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- 저자 : Masato Hoshi (검색결과 3 건)
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Interactively Instructing a Guide Robot through a Network
Yosuke Hoshi,Yoshinori Kobayashi,Tomoki Kasuya,Masato Fueki,Yoshinori Kuno 제어로봇시스템학회 2008 제어로봇시스템학회 국제학술대회 논문집 Vol.2008 No.10
In this paper, we propose a remote-interactive mode for a museum guide robot. In this mode, the remote operator can interact with the robot by using voice and gestures through a network. The operator can instruct the robot what to do using nonverbal behaviors such as touching an object on the display screen while saying an instruction. For example, the operator can ask the robot, “Bring this brochure to him,” while first touching the brochure and then the person on the display. The brochure is detected and tracked using the SIFT feature matching between video camera images. After the robot takes the brochure, the robot detects and tracks the person, and then hands it to him to the person.
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RET signaling is required for survival and normal function of nonpeptidergic nociceptors.
Golden, Judith P,Hoshi, Masato,Nassar, Mohammed A,Enomoto, Hideki,Wood, John N,Milbrandt, Jeffrey,Gereau, Robert W,Johnson, Eugene M,Jain, Sanjay The Society 2010 The Journal of neuroscience Vol.30 No.11
<P>Small unmyelinated sensory neurons classified as nociceptors are divided into two subpopulations based on phenotypic differences, including expression of neurotrophic factor receptors. Approximately half of unmyelinated nociceptors express the NGF receptor TrkA, and half express the GDNF family ligand (GFL) receptor Ret. The function of NGF/TrkA signaling in the TrkA population of nociceptors has been extensively studied, and NGF/TrkA signaling is a well established mediator of pain. The GFLs are analgesic in models of neuropathic pain emphasizing the importance of understanding the physiological function of GFL/Ret signaling in nociceptors. However, perinatal lethality of Ret-null mice has precluded the study of the physiological role of GFL/Ret signaling in the survival, maintenance, and function of nociceptors in viable mice. We deleted Ret exclusively in nociceptors by crossing nociceptor-specific Na(v)1.8 Cre and Ret conditional mice to produce Ret-Na(v)1.8 conditional knock-out (CKO) mice. Loss of Ret exclusively in nociceptors results in a reduction in nociceptor number and size, indicating that Ret signaling is important for the survival and trophic support of these cells. Ret-Na(v)1.8 CKO mice exhibit reduced epidermal innervation but normal central projections. In addition, Ret-Na(v)1.8 CKO mice have increased sensitivity to cold and increased formalin-induced pain, demonstrating that Ret signaling modulates the function of nociceptors in vivo. Enhanced inflammation-induced pain may be mediated by decreased prostatic acid phosphatase (PAP), as PAP levels are markedly reduced in Ret-Na(v)1.8 CKO mice. The results of this study identify the physiological role of endogenous Ret signaling in the survival and function of nociceptors.</P>
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Katsuyoshi Matsuoka,Kanae Togo,Noritoshi Yoshii,Masato Hoshi,Shoko Arai 대한장연구학회 2023 Intestinal Research Vol.21 No.1
Background/Aims: Patients with ulcerative colitis (UC) are at an increased risk of certain infections and malignancies compared with the general population. Incidence rates (IRs) of hospitalized infections, herpes zoster (HZ), and malignancies in patients with UC, stratified by treatment, in Japan were estimated. Methods: This retrospective study identified patients with UC treated with corticosteroids, immunosuppressants, or tumor necrosis factor inhibitors (TNFi) from 2 administrative databases (Japan Medical Data Center [JMDC] and Medical Data Vision [MDV]). IRs (unique patients with events per 100 patient‐years) were estimated for hospitalized infections, HZ, and malignancies, between June 2010 and May 2018. Results: Among 6,033 MDV patients with UC receiving corticosteroids, immunosuppressants, or TNFi, IRs (95% confidence intervals) were: hospitalized infections, 1.73 (1.52–1.93); HZ, 1.00 (0.85–1.16), and malignancies, 1.48 (1.29–1.66). Among 958 JMDC patients with UC receiving corticosteroids, immunosuppressants, or TNFi, IRs (95% confidence intervals) were: HZ, 1.82 (1.27–2.37) and malignancies, 1.35 (0.87–1.82). In both cohorts, IRs of malignancies were generally similar among patients receiving immunosuppressants, TNFi, or combination therapy (immunosuppressants and TNFi); this was also true for IRs of hospitalized infections and HZ in the MDV cohort. IRs of hospitalized infections, HZ, and malignancies were higher in patients receiving calcineurin inhibitors compared with immunosuppressants or TNFi, in both cohorts. Conclusions: IRs of hospitalized infections, HZ, and malignancies among patients with UC were generally similar regardless of UC treatment, except for calcineurin inhibitors.
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