• 제목/요약/키워드: ROS2

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Libclang 을 활용한 ROS2 의 스레드 안전성 분석 (Analyzing thread-safety on ROS2 with Libclang)

  • 신채원;강정환 ;권동현
    • 한국정보처리학회:학술대회논문집
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    • 한국정보처리학회 2023년도 춘계학술발표대회
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    • pp.149-150
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    • 2023
  • ROS2 코드에서, multi-threaded executor 은 여러 메시지 또는 이벤트를 병렬로 처리할 수 있도록 복수의 스레드를 만든다. Multi-threaded executor 을 사용하면 프로그램 성능이 가속화되고 메모리를 경제적으로 사용할 수 있지만, 하나의 시스템 자원을 여러 개의 프로세스가 동시에 참조하거나 수정하기 때문에 deadlock 등의 여러 문제가 발생한다. 이 논문에서는 libclang 인터페이스를 이용해 ROS2 코드를 구문 분석하고 스레드 안전성을 평가하는 방법과 그 한계점, 향후 연구 방향에 대해 논한다.

Robot Software Framework using Robot Operation System(ROS2) based on Behavior Tree

  • Sangho Lee;Hyejin Chang;Seulgi Jeon;Janghwan Kim;R. Young Chul, Kim
    • International Journal of Internet, Broadcasting and Communication
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    • 제15권4호
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    • pp.134-141
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    • 2023
  • As robotic technology expands into various fields, robots need to execute some complicated tasks in diverse environments. However, the previous robotic software solutions were limited to independent systems. We can not adapt to diverse functionalities and environments. This makes it hard to provide rapid and effective services and leads to costs and losses in the development process. To overcome these problems, we propose a robot software framework with behavior trees based on ROS2. This framework simplifies complex robot behaviors through behavior trees and makes it easy to modify, extend, and reuse robot behaviors. Furthermore, ROS2 standardizes connections between software modules, enhances the robot's flexibility, and enables independent development and testing of software. Our framework aims to provide a foundation for high-quality robot service provision by supporting the modularity, reusability, independent development, and testing required by intelligent robots that need to provide services in various environments.

쥐의 뇌실 하 영역(SVZ) 신경 줄기 세포의 신경 세포로의 분화 과정에서 Nox4의 역할 (Role of Nox4 in Neuronal Differentiation of Mouse Subventricular Zone Neural Stem Cells)

  • 박기엽;나예린;김만수
    • 생명과학회지
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    • 제26권1호
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    • pp.8-16
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    • 2016
  • 적절한 농도의 활성산소종(ROS)은 병원체에 대한 세포의 방어, 신호 전달, 세포 성장 및 유전자 발현을 포함한 다양한 정상 세포 기능을 매개한다. 최근의 연구는 ROS와 ROS를 생성하는 NADPH 산화 효소(Nox)가 성인 쥐 뇌의 뇌실 하 영역(SVZ)에 있는 신경 줄기세포의 자가 복제와 신경 세포 분화에 중요하다는 것을 보여 주었다. 본 연구에서 세포 내 ROS가 갓 태어난 쥐의 뇌에서 적출되어 배양된 SVZ 신경 줄기세포에서 검출된 것으로 나타났다. Nox 유사 유전자들 중 Nox4가 배양된 세포에서 주로 발현되었고, Nox1과 Nox2는 거의 발현되지 않았다. 또한, Nox4 유전자는 신경 세포 분화 동안 최대 10배까지 발현이 크게 증가하였다. Immunocytochemistry결과 Nox4 단백질은 신경 세포 특이적인 tubulin인 Tuj1-양성 신경 세포에서 주로 발견되었다. 이와 맥을 같이 하여, 내인성 ROS는 분화 후 축삭돌기를 가지고 있으며 신경 세포로 보이는 세포에서만 검출되었다. 또한, ROS를 제거하는N-acetyl cysteine에 의해 세포 산화 환원 상태가 교란되었을 때, 신경 세포로의 분화가 크게 감소하였다. 마지막으로, shRNA를 이용하 여 Nox4를 knockdown한 세포에서 신경 세포로의 분화가 감소하였다. 이러한 연구 결과는 Nox4가 갓 태어난 쥐의 SVZ 신경 줄기 세포의 주요한 ROS 생성 효소이고, Nox4에 의한 ROS생성이 신경 세포 분화에 중요하다는 것을 암시한다.

Effects of NaOCl on Neuronal Excitability and Intracellular Calcium Concentration in Rat Spinal Substantia Gelatinosa Neurons

  • Lee, Hae In;Park, A-Reum;Chun, Sang Woo
    • International Journal of Oral Biology
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    • 제38권1호
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    • pp.5-12
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    • 2013
  • Recent studies indicate that reactive oxygen species (ROS) can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In this study, we investigated the effects of NaOCl, a ROS donor, on neuronal excitability and the intracellular calcium concentration ($[Ca^{2+}]_i$) in spinal substantia gelatinosa (SG) neurons. In current clamp conditions, the application of NaOCl caused a membrane depolarization, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN), a ROS scavenger. The NaOCl-induced depolarization was not blocked however by pretreatment with dithiothreitol, a sulfhydryl-reducing agent. Confocal scanning laser microscopy was used to confirm whether NaOCl increases the intracellular ROS level. ROS-induced fluorescence intensity was found to be increased during perfusion of NaOCl after the loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF$-DA). NaOCl-induced depolarization was not blocked by pretreatment with external $Ca^{2+}$ free solution or by the addition of nifedifine. However, when slices were pretreated with the $Ca^{2+}$ ATPase inhibitor thapsigargin, NaOCl failed to induce membrane depolarization. In a calcium imaging technique using the $Ca^{2+}$-sensitive fluorescence dye fura-2, the $[Ca^{2+}]_i$ was found to be increased by NaOCl. These results indicate that NaOCl activates the excitability of SG neurons via the modulation of the intracellular calcium concentration, and suggest that ROS induces nociception through a central sensitization.

RBL-2H3에서 IgE-dependent Histamine-releasing Factor에 의한 활성산소종 생성에 관한 연구 (Generation of ROS by IgE-Dependent Histamine-Releasing Factor in RBL-2H3 Cells)

  • 주이신;이경림
    • 한국미생물·생명공학회지
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    • 제33권3호
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    • pp.231-235
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    • 2005
  • RBL-2H3 cell에서 HRE에 의하여 histamine이 분비되는 과정에서 ROS가 생성되는지 실험해 본 결과, ROS가 HRF를 처리한지 5분대에 최대치를 보이며 생성되었다가 소멸되는 것을 관찰할 수 있었다. 따라서 HRF가 세포내 second messenger로써의 ROS를 생성하였다고 확인할 수 있었다. 또한 ROS는 단백질 정제 과정에서의 endotoxin오염에 의해 영향을 받지만,본 실험에서 규명한 HRF에 의한 ROS 생성은 endotoxin에 의한 것이 아닌, 순수하게 HRF에 의한 signaling의 결과라는 것도 확인할 수 있었다.

인진과 황련 추출물의 췌장암 세포주 MIA PaCa-2에 대한 세포사멸 효과 (Apoptotic Effect of ARTEMISIAE CAPILLARIS HERBA and COPTIDIS RHIZOMA Extracts on MIA PaCa-2 Cells)

  • 주현아;배현진;황충연
    • 한방안이비인후피부과학회지
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    • 제27권4호
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    • pp.158-176
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    • 2014
  • Purpose : The purpose of this study is to investigate the effect of ARTEMISIAE CAPILLARIS HERBA and COPTIDIS RHIZOMA Extracts on cell death in pancreatic cancer cells. Method : Human-derived pancreatic cancer cell line, MIA PaCa-2 cells were treated by Prescription A with various concentrations and the cytotoxicity was determined by MTT assay. To investigate the effects of Prescription A on pancreatic cancer cells, the staining of Annexin V/PI, cell cycle arrest, nuclear chromatin condensation and the production of reactive oxygen species (ROS) were examined. The effect of Prescription A's effective components, ARTEMISIAE CAPILLARIS HERBA and COPTIDIS RHIZOMA Extracts on cell death were also observed. Results : The viability of MIA PaCa-2 cells treated with Prescription A were decreased in a dose dependent manner. Prescription A induced cell death in MIA PaCa-2 cells as shown by result of Annexin V/PI double staining, chromatin condensation and cell cycle arrest. In addition, production of ROS was increased by Prescription A treatment, suggesting that ROS induced by Prescription A mediated cell death. Furthermore, Prescription A's effective components, ARTEMISIAE CAPILLARIS HERBA and COPTIDIS RHIZOMA Extracts were also induced apoptosis of MIA PaCa-2 cells through ROS production. Conclusion : These results suggest that Prescription A's effective components, ARTEMISIAE CAPILLARIS HERBA and COPTIDIS RHIZOMA Extracts induced death of MIA PaCa-2 through ROS production.

SOCS3 Attenuates Dexamethasone-Induced M2 Polarization by Down-Regulation of GILZ via ROS- and p38 MAPK-Dependent Pathways

  • Hana Jeong;Hyeyoung Yoon;Yerin Lee;Jun Tae Kim;Moses Yang;Gayoung Kim;Bom Jung;Seok Hee Park;Choong-Eun Lee
    • IMMUNE NETWORK
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    • 제22권4호
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    • pp.33.1-33.17
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    • 2022
  • Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages. Treatment of THP1 monocytic cells with dexamethasone (Dex) induced ROS generation and M2 polarization promoting IL-10 and TGF-β production, while suppressing IL-1β, TNF-α and IL-6 production. SOCS3 over-expression reduced, whereas SOCS3 ablation enhanced IL-10 and TGF-β induction with concomitant regulation of ROS. As a mediator of M2 differentiation, glucocorticoid-induced leucine zipper (GILZ) was down-regulated by SOCS3 and up-regulated by shSOCS3. The induction of GILZ and IL-10 by Dex was dependent on ROS and p38 MAPK activity. Importantly, GILZ ablation led to the inhibition of ROS generation and anti-inflammatory cytokine induction by Dex. Moreover, GILZ knock-down negated the up-regulation of IL-10 production induced by shSOCS3 transduction. Our data suggest that SOCS3 targets ROS- and p38-dependent GILZ expression to suppress Dex-induced M2 polarization.

Relationship between reactive oxygen species and autophagy in dormant mouse blastocysts during delayed implantation

  • Shin, Hyejin;Choi, Soyoung;Lim, Hyunjung Jade
    • Clinical and Experimental Reproductive Medicine
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    • 제41권3호
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    • pp.125-131
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    • 2014
  • Objective: Under estrogen deficiency, blastocysts cannot initiate implantation and enter dormancy. Dormant blastocysts live longer in utero than normal blastocysts, and autophagy has been suggested as a mechanism underlying the sustained survival of dormant blastocysts during delayed implantation. Autophagy is a cellular degradation pathway and a central component of the integrated stress response. Reactive oxygen species (ROS) are produced within cells during normal metabolism, but their levels increase dramatically under stressful conditions. We investigated whether heightened autophagy in dormant blastocysts is associated with the increased oxidative stress under the unfavorable condition of delayed implantation. Methods: To visualize ROS production, day 8 (short-term dormancy) and day 20 (long-term dormancy) dormant blastocysts were loaded with $1-{\mu}M$ 5-(and-6)-chloromethyl-2', 7'-dichlorodihydrofluorescein diacetate, acetyl ester (CM-$H_2DCFDA$). To block autophagic activation, 3-methyladenine (3-MA) and wortmannin were used in vivo and in vitro, respectively. Results: We observed that ROS production was not significantly affected by the status of dormancy; in other words, both dormant and activated blastocysts showed high levels of ROS. However, ROS production was higher in the dormant blastocysts of the long-term dormancy group than in those of the short-term group. The addition of wortmannin to dormant blastocysts in vitro and 3-MA injection in vivo significantly increased ROS production in the short-term dormant blastocysts. In the long-term dormant blastocysts, ROS levels were not significantly affected by the treatment of the autophagy inhibitor. Conclusion: During delayed implantation, heightened autophagy in dormant blastocysts may be operative as a potential mechanism to reduce oxidative stress. Further, ROS may be one of the potential causes of compromised developmental competence of long-term dormant blastocysts after implantation.

산화방지제 파이토케미컬이 건강에 미치는 영향에 대해 고려할 점 (Considerations for the effects of antioxidant phytochemicals on human health)

  • 김대옥;이창용
    • 한국식품과학회지
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    • 제53권2호
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    • pp.111-114
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    • 2021
  • 과일, 채소, 곡물, 견과류 등에 함유된 파이토케미컬은 심혈관질환, 암, 퇴행성신경질환 등을 유발하는 활성산소의 바람직하지 않은 영향을 방지하는 산화방지제로 역할을 한다. 이처럼 유해물질로 간주되었던 활성산소는 최근에 면역 및 다른 생리적 반응 신호에서 인체에 유익한 역할을 하는 것으로 밝혀졌다. 여러 연구에 따르면 활성산소는 신진대사 건강을 증진시키는 필수 신호 전달 물질로 작용한다. 따라서, 산화방지제가 활성산소의 신호 전달에 간섭하는 것은 전반적인 이점에 의문의 여지가 있다. 그러므로 건강상의 이익을 위해 파이토케미컬을 기능성 식품과 보충제에 적용할 때 활성산소가 미치는 영향을 이해하기 위한 연구가 반드시 필요하다. 본 논문은 활성산소에 관한 연구를 계획하는 식품학자 및 영양학자들에게 가능한 연구 방향을 제공하고자 활성산소의 새로운 역할과 다양한 파이토케미컬의 호메시스를 간략하게 다루고 있다.

LPS 자극 RAW 264.7 세포에 있어서 칼슘의존성 ROS와 NO 생산 및 NF-${\kappa}B$ 활성에 대한 CLA의 억제효과 (Effect of trans-10, cis-12 Conjugated Linoleic Acid on Calcium-Dependent Reactive Oxygen Species and Nitric Oxide Production and Nuclear Factor-${\kappa}B$ Activation in Lipopolysaccharide-Stimulated RAW 264.7 Cells)

  • 최태원;강병택;강지훈;양만표
    • 한국임상수의학회지
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    • 제32권2호
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    • pp.135-140
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    • 2015
  • 염증상태에서의 CLA의 효과와 작용기전을 알아보기 위해 LPS로 자극한 RAW 264.7 세포에 있어서 ROS와 NO생산 및 NF-${\kappa}B$ 활성에 대한 t10c12-CLA의 효과를 검토하였다. 또한 이러한 효과가 세포질 내 칼슘이온의 변화와 관련이 있는지도 알아보았다. LPS 자극으로 ROS 생산은 증가하였고 이러한 증가는 칼슘결합제인 BAPTA/AM에 의해 감소하였다. t10c12-CLA 또한 LPS 자극 RAW 264.7 세포의 ROS 생산 증가를 억제시켰으며 BAPTA/AM과 함께 처리시 더욱 억제되었다. NO의 생산과 NF-${\kappa}B$ p65 활성도 t10c12-CLA, BAPTA/AM, t10c12-CLA와 BAPTA/AM의 동시처리 모두에서 현저하게 억제되었다. 이상의 결과로부터 염증 조건에서 CLA는 과도한 ROS와 NO의 생산 및 NF-${\kappa}B$의 활성을 칼슘 의존적으로 억제하여 항염증 효과를 발휘하는 것으로 생각되었다.