A study on the heavy payloads underwater manipulator for deep-sea driven by electric motor

In this study, a development of a 6 D.O.F underwater manipulator which is actuated by electric motors capable of carrying over 70kg payload. It designed to be driven at 3,000m. Balancing weight is applied to reduce the capacity of the joint-2 actuator. I calculated the ideal motor capacity by interpreting inertia torque where is on the each joint actuator. The joint actuator for the manipulator is designed as a double oil jacket for waterproofness in high pressure. Each link is designed the modularization to assemble and replace the parts easily. The kinematics and dynamics of the manipulator has been analyzed based on new designed manipulator. By doing this, I can figured out the feature of 6-axis manipulator motion and stability evaluation of link structure. Also, Thickness of link cylinder at 3,000m has been verified through FEM simulation.1. 서 론 1.1 개요 1.2 기존 매니퓰레이터 분석 1.2.1 유압 구동 방식의 수중 매니퓰레이터 1.2.2 전기 모터 방식의 수중 매니퓰레이터 1.3 연구범위 및 목적 2. 수중 매니퓰레이터의 구조설계 2.1 수중 6축 매니퓰레이터의 구성 및 설계조건 2.2 수중 6축 매니퓰레이터의 관절구동기 용량설계 2.2.1 각 관절의 관성모멘트 가정 및 해석 2.2.2 각 관절의 각속도 및 각가속도 해석 2.2.3 각 관절의 관성력에 의한 토크 해석 2.2.4 링크중량에 의해 발생하는 각 관절의 토크 해석 2.2.5 항력에 의해 발생하는 각 관절의 토크 해석 2.2.6 각 관절의 관성력과 무게, 항력에 의한 토크 해석 2.3 관절구동기 기구구조 설계 2.3.1 관절구동기의 수밀구조 2.3.2 관절구동기 배치설계 2.4 수중 6축 매니퓰레이터의 기구부 설계 3. 수중 6축 매니퓰레이터의 기구학 및 동역학 해석 3.1 매니퓰레이터의 순기구학 해석 3.2 매니퓰레이터의 역기구학 해석 3.3 매니퓰레이터의 속도 기구학 해석 3.4 매니퓰레이터의 동역학 해석 4. 수중 6축 매니퓰레이터 링크의 유한요소해석 4.1 매니퓰레이터의 링크 실린더 내압 해석 4.1.1 실린더 모델링과 경계조건 4.1.2 실린더 압력 해석 결과 4.1.3 실린더 좌굴 해석 결과 5. 결론 참고문

취업여부에 따른 기혼여성의 추가 출산의향

학위논문 (석사)-- 서울대학교 대학원 : 경제학부, 2013. 2. 류근관.본 연구는 우리나라 기혼여성의 취업여부에 따라 경제적, 문화가치관, 지역적 특성이 추가출산의향에 미치는 영향을 알아보고자 하였다. 분석을 위해 통계청의 2005년 인구주택총조사 마이크로데이터를 활용하였고 만 20-40세 기혼여성 76,385명을 대상으로 하여 프로빗 회귀 모형을 사용하였다. 분석 결과, 경제적, 문화가치관 변수뿐만 아니라 지역별 변수가 추가 출산의향에 영향을 미치는 것으로 나타났다. 지역별 실업률은 취업여성과 미취업여성의 추가 출산의향을 감소시키는 것으로 나타났으며 보육시설 공급률 변수는 미미하지만 미취업여성과 취업여성의 추가 출산의향을 높이는 것으로 나타났다. 또한 취업여부에 따라 각 독립 변인들이 추가 출산의향에 상이하게 영향을 미치는 것으로 나타났다. 미취업여성은 경제적 특성을 나타내는 변수인 남편의 소득이나 지역별 실업률 등에서 영향을 받는 것으로 나타났다. 반면, 취업여성의 경우 임금근로 여부에 따라 의향의 차이를 보였으며, 보육시설 공급률이 출산의향에 미치는 영향 또한 미취업여성에 비해 큰 것으로 나타나 자녀 양육과 관련된 특성이 중요하게 고려되고 있음을 파악할 수 있었다. 결론적으로 본 연구는 실증분석을 통해 여성의 취업 여부 및 지역별 특성이 출산의향에 영향을 줄 수 있음을 보였다. 이를 바탕으로 출산율 제고를 위한 정책 수립 시 여성의 취업여부 및 지역별 특성을 고려한 차별화된 정책들이 수립 및 시행되어야 한다는 정책적 함의를 제시하였다.제 1 장 서론 1 1-1. 연구 동기 1 1-2. 연구 의의 3 제 2 장 이론적 배경 및 선행연구 4 2-1. 경제학적 접근 4 2-2. 문화가치관 접근 6 2-3. 지역적 접근 7 제 3 장 데이터 및 기술통계량 10 3-1. 분석자료 10 3-2. 기술통계량 11 제 4 장 연구방법 및 변수설명 14 4-1. 연구방법 14 4-2. 변수설명 16 제 5 장 분석결과 20 5-1. 취업여부에 따른 추가 출산의향 20 5-2. 경제적·문화가치관 변수의 영향 분석 21 5-3. 부모와의 동거여부와 남아선호사상의 관계 26 5-4. 경제적·문화가치관·지역적 변수의 영향 분석 27 제 6 장 결론 및 함의 31Maste

Effects of Post Ischemia-Reperfusion Treatment with Trimetazidine on Renal Injury in Rats: Insights on Delayed Renal Fibrosis Progression

Even after recovery from acute kidney injury, glomeruli remain vulnerable to further injury by way of interstitial fibrosis. This study is aimed at elucidating the effects of post ischemia-reperfusion (I/R) treatment with trimetazidine on the progression to renal fibrosis as well as short- and intermediate-term aspects. Trimetazidine 3 mg/kg or 0.9% saline was given intraperitoneally once upon reperfusion or daily thereafter for 5 d or 8 w. Renal histologic changes and related signaling proteins were assessed. After 24 h, post I/R treatment with trimetazidine significantly reduced serum blood urea nitrogen and creatinine levels and tubular injury accompanied with upregulation of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor (VEGF), and Bcl-2 expression. After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1α-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels. After 8 w, however, post I/R treatment with trimetazidine did not modify the progression of renal fibrosis. In conclusion, post I/R treatment with trimetazidine allows ischemic kidneys to regain renal function and structure more rapidly compared to nontreated kidneys, but not enough to resolute renal fibrosis in long-term aspect.ope

Renoprotective effects of dexmedetomidine against ischemia-reperfusion injury in streptozotocin-induced diabetic rats.

BACKGROUND: Diabetic patients are susceptible to renal ischemia-reperfusion injury, which leads to perioperative complications. Activation of NOD-like receptor protein 3 (NLRP3) inflammasome participates in the development of diabetes, and contributes to renal ischemia-reperfusion injury. Dexmedetomidine (DEX), a highly selective α2-adrenoreceptor agonist, shows renoprotective effects against ischemia-reperfusion injury. We aimed to elucidate the effects, underlying mechanisms, and optimal timing of DEX treatment in diabetic rats. METHODS: Male Sprague-Dawley rats (n = 12 per group) were randomly divided into normal-sham, diabetes-sham, diabetes-ischemia-reperfusion-control, diabetes-ischemia-reperfusion-DEX-pre-treatment, and diabetes-ischemia-reperfusion-DEX-post-treatment groups. Renal ischemia-reperfusion injury was induced in diabetic rats by occlusion of both renal arteries for 45 min, followed by reperfusion for 24 h. DEX (10 μg/kg) was administered intraperitoneally 1 h before ischemia (pre-treatment) or upon reperfusion (post-treatment). After reperfusion, renal tissue was biochemically and histopathologically evaluated. RESULTS: DEX treatment attenuated ischemia reperfusion-induced increase in NLRP3, caspase-1, IL-1β, phospho-AKT, and phospho-ERK signaling. Moreover, oxidative stress injury, inflammatory reactions, apoptosis, and renal tubular damage were favorably modulated by DEX treatment. Furthermore, post-reperfusion treatment with DEX was significantly more effective than pre-treatment in modulating NLRP3 inflammasome, AKT and ERK signaling, and oxidative stress. CONCLUSIONS: This study shows that the protective effects of DEX in renal ischemia-reperfusion injury are preserved in diabetic conditions and may potentially provide a basis for the use of DEX in clinical treatment of renal ischemia-reperfusion injury.ope

Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation

Emerging evidence indicates the pronounced role of inflammasome activation linked to reactive oxygen species (ROS) in the sterile inflammatory response triggered by ischemia/reperfusion (I/R) injury. Ethyl pyruvate (EP) is an antioxidant and conveys myocardial protection against I/R injury, while the exact mechanisms remain elusive. We aimed to investigate the effect of EP on myocardial I/R injury through mechanisms related to ROS and inflammasome regulation. The rats were randomly assigned to four groups: (1) sham, (2) I/R-control (IRC), (3) EP-pretreatment + I/R, and (4) I/R + EP-posttreatment. I/R was induced by a 30 min ligation of the left anterior descending artery followed by 4 h of reperfusion. EP (50 mg/kg) was administered intraperitoneally at 1 h before ischemia (pretreatment) or upon reperfusion (posttreatment). Both pre- and post-EP treatment resulted in significant reductions in myocardial infarct size (by 34% and 31%, respectively) and neutrophil infiltration. I/R-induced myocardial expressions of NADPH oxidase-4, carnitine palmitoyltransferase 1A, and thioredoxin-interacting protein (TXNIP) were mitigated by EP. EP treatment was associated with diminished inflammasome activation (NOD-like receptor 3 (NLRP3), apoptosis-associated speck-like protein, and caspase-1) and interleukin-1β induced by I/R. I/R-induced phosphorylation of ERK and p38 were also mitigated with EP treatments. In H9c2 cells, hypoxia-induced TXNIP and NLRP3 expressions were inhibited by EP and to a lesser degree by U0126 (MEK inhibitor) and SB203580 (p38 inhibitor) as well. EP's downstream protective mechanisms in myocardial I/R injury would include mitigation of ROS-mediated NLRP3 inflammasome upregulation and its associated pathways, partly via inhibition of hypoxia-induced phosphorylation of ERK and p38.ope

Effect of pregabalin administration upon reperfusion in a rat model of hyperglycemic stroke: Mechanistic insights associated with high-mobility group box 1

Hyperglycemia, which reduces the efficacy of treatments and worsens clinical outcomes, is common in stroke. Ability of pregabalin to reduce neuroexcitotoxicity may provide protection against stroke, even under hyperglycemia. We investigated its protective effect against hyperglycemic stroke and its possible molecular mechanisms. Male Wistar rats administered dextrose to cause hyperglycemia, underwent middle cerebral artery occlusion for 1 h and subsequent reperfusion. Rats were treated with an intraperitoneal injection of 30 mg/kg pregabalin or an equal amount of normal saline at the onset of reperfusion (n = 16 per group). At 24 h after reperfusion, neurological deficit, infarct volume, and apoptotic cell count were assessed. Western blot analysis was performed to determine protein expression of high-mobility group box 1 (HMGB1), toll-like receptor-4 (TLR-4), phosphorylated nuclear factor-kappa B (p-NF-κB), interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), phosphorylated inducible and endothelial nitric oxide synthase (p-iNOS, p-eNOS), Bcl-2, Bax, Cytochrome C, and caspase-3 in the brain. Pregabalin-treated rats showed significantly improved neurological function (31% decrease in score), reduced infarct size (by 33%), fewer apoptotic cells (by 63%), and lower expression levels of HMGB1, TLR4, p-NF-κB, IL-1β, and TNF- α, compared with control rats. Decreased p-iNOS and increased p-eNOS expressions were also observed. Expression of Bax, Cytochrome C, and cleaved caspase-3/caspase3 was significantly downregulated, while Bcl-2 expression was increased by pregabalin treatment. Pregabalin administration upon reperfusion decreased neuronal death and improved neurological function in hyperglycemic stroke rats. Cogent mechanisms would include attenuation of HMGB1/TLR-4-mediated inflammation and favorable modulation of the NOS.ope

Effects of propofol on the expression of matric metalloproteinases in rat cardiac fibroblasts after hypoxia and reoxygenation.

BACKGROUND: Propofol is known to protect the myocardium against ischaemia/reperfusion (I/R) injury through its antioxidant and anti-inflammatory properties. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are involved in cell migration and invasion, and mediate tissue remodelling during I/R injury. They are regulated by various mechanisms including oxidative stress and AKT and ERK pathways. We investigated whether propofol affected the expression of MMPs and subsequent cell migration and invasion and the signalling pathways involved in primary rat cardiac fibroblasts undergoing hypoxia and reoxygenation. METHODS: The phosphorylation of ERK and AKT signalling pathways was examined by western blot analysis in rat primary cardiac fibroblasts after hypoxia and reoxygenation. mRNA expression of MMP and TIMPS was analysed by real-time PCR, and proteolytic activities of MMP-2 and -9 were assessed. The effects of propofol on migration, invasion, wound healing, and cell proliferation activity were evaluated after reoxygenation. RESULTS: Propofol induced AKT and ERK1/2 activation. Subsequent activation of MMPs resulted in increased cell migration, invasion, and wound-healing activity under hypoxia-reoxygenation, which was decreased by LY294002 (AKT inhibitor) and U0126 (ERK inhibitor) in rat cardiac fibroblasts. However, propofol had no effect on proliferation or viability of cardiac fibroblasts after hypoxia-reoxygenation. CONCLUSIONS: Propofol affected the expression of MMPs and TIMPs and subsequently induced cell migration and invasive ability, through activation of the ERK and AKT signalling pathway in hypoxia-reoxygenated rat cardiac fibroblastsope

A study on the Prevalence and Related Factors of Post-Intensive Care Syndrome(PICS) of Intensive Care Survivors

학위논문 (석사)-- 서울대학교 대학원 : 간호학과, 2017. 2. 강승완.집중치료 후 증후군(Post Intensive Care Syndrome: PICS)'은 중증 질환이나 급성 입원 치료 후 나타나는 복합적인 증상으로서 이전보다 악화되거나 새로 생겨난 건강 문제로 크게 신체적, 인지적, 정신적 증상으로 나뉜다. 본 연구는 중환자 생존자의 집중치료 후 증후군의 실태와 관련요인을 파악하기 위한 서술적 상관관계 연구이다. 연구의 목적은 중환자관련 의료진 및 건강관련 종사자, 중환자 생존자에게 집중치료 후 증후군에 대해 인식하게 하고 예방과 치료의 중요성을 알려 중환자실 생존자의 삶의 질을 위해 장기적으로 관리할 수 있는 제도를 마련하는 것이다. 자료 수집은 2016년 8월 1일부터 9월 30일까지 서울 시내 일개 대학병원의 환자 104명을 대상으로 시행하였다. 집중치료 후 증후군 측정을 위해 신체적 기능(K-ADL), 인지적 기능(MMSE-K), 정신적 기능(HADS, IES-R-K)의 구조화된 설문지가 사용되었다. 자료는 기술통계, t-test, one-way ANOVA, Pearsons correlation coefficient, Multiple regression 방법을 이용하여 분석하였다. 연구 결과는 다음과 같다. 1. 중환자 생존자 중 89명(85.6%)이 집중치료 후 증후군에 해당하였고, 이들은 본 연구에서 측정한 5개의 증상 중 평균 2개의 증상을 경험 하는 것으로 나타났다. 또한 PICS 증상 중 인지적 · 신체적 문제에 비해 정신적 문제(불안, 우울, PTSD)가 많이 발생하였다. 2. K-ADL로 측정한 신체기능장애가 있는 대상자는 28명(26.9%), MMSE-K로 측정한 인지기능장애가 의심되거나 인지기능장애가 있는 대상자는 30명(28.9%)이었다. HADS로 측정한 불안 증상을 호소하는 대상자는 총 36명(34.7%), 우울 증상을 호소하는 대상자는 총 75명(72.1%)이었다. IES-R-K로 측정한 PTSD를 호 소하는 대상자는 총 38명(36.5%)이었다. 3. 신체적 · 인지적 · 정신적 증상에 유의한 차이가 있는 것으로 나타난 대상자의 질병 특성은 다음과 같다. 일상생활기능은 패혈증 (p=.047), 중환자실 재원 일수(p=.020), 승압제(p=.031)에서, 인지기능은 질병중증도(p<.001), 중환자실 입 · 퇴실 시 의식수준(p=.045, p<.001)에서, 불안은 패혈증(p=.042), 우울은 지속적 인슐린(p=.002),스테로이드 치료(p=.004), PTSD는 중환자실 입실 횟수(p=.012)에서 유의한 차이를 보였다. 4. PICS에 영향을 미치는 요인은 스테로이드 치료(p<.001), 질병중증도(p=.010), 성별(p=.011), 지속적 인슐린 치료(p=.022)였으며 이 변수들은 PICS를 33.7% 설명하였다. 본 연구에서 스테로이드와 지속적 인슐린 치료는 PICS의 증상을 감소시키는 요인으로 나타났다. 또한 중증도가 높을수록, 남자보다 여자가 PICS의 증상을 더 많이 경험하는 것으로 나타났다. 국내에서는 PICS의 실태를 파악한 연구가 드물기에 지역사회, 병원, 가정 등 다양한 환경에 있는 중환자 생존자를 대상으로 반복 연구가 필요하다. 또한 중환자 의료진은 중환자 생존자가 더 나은 삶의 질을 영위할 수 있도록 PICS에 영향을 미치는 관련 요인을 파악하여 PICS의 발생을 줄일 수 있도록 노력해야 할 것이다. 주요어: 중환자실, 중환자 생존자, 집중치료 후 증후군 학 번: 2015-20552I. 서론 1 1. 연구 필요성 1 2. 연구 목적 4 3. 용어 정의 4 II. 문헌고찰 6 1. 중환자실 환자의 경험 6 2. 집중치료 후 증후군 9 III. 연구의 이론적 기틀 18 1. 나이팅게일 환경이론 18 2. 본 연구의 이론적 기틀 19 IV. 연구 방법 21 1. 연구 설계 21 2. 연구 대상 및 기간 21 3. 연구 도구 22 4. 자료 수집 방법 및 절차 26 5. 자료 분석 방법 26 6. 윤리적 고려 27 7. 연구의 제한점 28 V. 연구결과 29 1. 대상자 특성 29 2. 집중치료 후 증후군 40 3. 질병 특성에 따른 일상생활기능, 불안, 우울, PTSD, 인지기능 43 4. 대상자 특성에 따른 집중치료 후 증후군 48 5. 집중치료 후 증후군 증상 간의 상관관계 55 6. 집중치료 후 증후군에 영향을 미치는 요인 57 VI. 논 의 59 1. 집중치료 후 증후군의 실태 59 2. 집중치료 후 증후군의 관련요인 62 VII. 결론 및 제언 66 1. 결 론 66 2. 제 언 68 참고문헌 69 부 록 81 Abstract 92Maste

조골세포 분화에서 ERK 12 통한 Runx2 안정성 조절에 관한 연구

Thesis(doctors) --서울대학교 대학원 :치의학과(두개악안면 세포 및 발생생물학전공),2008. 8.Docto

Nano-fibrous scaffolding promotes osteoblast differentiation and biomineralization

Nano-fibrous poly(l-lactic acid) (PLLA) scaffolds with interconnected pores were developed under the hypothesis that nano-fibrous scaffolding would mimic a morphological function of collagen fibrils to create a more favorable microenvironment for cells versus solid-walled scaffolds. In this study, an in vitro system was used to examine biological properties of the nano-fibrous scaffolds compared with those of solid-walled scaffolds for their potential use in bone tissue engineering. Biomineralization was enhanced substantially on the nano-fibous scaffolds compared to solid-walled scaffolds, and this was confirmed by von Kossa staining, measurement of calcium contents, and transmission electron microscopy. In support of this finding, osteoblasts cultured on the nano-fibrous scaffolds exhibited higher alkaline phosphatase activity and an earlier and enhanced expression of the osteoblast phenotype versus solid-walled scaffolds. Most notable were the increases in runx2 protein and in bone sialoprotein mRNA in cells cultured on nano-fibrous scaffolds versus solid-walled scaffolds. At the day 1 of culture, α2 and β1 integrins as well as αv and β3 integrins were highly expressed on the surface of cells seeded on nano-fibrous scaffolds, and linked to this were higher levels of phospho-Paxillin and phospho-FAK in cell lysates. In contrast, cells seeded on solid-walled scaffolds expressed significantly lower levels of these integrins, phospho-Paxillin, and phospho-FAK. To further examine the role of nano-fibrous architecture, we inhibited the formation of collagen fibrils by adding 3,4-dehydroproline to cultures and then assayed cells for expression of α2 integrin. Cells seeded on nano-fibrous scaffolds sustained expression of α2 integrin in the presence of dehydroproline, while suppression of α2 integrin was evident in cells seeded on solid-walled scaffolds. These results provide initial evidence that synthetic nano fibers may exhibit certain properties that are comparable to natural collagen fibers, and thus, the nano-fibrous architecture may serve as a superior scaffolding versus solid-walled architecture for promoting osteoblast differentiation and biomineralization.ope