their possible clinical application. Intriguingly, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a reduced PIM2 protein levels and impaired MM cell survival preferentially in acidic conditions, in contrast to other types of PIM inhibitors, including AZD1208, CX-6258 and PIM447. SMI-16a also suppressed the drug efflux function of breast cancer resistance protein, minimized the sizes of side populations and reduced in vitro colony-forming capacity and in vivo tumourigenic activity in MM cells, suggesting impairment of their clonogenic capacity. PIM2 is known to be subject to ubiquitination-independent proteasomal degradation. Consistent with this, the proteasome inhibitors bortezomib and carfilzomib increased PIM2 protein levels in MM cells without affecting its mRNA levels. However, SMI-16a mitigated the PIM2 protein increase and cooperatively enhanced anti-MM effects in combination with carfilzomib. Collectively, the thiazolidine-2,4-dione-family compounds SMI-16a and SMI-4a uniquely reduce PIM2 protein in MM cells, which may contribute to their profound efficacy in addition to their immediate kinase inhibition. Their combination with proteasome inhibitors is envisioned. (Keyword) Animals / Antineoplastic Agents / Cell Line, Tumor / Cell Survival / Cell Transformation, Neoplastic / Disease Models, Animal / Humans / Hydrogen-Ion Concentration / Mice / Multiple Myeloma / Proteasome Inhibitors / Protein-Serine-Threonine Kinases / Proteolysis / Proto-Oncogene Proteins / Thiazolidinediones (Tokushima University Institutional Repository) ● Metadata: 112752 (Link to Publication Site) ● Publication site (DOI): 10.1111/bjh.15033 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29327347 ● Summary page in Scopus @ Elsevier: 2-s2.0-85040344893 (Tokushima University Institutional Repository: 112752, DOI: 10.1111/bjh.15033, PubMed: 29327347, Elsevier: Scopus)
23.	山口純代, Shingen Nakamura, 住田智志, 前田悠作, Masahiro Oura, 高橋真美子, 岩佐昌美, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Jun Kishi and Masahiro Abe : Development of adult T-cell leukemia/lymphoma during immunosuppressive Therapy for human T-cell leukemia virus type 1 associated arthropathy, Shikoku Acta Medica, Vol.73, No.5,6, 301-308, 2017. (Summary) A 64-year-old woman presented with lower leg edema, fever, and bilateral joint pain, involving the wrists, fingers, and knees, in April 201X. Serological test results were negative for rheumatoid factor, antinuclear antibody, and anti-cyclic citrullinated peptide antibody. A diagnosis of remitting seronegative symmetrical synovitis with pitting edema syndrome, a type of seronegative rheumatoid arthritis, was made and prednisolone was administered. The joint pain was refractory to prednisolone therapy. In February, 201X+2, the patient presented with right cervical lymphadenopathy. The CT scan revealed swelling of the cervical, axillary, and inguinal lymph nodes bilaterally and rapidly enlarged. In April, 18F-fluorodeoxyglucose PET/CT scan showed an abnormal collection in the enlarged lymph nodes. The patient subsequently developed hoarseness with dyspnea and attended our department. Blood test results showed high levels of lactate dehydrogenase (547U/L) and soluble interleukin‐2 receptor (34200 IU/L) and were positive for anti-human T-cell leukemia virus type1 (HTLV‐1) antibody. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells positive for CD3, CD4, and CD25 and negative for CD7. Monoclonal integration of HTLV‐1 proviral DNA was detected in the lymph node. A diagnosis of adult T-cell leukemia/lymphoma (ATLL), lymphoma type was made. The pain involving multiple joints was attributed to HTLV‐1associated arthropathy. Immunosuppressive therapy for HTLV‐1 carrier status may have played a role in the development of ATLL. (Keyword) Adult T-cell leukemia/lymphoma / HTLV-1 / rheumatoid arthritis / immunosuppressive therapy (Tokushima University Institutional Repository) ● Metadata: 112059 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050020697876757248 (Tokushima University Institutional Repository: 112059, CiNii: 1050020697876757248)
24.	Hirokazu Miki, Shingen Nakamura, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Ariunzaya Bat-Erdene, Yusaku Maeda, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kiyoe Kurahashi, Sumiko Yoshida, Kumiko Kagawa, Itsuro Endo, Aihara Kenichi, Mariko Ikuo, Kouji Itou, Koichiro Hayashi, Michihiro Nakamura and Masahiro Abe : Effective impairment of myeloma cells and their progenitors by hyperthermia., Oncotarget, Vol.9, No.12, 10307-10316, 2017. (Summary) Multiple myeloma (MM) remains incurable, and MM-initiating cells or MM progenitors are considered to contribute to disease relapse through their drug-resistant nature. In order to improve the therapeutic efficacy for MM, we recently developed novel superparamagnetic nanoparticles which selectively accumulate in MM tumors and extirpate them by heat generated with magnetic resonance. We here aimed to clarify the therapeutic effects on MM cells and their progenitors by hyperthermia. Heat treatment at 43°C time-dependently induced MM cell death. The treatment upregulated endoplasmic reticulum (ER) stress mediators, ATF4 and CHOP, while reducing the protein levels of Pim-2, IRF4, c-Myc and Mcl-1. Combination with the proteasome inhibitor bortezomib further enhanced ER stress to potentiate MM cell death. The Pim inhibitor SMI-16a also enhanced the reduction of the Pim-2-driven survival factors, IRF4 and c-Myc, in combination with the heat treatment. The heat treatment almost completely eradicated "side population" fractions in RPMI8226 and KMS-11 cells and suppressed their clonogenic capacity as determined by colony formation and tumorigenic capacity in SCID mice. These results collectively demonstrated that hyperthermia is able to impair clonogenic drug-resistant fractions of MM cells and enhance their susceptibility to chemotherapeutic drugs. (Tokushima University Institutional Repository) ● Metadata: 113059 (Link to Publication Site) ● Publication site (DOI): 10.18632/oncotarget.23121 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29535808 ● Summary page in Scopus @ Elsevier: 2-s2.0-85041952629 (Tokushima University Institutional Repository: 113059, DOI: 10.18632/oncotarget.23121, PubMed: 29535808, Elsevier: Scopus)

Academic Letter:

1.	Yusaku Maeda, Shoichiro Takao, Shiori Morita, Shin Kondo, Michiko Yamashita, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Mamiko Takahashi, Shiroh Fujii, Takeshi Harada, Hirokazu Miki, Masahiro Abe and Shingen Nakamura : Quality of skeletal muscles during allogeneic stem-cell transplantation: a pilot study, BMJ Supportive & Palliative Care, 2024. (Link to Publication Site) ● Publication site (DOI): 10.1136/spcare-2024-005070 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1136/spcare-2024-005070 (DOI: 10.1136/spcare-2024-005070)

Review, Commentary:

1.	山口普史, Hiroshi Bandou, 新谷保実, Hiroaki Yanagawa, Naoko Matsui, 重清俊雄, 田邊舞, 高岡奨, 飯間努, Masahiro Oura, 喜多秀仁, 戸根沙織, 野田和克 and 森住俊 : 意識障害患者の鑑別診断における詳細な病歴確認の重要性, 日本内科学会雑誌, Vol.104, No.7, 1495-1503, Jul. 2015.

Proceeding of International Conference:

1.	Shingen Nakamura, Yusaku Maeda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Hikaru Yagi, Shiro Fujii, Takeshi Harada and Hirokazu Miki : False-positive aspergillus galactomannan test in multiple myeloma, ID week 2024, Oct. 2024.
2.	Takeshi Harada, Asuka Oda, Yosuke Matsushita, Ryohei Sumitani, Yusuke Inoue, Tomoyo Hara, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Kiyoe Kurahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, Toyomasa Katagiri and Masahiro Abe : ADAR1-dsRNA metabolism in myeloma cells with 1q amplification: a novel therapeutic target, 19th International Myeloma Society Annual Meeting, Aug. 2022.
3.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Asuka Oda, Takeshi Harada, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, Tomoyo Hara, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Mechanical unloading promotes bone destruction and myeloma tumor expansion, Cancer and bone society young investigator symposium, Online, Feb. 2022.
4.	Hirofumi Tenshin, Takeshi Harada, Yusuke Inoue, Jumpei Teramachi, Masahiro Hiasa, Sou Shimizu, Emiko Nakaue, Kotaro Tanimoto, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Targeting SLAMF7 to disrupt myeloma-osteoclast interaction: elotuzumabs ADCC activity with Th1-like gamma delta T cells towards osteoclasts and myeloma cells., Cancer and bone society young investigator symposium, Feb. 2022.
5.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Novel strategy of elotuzumab and zoledronic acid with Th1-like T cells against myeloma, 18th International Myeloma Workshop, Wien, Sep. 2021.
6.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Induction of elotuzumabs ADCC activity by Th1-like T cells towards osteoclasts as well as myeloma cells, EHA2021 Virtual Congress, Jun. 2021.
7.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The anti-SLAMF7 elotuzumab enhances ADCC activity with Th1-like γδT cells towards osteoclasts and myeloma cells., The European Calcified Tissue Society 2021 Digital Congress 2021, web, Mar. 2021.
8.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Eiji Tanaka, Kotaro Tanimoto, Sou Shimizu, Masahiro Oura, Kimiko Sogabe, Masahiro Abe, Toshio Matsumoto and Itsuro Endo : The novel therapeutic approaches with TAK1 inhibition against the aberrant NLRP3 inflammasome activation in rheumatoid arthritis, ECTS 2020 Digital Congress, Oct. 2020.
9.	Takeshi Harada, Asuka Oda, Hiroto Ohguchi, Yohann Grondin, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe : Novel therapeutic rationale for targeting HDAC1 and PIM2 in multiple myeloma, 61th ASH Annual Meeting & Exposition, Orlando, Dec. 2019. (Link to Publication Site) ● Publication site (DOI): 10.1182/blood-2019-127679 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1182/blood-2019-127679 (DOI: 10.1182/blood-2019-127679)
10.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Asuka Oda, Ashtar Mohannad, Kotaro Tanimoto, Soh Shimizu, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The role of NLRP3 inflammasome activation in joint inflammation and destruction in rheumatoid arthritis: novel therapeutic approaches with TAK1 inhibition., 29th Australian and New Zealand Bone and Mineral Society Annual Scientific Meeting, Oct. 2019.
11.	Takeshi Harada, Asuka Oda, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Teru Hideshima, C. Kenneth Anderson and Masahiro Abe : Targeting myeloma metabolisms regulated by HDAC1-IRF4 axis can be a novel therapeutic strategy, 17th International Myeloma Workshop, Sep. 2019.
12.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Oda Asuka, Iwasa Masami, Takeshi Harada, Bat-Erdene Ariunzaya, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Shingen Nakamura, Hirokazu Miki, Toshio Matsumoto, Masahiro Abe and Eiji Tanaka : Peri-implantitis and the role of Febuxostat in osteoclast differentiation., AEEDC Dubai World Orthodontic Conference, Dubai, UAE, Feb. 2019.
13.	Takeshi Harada, Asuka Oda, Yohann Grondin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masami Iwasa, Masahiro Oura, Shingen Nakamura, Kumiko Kagawa, Yasunobu Okamoto, Kimiko Sogabe, Shiroh Fujii, Hirokazu Miki, Shuji Ozaki, Teru Hideshima, Kenneth C. Anderson and Masahiro Abe : The critical role of the HDAC1-IRF4-Pim-2 axis in myeloma cell growth and survival: therapeutic impacts of targeting the HDAC1-IRF4-Pim-2 axis, 60th ASH Annual Meeting & Exposition, San Diego, Dec. 2018.
14.	Shingen Nakamura, Hirokazu Miki, Ariunzaya Bat-Erdene, Yasunobu Okamoto, Kimiko Sogabe, Masahiro Oura, Mamiko Takahashi, Masami Iwasa, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa and Masahiro Abe : Alteration of muscle mass after chemotherapy in patients with newly diagnosed multiple myeloma., Esmo asia 2018, Nov. 2018.
15.	Noriyuki Shimizu, Masahiro Oura, Sachiko Chikahisa and Hiroyoshi Sei : EEG delta power in NREM sleep is enhanced by refeeding after 24-hr fasting in time-dependent manner, 36th International Union of Physiological Sciences, Kyoto, Aug. 2009.

Proceeding of Domestic Conference:

1.	住谷龍平, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Shiroh Fujii, Takeshi Harada, Hirokazu Miki and 安倍正博 : 周期的な発熱，血小板減少，高LDH血症で発症したびまん性大細胞型B細胞リンパ腫の1例, 第128回日本内科学会四国地方会,
2.	Yusaku Maeda, Shingen Nakamura, Saki Saijo, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Shiroh Fujii, Takeshi Harada and Hirokazu Miki : 多職種による集学的ケアを行ったインヒビター保有重症先天性血友病Aの1例, 第129回内科学会四国地方会,
3.	阪本朋香, Yoshie Imai, 三木こずえ, Shiroh Fujii, Hirokazu Miki, Kimiko Sogabe, Masahiro Oura, Ryohei Sumitani, 八木ひかる, 高橋真美子, Takeshi Harada, 前田悠作, Shingen Nakamura and Ken-ichi Matsuoka : 治療過程にある多発性骨髄腫患者が治療を続ける意味, 第39回日本がん看護学会学術集会, Feb. 2025.
4.	明石和子, Yoshie Imai, Shingen Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 初回再発した老年期の造血器腫瘍患者が捉える化学療法への構え, 第9回日本がんサポーティブケア学会学術集会, May 2024.
5.	Ryohei Sumitani, Hirokazu Miki, Kazumi Okamura, 前田悠作, Masahiro Oura, Kimiko Sogabe, 八木ひかる, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Takeshi Oya, Masahiro Abe and 佐藤亜紀 : KRAS変異を認めた治療抵抗性Rosai-Dorfman病の1例, 臨床血液, Vol.65, No.5, 473, May 2024.
6.	明石和子, Yoshie Imai, Shingen Nakamura, 西條早希, 前田悠作, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 初回再発した成人期の造血器腫瘍患者が捉える化学療法への構え, 第21回日本臨床腫瘍学会学術集, Feb. 2024.
7.	Shingen Nakamura, 手束宏明, 山上圭, Yuishin Izumi, 西條早希, 前田悠作, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, 藤井志朗, Takeshi Harada and 三木浩和 : 免疫再構築症候群により急速な経過で死亡に至ったHIV関連進行性多巣性白質脳症の一剖検例, 日本エイズ学会誌, Vol.25, No.4, 461, Nov. 2023. (Keyword) AIDS(合併症,薬物療法,病理学) 白質脳症-進行性多巣性(病因,薬物療法,病理学) 剖検免疫再構築症候群(病因,病理学) ヒト中年(45∼64) 男
8.	明石和子, Yoshie Imai, Shingen Nakamura, 西條早希, 前田悠作, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Takeshi Harada, Shiroh Fujii and Hirokazu Miki : 再発・難治性造血器腫瘍患者が捉えるアドバンス・ケア・プランニング, 第61回日本癌治療学会学術集会, Oct. 2023.
9.	Ryohei Sumitani, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, Shiroh Fujii, Takeshi Harada, Hirokazu Miki and Masahiro Abe : 周期的な発熱，血小板減少，高LDH血症で発症したびまん性大細胞型B細胞リンパ腫の1例, 第128回日本内科学会四国地方会, Jul. 2023.
10.	Ryohei Sumitani, Shingen Nakamura, 林成樹, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Takeshi Harada, 藤井志朗, 三木浩和, 東航平 and 安倍正博 : Lipiodolでのリンパ管造影により難治性乳糜腹水が軽快した濾胞性リンパ腫, 臨床血液, Vol.64, No.6, 560, Jun. 2023. (Keyword) エチヨード化油(診断的利用,治療的利用) 乳び腹水(治療,X線診断,合併症) リンパ管造影リンパ腫-濾胞性(合併症) ヒト高齢者(65∼79) 女
11.	林成樹, Ryohei Sumitani, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Ayaka Mori, Masanori Tamaki and Masahiro Abe : ITP，自己免疫性出血病F13に続発しTAFRO症候群を発症した1例, 第127回日本内科学会四国地方会, Dec. 2022.
12.	Mamiko Takahashi, Shingen Nakamura, Shin Kondo, Masafuumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki and Masahiro Abe : Importance of skeletal muscle mass during chemotherapies in patients with hematological malignancies, JSH2022, Oct. 2022.
13.	Takeshi Harada, Ryohei Sumitani, Asuka Oda, Yusuke Inoue, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Mamiko Takahashi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Shuji Ozaki, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : The therapeutic potential targeting ADAR1-dsRNA metabolism in myeloma cells with 1q amplification, The 84th Annual Meeting of the Japanese Society of Hematology, Oct. 2022.
14.	新居寛子, 髙橋真美子, Shiroh Fujii, Kimiko Sogabe, 林成樹, Ryohei Sumitani, Masahiro Oura, Takeshi Harada, Shingen Nakamura, 安積麻衣, 湊将典, Hirokazu Miki and Masahiro Abe : ループス腎炎に対してミコフェノール酸モフェチル投与中に発症した他の医原性免疫不全関連リンパ増殖性疾患の1例, 第265回徳島医学会学術集会, Jul. 2022.
15.	Ryohei Sumitani, Makiko Mizuguchi, Masahiro Oura, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Toshihiro Hashimoto, Takeshi Harada and Masahiro Abe : 126, 第126回日本内科学会四国地方会, Jun. 2022.
16.	中村昌史, Hirokazu Miki, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, 西尾進, Tetsu Tomonari and Masahiro Abe : ALアミロイドーシスの肝病変の評価における超音波エラストグラフィの有用性, The Japanese Journal of Clinical Hematology, Vol.63, No.6, 685-686, Jun. 2022. (Keyword) 肝臓疾患(超音波診断,薬物療法) 組織弾性イメージング *アミロイドーシス-免疫グロブリン軽鎖(超音波診断,薬物療法) ヒト中年(45∼64) 男女
17.	Shingen Nakamura, HORI Taiki, Masafumi Nakamura, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada and Masahiro Abe : Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia, The 47th annual meeting of Japanese Society of Myeloma, May 2022.
18.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, 菊池次郎, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐 and Masahiro Abe : Osteoclasts robustly express SLAMF7 and secrete soluble SLAMF7, The 47th Annual Meeting of the Japanese Society of Myeloma, May 2022.
19.	井上雄介, Takeshi Harada, Hirofumi Tenshin, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Shingen Nakamura, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Leverage of Th1-like γδT cells into antibody-mediated immunotherapy against myeloma, The 47th Annual Meeting of the Japanese Society of Myeloma, May 2022.
20.	Takeshi Harada, Ryohei Sumitani, Asuka Oda, Inoue Yusuke, Masahiro Oura, Kimiko Sogabe, Tomoko Maruhashi, Takahashi Mamiko, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Therapeutic impact of targeting RNA editing enzyme ADAR1 on myeloma cells with 1q amplification, 第47回日本骨髄腫学会学術集会, May 2022.
21.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, 小田明日香, Sou Shimizu, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Takeshi Harada and Masahiro Abe : TAK1 阻害は骨髄腫の細胞間相互作用による骨破壊と薬剤耐性を改善する, 第47回日本骨髄腫学会学術集会, May 2022.
22.	丸橋朋子, Hirokazu Miki, Kimiko Sogabe, Takeshi Harada, 小田明日香, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, 高橋真美子, Shiroh Fujii and Masahiro Abe : 骨髄腫細胞のプロテアソーム阻害薬への抵抗性の機序と温熱療法によるその克服の可能性, 第47回日本骨髄腫学会学術集会, May 2022.
23.	Shingen Nakamura, 堀太貴, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 髙橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada and Masahiro Abe : 形質細胞疾患における新型コロナワクチンの有効性, 第47回日本骨髄腫学会学術集会, May 2022.
24.	Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, 西尾進, 友成哲 and Masahiro Abe : 肝臓アミロイドーシスに対する超音波エラストグラフィを用いた非侵襲的診断法の有用性, 第47回日本骨髄腫学会学術集会, May 2022.
25.	Shingen Nakamura, 堀太貴, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Hirokazu Miki, Takeshi Harada, Ken-ichi Aihara and Masahiro Abe : 形質細胞異常症患者におけるSARS-CoV-2に対するmRNAワクチンの液性免疫応答の評価(Humoral response of the mRNA vaccine against SARS-CoV-2 in patients with plasma cell dyscrasia), International Journal of Myeloma, Vol.12, No.3, 199, May 2022. (Keyword) 予防接種単クローン性免疫グロブリン血症-良性(免疫学) 液性免疫アミロイドーシス-免疫グロブリン軽鎖(免疫学) *COVID-19ワクチン(治療的利用,薬理学)
26.	Emiko Nakaue, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka and Masahiro Abe : The impact of pulsatile proteasome inhibitor on bone metabolism, International Journal of Myeloma, Vol.12, No.3, 152, May 2022. (Keyword) 骨髄腫-多発性(薬物療法,病理学) / 骨組織リモデリング / パルス療法(薬物療法) / Proteasome Inhibitors(治療的利用,薬理学) / Homo sapiens
27.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, 菊池次郎, 小田明日香, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 高橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Masahiro Hiasa, Jumpei Teramachi, 鈴木敦, 角川学士, 峯畑健一, 古川雄祐 and Masahiro Abe : 破骨細胞はSLAMF7を強発現し可溶性SLAMF7を産生する(Osteoclasts robustly express SLAMF7 and secrete soluble SLAMF7), International Journal of Myeloma, Vol.12, No.3, 150, May 2022. (Keyword) 骨髄腫-多発性(遺伝学,病理学) 破骨細胞 Signaling Lymphocytic Activation Molecule Family(血液) SLAMF7 Protein(血液) ヒト
28.	高原由実子, Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Masahiro Abe, 岡本秀樹, 岡田直人, 矢野由美子, 高橋真理, 青田桂子 and Shuji Ozaki : HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題, Shikoku Acta Medica, Vol.78, No.1-2, 89, Apr. 2022.
29.	Ryohei Sumitani, Takeshi Harada, 中村昌史, 水口槙子, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 髙橋真美子, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Mio Yada, Yoshihiro Matsudate, Hisanori Uehara and Masahiro Abe : 少量methotrexate療法が有効であった進行期原発性皮膚未分化大細胞型リンパ腫., The Japanese Journal of Clinical Hematology, Vol.63, No.6, 536-543, Mar. 2022. (Summary) 進行期の原発性皮膚未分化大細胞リンパ腫(pcALCL)に対する標準治療は定まっていない．症例は71歳,男性．多発性の皮膚紅斑と結節病変を認め,左耳介後部からの生検でリンパ腫性丘疹症(LyP)と診断された．局所電子線照射にて全ての病変は消退したが,5ヵ月後に両内眼角に結節病変が出現し,同部位の生検ではCD30陽性大型細胞が大部分を占めpcALCLと診断された．PET/CTにて右口蓋扁桃腫大,頸部,鼠径部の表在リンパ節腫大およびFDG集積を認め,TNM分類T3bN3M0であった．慢性閉塞性肺疾患による呼吸機能低下と肺炎を反復していたため,多剤併用化学療法ではなくmethotrexate(MTX)15mg/週の内服療法を選択した．皮膚,リンパ節病変は縮小し,副作用なく長期間病勢コントロールが可能であった．pcALCLの標準治療は確立されていないが様々な治療法が開発されてきており,少量MTX療法は呼吸器感染症を繰り返すフレイルな患者に有用であった．LyPにpcALCLが続発する機序や本疾患群に対する少量MTX療法の作用機序の解明が望まれる．(著者抄録) (Keyword) Etoposid / Methotrexate / 顔面腫瘍 / lung disease / 皮膚疾患-顔面 / 皮膚腫瘍 / 扁桃腫瘍 / 放射線療法 / Folic Acid / リンパ腫-未分化大細胞 / 心筋症-たこつぼ型 / PET-CT検査 / フレイル / Homo sapiens / 高齢者 (Link to Publication Site) ● Publication site (DOI): 10.11406/rinketsu.63.536 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11406/rinketsu.63.536 (DOI: 10.11406/rinketsu.63.536)
30.	高原由実子, Hirokazu Miki, Shingen Nakamura, 中村昌史, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, Takeshi Harada, Shiroh Fujii, Keiko Aota, Shuji Ozaki and Masahiro Abe : HIV感染症および後天性免疫不全症候群患者の臨床的特徴と今後の課題., --- 264 ( 3 ) ---, 第264回徳島医学会学術集会(令和3年度冬期), 2022年2月20日(Web開催), Feb. 2022.
31.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Resumption of myeloma cell sensitivity to proteasome inhibitors by PIM and Akt inhibition, The 83rd Annual Meeting of the Japanese Society of Hematology, Sep. 2021.
32.	Hirofumi Tenshin, 寺町順平日浅雅博小田明日香原田武志, Masahiro Hiasa, 小田明日香, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Eiji Tanaka, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome aggravates osteoclastic bone destruction in myeloma, 日本血液学会学術集会83回 Page 83回 Page OS2-4B-4(2021.09), Sep. 2021.
33.	Kotaro Tanimoto, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Takeshi Harada, 小田明日香, Masahiro Oura, Kimiko Sogabe, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Extraosseous dissemination of myeloma by mechanical unloading, 日本血液学会学術集会83回 Page 83回 Page OS2-11C-3(2021.09), Sep. 2021.
34.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Expansion of γδT cells by CELMoDs and enhancement of their anti-myeloma effects by elotuzumab, The 83rd Annual Meeting of Japanese Society of Hematology, Sep. 2021.
35.	Shingen Nakamura, 上野宜久, Sumiko Yoshida, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, 広津崇亮 and Masahiro Abe : 血液がんにおける線虫がん検査 N-NOSEの検討(Detection of hematological malignancies using N-NOSE(Nematode-NOSE)), 日本血液学会学術集会, OS1-11B-2, Sep. 2021. (Keyword) 検尿走化性 Caenorhabditis elegans 造血器腫瘍(診断) ヒト男女
36.	Hirokazu Miki, Shingen Nakamura, Shiroh Fujii, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Kumiko Kagawa, Nishio Susumu, Tetsu Tomonari and Masahiro Abe : 肝臓アミロイドーシスに対する超音波エラストグラフィの診断的有用性., 第83回日本血液学会学術集会, OS1-8D-2, Sep. 2021.
37.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, 丸橋朋子, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : PIMとAkt阻害による骨髄腫細胞のプロテアソーム阻害薬感受性の増強(Sensitization of myeloma cells to proteasome inhibitors by PIM and Akt inhibition), 日本血液学会学術集会, OS2-11D-3, Sep. 2021.
38.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Development of combinatory treatment of Th1-like γδT cells with elotuzumab against osteoclasts as well as myeloma cells, 第46回日本骨髄腫学会学術集会, May 2021.
39.	Hirokazu Miki, Shingen Nakamura, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 髙橋真美子, 丸橋朋子, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Masateru Kondo, Naoto Okada, Yoshimi Bando, Itsuro Endo and Masahiro Abe : The importance of retaining physical functions to prevent SRE in multiple myeloma., 第46回日本骨髄腫学会学術集会, May 2021.
40.	Kimiko Sogabe, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, 小田明日香, 井上雄介, Ryohei Sumitani, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirofumi Tenshin, Masahiro Hiasa, Jumpei Teramachi, 李政樹, 飯田真介 and Masahiro Abe : 骨髄腫細胞のプロテアソーム阻害薬の耐性機序におけるPIM2とAkt活性およびNRF2蓄積の役割(Mechanisms for the resistance to proteasome inhibitors in myeloma cells: the role of PIM2 and Akt kinase activation and NRF2 accumulation), International Journal of Myeloma, Vol.11, No.2, 85, May 2021. (Keyword) 癌原遺伝子タンパク質骨髄腫-多発性(遺伝学,実験的) Protein-Serine-Threonine Kinases 抗腫瘍剤耐性 c-akt癌原遺伝子タンパク質 NF-E2-Related Factor 2 Proteasome Inhibitors(薬理学) *PIM2 Protein
41.	石田卓也, Hirokazu Miki, 髙橋真美子, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 丸橋朋子, 岡本秀樹, Naoto Okada, 矢野由美子, 高橋真理, Tetsu Tomonari, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, Keiko Aota, Hiroyoshi Watanabe and Masahiro Abe : HIV感染血友病患者における臨床的特徴と今後の課題, 第262回徳島医学会学術集会, Mar. 2021.
42.	Maruhashi Tomoko, Shiroh Fujii, Kumiko Kagawa, Nakamura Masafumi, Shiyori Kawata, Makiko Mizuguchi, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, Takahashi Mamiko, Takeshi Harada, Shingen Nakamura, Hirokazu Miki and Masahiro Abe : 造血幹細胞移植(allo-SCT)が奏効したMLL遺伝子変異合併CML急性転化(CML-BP)の2例, 第43回日本造血細胞移植学会総会, Mar. 2021.
43.	清重尚希, Ryohei Sumitani, 水口槙子, 中村昌史, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, 賀川久美子, Masahiro Abe, Shingen Nakamura, Hirokazu Miki, 曽賀愛未, 一宮由貴 and Yuri Yamamoto : 急性転化をきたしたAYA世代慢性骨髄性白血病の1例, Shikoku Acta Medica, Vol.76, No.5-6, 354-355, Dec. 2020. (Keyword) 同種移植抗腫瘍剤(治療的利用) *白血病-BCR-ABL陽性慢性骨髄性(診断,治療,薬物療法) 急性転化(白血病) 障害者の子供造血幹細胞移植家族介護者ヒト青年期(13~18) 女
44.	Hirokazu Miki, 悦子李, 佃恵里加, 小田直輝, 瀧本朋美, 中村昌史, 水口槙子, Ryohei Sumitani, Masahiro Oura, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, Kumiko Kagawa, Masahiro Abe and Shingen Nakamura : Daratumumab投与による輸血関連検査への影響とその対策, Shikoku Acta Medica, Vol.76, No.5-6, 341, Dec. 2020. (Keyword) Coombsテスト / 骨髄腫-多発性(診断,薬物療法) / Daratumumab(治療的利用) / ヒト / 中年(45~64) / 高齢者(65~79) / 高齢者(80~) / 男 / 女
45.	Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Hirokazu Miki, 小田明日香, Takeshi Harada, Ryohei Sumitani, Masahiro Oura, Kumiko Kagawa, Hirofumi Tenshin, Jumpei Teramachi, Masaki Ri, Shinsuke Iida and Masahiro Abe : Immediate accumulation of anti-apoptotic PIM2 in myeloma cells by proteasome inhibitors, 第82回日本血液学会学術集会, Oct. 2020.
46.	Hirofumi Tenshin, Mohannad Ashtar, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する:Xanthine oxidase阻害剤febuxostatの治療効果．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020.
47.	Takeshi Harada, Yusuke Inoue, Hirofumi Tenshin, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Ryohei Sumitani, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa, Masahiro Hiasa, Jumpei Teramachi and Masahiro Abe : Versatile anti-myeloma effects by elotuzumab: impact on γδT cells and osteoclasts, The 82nd Annual Meeting of Japanese Soceity of Hematology, Oct. 2020.
48.	Hirofumi Tenshin, アシテルモハナッド, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, 比嘉佳基, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する Xanthine oxidase阻害剤febuxostatの治療効果, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020. (Keyword) Xanthine Oxidase(拮抗物質・阻害物質) / reactive oxygen species / 抗腫瘍剤(毒性・副作用) / 骨吸収(化学的誘発,薬物療法,実験的) / cell differentiation / osteoclast / 破骨細胞分化因子 / Febuxostat(治療的利用) / RAW264.7細胞 / マウス / animal
49.	Masahiro Oura, Shingen Nakamura, 堀太貴, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Tomoko Kobayashi, Takeshi Oya and Masahiro Abe : 結節性紅斑と悪性腫瘍関連血球貪食症候群を惹起した骨髄異形成症候群の1例, The Japanese Journal of Clinical Hematology, Vol.61, No.10, 1542, Oct. 2020. (Keyword) 骨髄異形成症候群(合併症) 紅斑-結節性(病因) *血球貪食性リンパ組織球症(病因) ヒト中年(45~64) 男
50.	中村昌史, Hirokazu Miki, Masahiro Oura, 川田知代, 堀太貴, 村井純平, Ryohei Sumitani, Kimiko Sogabe, 高橋真美子, Takeshi Harada, Shiroh Fujii, Shingen Nakamura, Kumiko Kagawa, 菅崎幹樹, 徳永尚樹, Akishige Ikegame, 森下英理子 and Masahiro Abe : クロスミキシングテストの特徴的な所見が診断の契機となったプレカリクレイン欠乏症の1例, The Japanese Journal of Clinical Hematology, Vol.61, No.10, 1537-1538, Oct. 2020. (Keyword) Prekallikrein(欠損・欠乏) 血液凝固異常(診断) *血液凝固検査ヒト中年(45~64) 男
51.	山崎佳那子, 祖川麻衣子, Kazutoshi Murao, Yoshiaki Kubo, Masahiro Oura, Takeshi Harada, Shingen Nakamura and Kumiko Kagawa : 骨髄異形成症候群の患者に生じた晩発性皮膚ポルフィリン症の1例, The Nishinihon Journal of Dermatology, Vol.82, No.3, 238-239, Jun. 2020. (Keyword) 骨髄異形成症候群(合併症) Uroporphyrins(尿) ポルフィリン症-晩発性皮膚(合併症,診断) ヒト中年(45~64) 男
52.	Kotaro Tanimoto, Masahiro Hiasa, Akihiko Iwasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, 曾我部公子, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる．, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, Oct. 2019.
53.	谷本幸太朗, Masahiro Hiasa, Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masami Iwasa, 小田明日香, Kimiko Sogabe, Masahiro Oura, Takeshi Harada, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 不動性骨吸収の亢進は骨髄内の骨髄腫進展を促進させる, 第37回日本骨代謝学会学術集会, Oct. 2019.
54.	安宅克博, Shingen Nakamura, Masahiro Oura, Kimiko Sogabe, Takeshi Harada, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Yasuhiko Nishioka and Masahiro Abe : 長期にわたる血小板減少が先行した芽球性形質細胞様樹状細胞腫瘍の1例, 第120回日本内科学会四国地方会, May 2019.
55.	Takeshi Harada, Oda Asuka, Hirofumi Tenshin, Jumpei Teramachi, Masahiro Oura, Kimiko Sogabe, Masami Iwasa, Shiroh Fujii, Hirokazu Miki, Kumiko Kagawa, Teru Hideshima, Anderson C. Kenneth and Masahiro Abe : The novel therapeutic strategy targeting the HDAC1-IRF4-PIM2 pathway in myeloma cells, The 44th Annual Meeting of the Japanese Society of Myeloma, May 2019. (Keyword) Multiple myeloma / Class-I HDAC / IRF4 / Pim-2
56.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Oda Asuka, Bat-Erdene Ariunzaya, Takeshi Harada, Iwasa Masami, Shiroh Fujii, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Masahiro Oura, Kumiko Kagawa, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Mechanisms of TAK1 over-activation in myeloma cells and TAK1-mediated myeloma growth and bone destruction, 第80回日本血液学会学術集会, Oct. 2018.
57.	Masami Iwasa, Takeshi Harada, Bat-Erdene Ariunzaya, 小田明日香, Kimiko Sogabe, Masahiro Oura, Jumpei Teramachi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : HDAC阻害による骨髄腫細胞のIFN-γ-STAT1- PD-L1経路の増強効果, 第80回日本血液学会学術集会, Oct. 2018. (Keyword) Multiple myeloma
58.	Masami Iwasa, Takeshi Harada, Bat-Erdene Ariunzaya, 小田明日香, 前田悠作, 高橋真美子, Masahiro Oura, Jumpei Teramachi, Shiroh Fujii, Shingen Nakamura, Hirokazu Miki, Kumiko Kagawa and Masahiro Abe : Amplification of the IFN- γ -STAT1- PD-L1 pathway in myeloma cells by panobinostat, The 43rd Annual Meeting of the Japanese Society of Myeloma, May 2018. (Keyword) Multiple myeloma
59.	Shoko Iwahashi, Mitsuo Shimada, Kouzou Yoshikawa, Jun Higashijima, Takuya Tokunaga, Masaaki Nishi, Chie Takasu, Hideya Kashihara, Daichi Ishikawa, Hirokazu Miki and Masahiro Oura : MDS・発作性夜間血色素尿症を合併する胃癌に対する手術が安全に施行可能であった1例, 第118回日本外科学会定期学術集会, Apr. 2018.
60.	Jumpei Teramachi, Masahiro Hiasa, Oda Asuka, Hirofumi Tenshin, Ryota Amachi, Takeshi Harada, Shingen Nakamura, Masami Iwasa, Masahiro Oura, Yusaku Maeda, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : Disruption of myeloma cell-bone marrow interaction by TAK-1 inhibition, 第80回日本血液学会学術集会, Oct. 2017.

Et cetera, Workshop:

1.	岩脇文香, 山﨑佳那子, 中島美世, Kazutoshi Murao, Yoshiaki Kubo and Masahiro Oura : シアナミドによる薬疹を契機に丘疹-紅皮症を生じたHTLV-1キャリアの1例, 第73回日本皮膚科学会西部支部学術大会, Oct. 2021.

Associate Professor : Oura, Masahiro

Research

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Academic Letter:

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

Et cetera, Workshop: