• 한국항공우주학회지
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• 제49권4호
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• pp.321-328
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• 2021

본 연구에서는 우주 발사체의 복합재 추진제 탱크 구조의 경량 설계를 위하여 좌굴 Knockdown factor를 ABAQUS를 이용한 수치해석 기반으로 새롭게 도출하였다. 복합재 원통 구조의 다양한 두께비(R/t)와 세장비(L/R)를 적절히 고려하였으며, 기하학적 초기 결함을 Single Perturbation Load Approach를 이용하여 구현하였다. 두께비 = 500 및 세장비 = 2.04를 갖는 복합재 원통 구조의 모델의 경우, NASA의 기존 좌굴 설계 기준보다 약 84.38%만큼 좌굴 Knockdown factor가 높게 도출되어 본 연구의 좌굴 설계 기준을 이용할 경우 복합재 추진제 탱크의 경량 구조 설계가 가능함을 확인하였다. 더불어, 복합재 원통 구조의 두께비와 세장비가 각각 증가함에 따라 전역 좌굴 하중과 좌굴 Knockdown factor가 모두 감소하는 경향을 알 수 있었다.

• Composites Research
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• 제34권5호
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• pp.283-289
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• 2021

본 연구에서는 압축력을 받는 얇은 복합재 원통 구조에 대하여 기하학적 혹은 하중에 대한 초기 결함 모델을 이용하여 수치해석적으로 좌굴 Knockdown factor를 새롭게 도출하였다. 전역 좌굴이 발생하기 이전에 타원형상의 변형 형상을 갖는 복합재 원통 구조를 사용하였다. 복합재 원통 구조의 기하학적 초기 결함만 고려하기 위하여 Single Perturbation Load Approach를 이용하였으며, 기하학적 초기 결함과 더불어 하중 불균일을 함께 구현하기 위하여 Single Boundary Perturbation Approach를 사용하였다. 기하학적 초기 결함 모델의 좌굴 Knockdown factor는 NASA의 기존의 좌굴 Knockdown factor보다 약 84% 높게 도출되었으며, 좌굴 시험에 비하여서는 약 9% 낮게 도출되었다. 기하학적 초기 결함과 하중 불균일을 함께 고려하는 모델의 좌굴 Knockdown factor는 NASA의 좌굴 Knockdown factor에 비하여서는 약 75% 높게, 그리고 좌굴 시험보다 약 14% 낮게 계산되었다. 따라서, 본 연구의 좌굴 설계 기준은 고려된 초기 결함 모델과 상관없이 기존의 좌굴 설계 기준에 비하여 경량 설계의 제공이 가능함과 동시에 좌굴 시험 대비 적절히 보수적인 설계 기준을 제공할 수 있음을 확인하였다.

• 한국항공우주학회지
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• 제48권9호
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• pp.653-661
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• 2020

본 논문에서는 우주 발사체 추진제 탱크 구조인 등방성 격자 원통 구조의 경량 설계를 위하여 축 방향의 압축력과 내부 압력을 함께 고려하여 좌굴 Knockdown factor를 수치해석 연구를 통하여 새롭게 정립하였다. 등방성 격자 원통 구조의 유한요소 모델링 및 비선형 후좌굴 해석을 위하여 비선형 유한요소 해석 프로그램인 ABAQUS를 사용하였다. 본 연구 결과, 축 방향의 압축력과 500 kPa의 내부 압력을 함께 받는 등방성 격자 원통 구조의 전역 좌굴 하중 및 좌굴 Knockdown factor가 축 방향의 압축력만을 받는 원통 구조에 비해 각각 304% 및 53%만큼 증가하였다. 따라서 발사체 탱크 구조의 좌굴 설계 시, 내부 압력과 압축력을 함께 고려한 본 연구의 좌굴 Knockdown factor를 이용할 경우, 내부 압력을 고려하지 않은 설계에 비하여 경량 구조 설계가 가능함을 확인하였다.

• Structural Engineering and Mechanics
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• 제87권5호
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• pp.419-429
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• 2023

This study conducts numerical analyses of a thin-walled composite cylinder under axial compression and internal pressure of 10 kPa. Numerical vibration correlation technique and nonlinear postbuckling analyses are conducted using the nonlinear finite element analysis program, ABAQUS. The single perturbation load approach and measured imperfection data are used to represent the geometric initial imperfection of thin-walled composite cylinder. The buckling knockdown factors are derived using present initial imperfection and analysis methods under axial compression without and with the internal pressure. Furthermore, the buckling knockdown factors are compared with the buckling test and computation time are calculated. In this study, derived buckling knockdown factors in present study have difference within 10% as compared with the buckling test. It is shown that nonlinear postbuckling analysis can derive relatively accurate buckling knockdown factor of present thin-walled cylinders, however, numerical vibration correlation technique derives reasonable buckling knockdown factors compared with buckling test. Therefore, this study shows that numerical vibration correlation technique can also be considered as an effective numerical method with 21~91% reduced computation time than nonlinear postbuckling analysis for the derivation of buckling knockdown factors of present composite cylinders.

• BMB Reports
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• 제48권10호
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• pp.583-588
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• 2015

Microtubule actin crosslinking factor 1 (MACF1), a widely expressed cytoskeletal linker, plays important roles in various cells by regulating cytoskeleton dynamics. However, its role in osteoblastic cells is not well understood. Based on our previous findings that the association of MACF1 with F-actin and microtubules in osteoblast-like cells was altered under magnetic force conditions, here, by adopting a stable MACF1-knockdown MC3T3-E1 osteoblastic cell line, we found that MACF1 knockdown induced large cells with a binuclear/multinuclear structure. Further, immunofluorescence staining showed disorganization of F-actin and microtubules in MACF1-knockdown cells. Cell counting revealed significant decrease of cell proliferation and cell cycle analysis showed an S phase cell cycle arrest in MACF1-knockdown cells. Moreover and interestingly, MACF1 knockdown showed a potential effect on cellular MTT reduction activity and mitochondrial content, suggesting an impact on cellular metabolic activity. These results together indicate an important role of MACF1 in regulating osteoblastic cell morphology and function.

• BMB Reports
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• 제48권8호
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• pp.467-472
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• 2015

Heat shock increases skin temperature during sun exposure and some evidence indicates that it may be involved in skin aging. The antioxidant response mediated by the transcription factor NF-E2-related factor 2 (Nrf2) is a critically important cellular defense mechanism that serves to limit skin aging. We investigated the effects of heat shock on collagenase expression when the antioxidant defense system was downregulated by knockdown of Nrf2. GSH and collagenases were analyzed, and the expression of inducible Nrf2, HO-1, and NQO1 was measured. HS68 cells were transfected with small interfering RNA against Nrf2. Heat shock induced the downregulation of Nrf2 in both the cytosol and nucleus and reduced the expression of HO-1, GSH, and NQO1. In addition, heat-exposed Nrf2-knockdown cells showed significantly increased levels of collagenase protein and decreased levels of procollagen. Our data suggest that Nrf2 plays an important role in protection against heat shock-induced collagen breakdown in skin. [BMB Reports 2015; 48(8): 467-472]

• Biomolecules & Therapeutics
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• 제31권6호
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• pp.648-654
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• 2023

Oxidative stress-induced melanocyte apoptosis is linked to the immune system and plays a critical role in the pathogenesis of vitiligo. Aquaporin-3 (AQP3), which is downregulated in vitiligo keratinocytes, regulates intracellular H₂O₂ accumulation. However, the role of AQP3 in oxidative stress is uncertain in vitiligo. This study investigated the effect of downregulated AQP3 on oxidative stress in vitiligo using lesional and non-lesional skin specimen sets from vitiligo patients and primary cultured adult normal human epidermal keratinocytes, with or without downregulation and overexpression of AQP3 in the presence or absence of H₂O₂ treatment. The levels of nuclear factor E2-related factor 2 (NRF2) and/or its main target, NAD(P)H quinone dehydrogenase 1 (NQO-1), were lower in the lesional keratinocytes and cultured keratinocytes with AQP3 knockdown, but were increased in keratinocytes upon AQP3 overexpression. Ratios of NRF2 nuclear translocation and NQO-1 expression levels were further reduced in AQP3-knockdown keratinocytes following H₂O₂ treatment. The conditioned media from AQP3-knockdown keratinocytes treated with H₂O₂ contained higher concentrations of reactive oxygen species (ROS). Moreover, the number of viable melanocytes was reduced when the conditioned media were added to the culture media. Overall, AQP3 downregulation in the keratinocytes of patients with vitiligo can induce oxidative stress in neighboring melanocytes, leading to melanocyte death.

• Molecules and Cells
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• 제38권9호
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• pp.789-795
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• 2015

A chromosome territory is composed of chromosomal subdomains. The internal structure of chromosomal subdomains provides a structural framework for many genomic activities such as replication and DNA repair, and thus is key to determining the basis of their mechanisms. However, the internal structure and regulating proteins of a chromosomal subdomain remains elusive. Previously, we showed that the chromosome territory expanded after BAF53 knockdown. Because the integrity of chromosomal subdomains is a deciding factor of the volume of a chromosome territory, we examined here the effect of BAF53 knockdown on chromosomal subdomains. We found that BAF53 knockdown led to the disintegration of histone H2B-GFP-visualized chromosomal subdomains and BrdU-labeled replication foci. In addition, the size of DNA loops measured by the maximum fluorescent halo technique increased and became irregular after BAF53 knockdown, indicating DNA loops were released from the residual nuclear structure. These data can be accounted for by the model that BAF53 is prerequisite for maintaining the structural integrity of chromosomal subdomains.

• International Journal of Oral Biology
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• 제43권3호
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• pp.161-169
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• 2018

We previously demonstrated that epidermal growth factor (EGF) enhances cell migration and invasion of breast cancer cells in a SMAD ubiquitination regulatory factor 1 (SMURF1)-dependent manner and that SMURF1 induces degradation of ${\beta}-catenin$ in C2C12 cells. However, the relationship between EGF-induced SMURF1 and ${\beta}-catenin$ expression in breast cancer cells remains unclear. So, we investigated if EGF and SMURF1 regulate ${\beta}-catenin$ expression in MDAMB231 human breast cancer cells. When MDAMB231 cells were incubated with EGF for 24, 48, and 72 hours, EGF significantly increased expression levels of SMURF1 mRNA and protein while suppressing expression levels of ${\beta}-catenin$ mRNA and protein. Overexpression of SMURF1 downregulated ${\beta}-catenin$ mRNA and protein, whereas knockdown of SMURF1 increased ${\beta}-catenin$ expression and blocked EGF-induced ${\beta}-catenin$ downregulation. Knockdown of ${\beta}-catenin$ enhanced cell migration and invasion of MDAMB231 cells, while ${\beta}-catenin$ overexpression suppressed EGF-induced cell migration and invasion. Furthermore, knockdown of ${\beta}-catenin$ enhanced vimentin expression and decreased cytokeratin expression, whereas ${\beta}-catenin$ overexpression decreased vimentin expression and increased cytokeratin expression. These results suggest that EGF downregulates ${\beta}-catenin$ in a SMURF1-dependent manner and that ${\beta}-catenin$ downregulation contributes to EGF-induced cell migration and invasion in MDAMB breast cancer cells.

• BMB Reports
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• 제52권6호
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• pp.373-378
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• 2019

The nucleotide-binding and oligomerization domain (NOD) is an innate pattern recognition receptor that recognizes pathogen- and damage-associated molecular patterns. The 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) is a matrix degradation product found in the synovial fluids of patients with osteoarthritis (OA). We investigated whether NOD2 was involved in 29-kDa FN-f-induced pro-catabolic gene expression in human chondrocytes. The expression of mRNA and protein was measured using quantitative real-time polymerase chain reaction (qrt-PCR) and Western blot analysis. Small interfering RNAs were used for knockdown of NOD2 and toll-like receptor 2 (TLR-2). An immunoprecipitation assay was performed to examine protein interactions. The NOD2 levels in human OA cartilage were much higher than in normal cartilage. NOD1 and NOD2 expression, as well as pro-inflammatory cytokines, including interleukin-1beta (IL-$1{\beta}$) and tumor necrosis factor-alpha (TNF-${\alpha}$), were upregulated by 29-kDa FN-f in human chondrocytes. NOD2 silencing showed that NOD2 was involved in the 29-kDa FN-f-induced expression of TLR-2. Expressions of IL-6, IL-8, matrix metalloproteinase (MMP)-1, -3, and -13 were also suppressed by TLR-2 knockdown. Furthermore, NOD2 and TLR-2 knockdown data demonstrated that both NOD2 and TLR-2 modulated the expressions of their adaptors, receptorinteracting protein 2 (RIP2) and myeloid differentiation 88, in 29-kDa FN-f-treated chondrocytes. 29-kDa FN-f enhanced the interaction of NOD2, RIP2 and transforming growth factor beta-activated kinase 1 (TAK1), an indispensable signaling intermediate in the TLR-2 signaling pathway, and activated nuclear factor-${\kappa}B$ (NF-${\kappa}B$), subsequently leading to increased expressions of pro-inflammatory cytokines and cartilage-degrading enzymes. These results demonstrate that 29-kDa FN-f modulated pro-catabolic responses via cross-regulation of NOD2 and TLR-2 signaling pathways.