• 멤브레인
• /
• 제26권1호
• /
• pp.76-85
• /
• 2016

반도체 및 디스플레이 공정에서 배출되는 $N_2/NF_3$ 혼합 가스 분리를 위한 폴리썰폰 중공사막 제조 연구를 수행하였다. 먼저 non-solvent induced phase separation (NIPS)와 vapor induced phase separation (VIPS) 혼합 공정을 이용하여 기체투과성이 높은 고분자 중공사막을 제조하였다. 제조된 중공사막 표면에 PDMS(polydimethylsiloxiane)와 Teflon AF1600(R) 고분자 소재를 이용하여 얇은 박막을 추가적으로 코팅하는 방법으로 기체 분리막을 완성하였다. 제조된 분리막은 코팅된 고분자 소재의 기체 분리 특성에 따라 상이한 $N_2/NF_3$ 분리 성능을 보여주었다. 특히 Teflon AF1600(R) 이 코팅된 중공사막의 경우 $N_2/NF_3$ 분리 성능(> 14)을 보여주었고, $N_2$ 투과도는 4.5 GPU를 나타내었다. 상용 폴리썰폰 막과 비교해 볼 때, 투과도는 약간 감소하였지만 기체 선택도는 크게 증가하였다. 이런 특징은 $N_2/NF_3$를 분리하는 분리막 구조로써 큰 가능성을 지니는 것으로 판단된다.

• Journal of Acupuncture Research
• /
• 제25권2호
• /
• pp.59-74
• /
• 2008

목적 : 이 연구는 봉약침의 봉독과 그 주요성분인 멜리틴이 $NF-{\kappa}B$의 활성억제와 세포자멸사 관련 단백질의 발현 조절을 통하여 세포자멸사를 유도하고 전립선 암세포주인 LNCaP 세포의 성장을 억제하는지를 확인하고 해당 기전을 살펴보고자 하였다. 방법 : 봉독이나 멜리틴을 처리한 후 LNCaP의 성장억제를 관찰하기 위해 WST-1 assay, CCK-8 assay를 시행하였고, 세포자멸사의 관찰에는 DAPI, TUNEL staining assay를 시행하였으며, 세포자멸사 조절단백질의 변동 관찰에는 western blot analysis를 시행하였고, 세포자멸사와 연관된 $NF-{\kappa}B$의 활성 변화를 관찰하기 위해 EMSA를 시행하였으며, LNCaP에서 봉독이나 멜리틴과 $NF-{\kappa}B$의 상호작용을 관찰하기 위해 transient transfection assay를 시행 시 세포생존율과 $NF-{\kappa}B$의 활성 변동을 측정하였다. 결과 : LNCaP 세포에 봉독이나 멜리틴을 처리한 후, 전립선암세포의 성장, 세포자멸사의 유발, 세포자멸사 관련 단백질의 발현, $NF-{\kappa}B$의 활성, $NF-{\kappa}B$의 p50 치환 후 $NF-{\kappa}B$의 활성과 LNCaP 세포 증식에 미치는 영향을 관찰하여 다음과 같은 결과를 얻었다. 1. LNCaP 세포에서 봉독이나 멜리틴을 처리한 후 세포자멸사가 유도되어 세포성장이 억제되었고, 세포자멸사 관련 단백질 중 분리된 PARP, caspase-9, Bax는 유의한 증가를, Bcl-2, p-Akt, MMP 13, XIAP, cXIAP는 유의한 감소를 나타내었다. 2. LNCaP 세포에서 봉독이나 멜리틴을 처리한 후 $NF-{\kappa}B$의 활성의 유의한 감소를 나타내었다. 3. LNCaP 세포에서 $NF-{\kappa}B$ p50를 치환하여 작용기를 없애고 봉독이나 멜리틴을 처리하였을 경우에도 $NF-{\kappa}B$의 활성의 유의한 감소를 나타내었다. 결론 : 이상의 결과는 봉독이나 멜리틴이 $NF-{\kappa}B$의 활성 억제를 통하여 인간 전립선암세포주인 LNCaP의 세포자멸사를 유발함으로써 증식억제 효과가 있음을 입증한 것으로 전립선암의 예방과 치료에 대한 효과적인 치료제 개발에 도움이 될 것으로 기대된다. 다만 그 기전에서 봉독이나 멜리틴은 기존연구와 달리 $NF-{\kappa}B$ p50의 작용기와 직접적으로 상호작용을 하지는 않는 것으로 보이므로 심화 연구를 요한다.

• Bulletin of the Korean Chemical Society
• /
• 제28권1호
• /
• pp.77-80
• /
• 2007

As neurofilament proteins are major cytoskeletal components of neuron, abnormality of neurofilament is proposed in brain with neurodegenerative disorders such as Parkinson's disease (PD). Since oxidative stress might play a critical role in altering normal brain proteins, we investigated the oxidative modification of neurofilament-L (NF-L) induced by the reaction of cytochrome c with H2O2. When NF-L was incubated with cytochrome c and H2O2, the protein aggregation was increased in cytochrome c and H2O2 concentrationsdependent manner. Radical scavengers, azide, formate and N-acetyl cysteine, prevented the aggregation of NFL induced by the cytochrome c/H2O2 system. The formations of carbonyl group and dityrosine were obtained in cytochrome c/H2O2-mediated NF-L aggregates. Iron specific chelator, desferoxamine, prevented the cytochrome c/H2O2 system-mediated NF-L aggregation. These results suggest that the cytochrome c/H2O2 system may be related to abnormal aggregation of NF-L which may be involved in the pathogenesis of PD and related disorders.

• Journal of Acupuncture Research
• /
• 제21권6호
• /
• pp.19-36
• /
• 2004

Objective : The purpose of this study was to investigate the effect of Bee Venom and Melittin Solution on the lipopolysaccharide(LPS) and sodium nitroprusside(SNP)-induced expression of prostaglandin $E_2(PGE_2)$, cyclooxygenase-2(COX-2), nuclear factor kappa B($NF-{\kappa}B$) and nuclear factor kappa B($NF-{\kappa}B$) dependent luciferase activity in RAW 264.7 cells, a murine macrophage cell line. Methods : The expression of PGE2 was determined by determination of $PEG_2$, COX-2 was by western blotting with corresponding antibodies, $NF-{\kappa}B$ was by gel mobility shift assay method and $NF-{\kappa}B$ dependent luciferase activity was investigated by luciferase assay in RAW 264.7 cells. Results : 1. LPS and SNP-induced expression of $PEG_2$ was significant after 24hour. 2. The 0.5, 1 and $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly LPS-induced expression of $PEG_2$ and, the $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly SNP-induced expression of $PEG_2$ compared with control, respectively. The 0.5 and $1{\mu}g/mL$ of bee venom could not significantly inhibit SNP-induced expression of $PEG_2$ compared with control. 3. The $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly LPS and SNP-induced expression of COX-2 compared with control, respectively. The 0.5 and $1{\mu}g/mL$ of bee venom inclined to decrease LPS and SNP-induced expression of COX-2 compared with control. 4. The 0.5, 1 and $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly LPS and SNP-induced expression of $NF-{\kappa}B$ compared with control, respectively. 5. The 0.5, 1 and $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly LPS-induced expression of $NF-{\kappa}B$ dependent luciferase activity and the 1 and $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly SNP-induced expression of $NF-{\kappa}B$ dependent luciferase activity compared with control, respectively. The $NF-{\kappa}B$ inhibitor also inhibited significantly LPS and SNP-induced expression of $NF-{\kappa}B$ dependent luciferase activity compared with control. 6. The 0.5, 1 and $5{\mu}g/mL$ of bee venom and the 5 and $10{\mu}g/mL$ of melittin solution inhibited significantly LPS + IFN-${\gamma}$, TNF-${\alpha}$ and LPS + TNF-${\alpha}$-induced expression of $NF-{\kappa}B$ dependent luciferase activity compared with control, respectively. The $NF-{\kappa}B$ inhibitor also inhibited significantly LPS and SNP-induced expression of $NF-{\kappa}B$ dependent luciferase activity compared with control. Conclusions : These results suggest the inhibitory action of bee venom and melittin solution on the inflammatory mediators such as $PEG_2$, COX-2 and $NF-{\kappa}B$.

• Structural Engineering and Mechanics
• /
• 제51권2호
• /
• pp.249-265
• /
• 2014

The mechanical characteristics of materials are very essential in structural analysis for the accuracy of structural calculations. The estimation modulus of elasticity of concrete ($E_c$), one of the most important mechanical characteristics, is a very complex area in terms of analytical models. Many attempts have been made to model the modulus of elasticity through the use of experimental data. In this study, the neuro-fuzzy (NF) technique was investigated in estimating modulus of elasticity of concrete and a new simple NF model by implementing a different NF system approach was proposed. A large experimental database was used during the development stage. Then, NF model results were compared with various experimental data and results from several models available in related research literature. Several statistic measuring parameters were used to evaluate the performance of the NF model comparing to other models. Consequently, it has been observed that NF technique can be successfully used in estimating modulus of elasticity of concrete. It was also discovered that NF model results correlated strongly with experimental data and indicated more reliable outcomes in comparison to the other models.

• Asian Pacific Journal of Cancer Prevention
• /
• 제15권2호
• /
• pp.595-598
• /
• 2014

Background: NF-${\kappa}B$ inhibits apoptosis through induction of antiapoptotic proteins and suppression of proapoptotic genes. Various chemotherapy agents induce NF-${\kappa}B$ translocation and target gene activation. We conducted the present study to assess the predictive value of NF-${\kappa}B$ regarding pathologic responses after receiving neoadjuvant chemotherapy. Materials and Methods: We enrolled 131 patients with locally advanced invasive ductal breast carcinoma. Immunohistochemistry (IHC) was used to detect NF-${\kappa}B$ expression. Evaluation of pathologic response was elaborated with the Ribero classification. Results: Expression of NF-${\kappa}B$ was significantly associated with poor pathological response (p=0.02). From the multivariate analysis, it was found that the positive expression of NF-${\kappa}B$ yielded RR=1.74 (95%CI 0.77 to 3.94). Conclusions: NF-${\kappa}B$ can be used as a predictor of poor pathological response after neoadjuvant chemotherapy.

• 생명과학회지
• /
• 제8권4호
• /
• pp.410-415
• /
• 1998

HPLC 및 electrospary mass spectrum으로부터 L-L dipeptide의 존제하에서 pepsin은 hexapeptide인 L-S-pNF-Nle-A-OMe를 가수분해하여 가수분해물외의 새로운 생성물을 합성하는 것이 확인되었다. 이 생성물은 254nm에서 p-nitro-Phe 잔기를 포함하는 peptide였다. 실험결과로부터 E(L-S-pNF)와 L-L 사이의 acyl transpeptidation에 의해 L-S-pNF-L-L가 생성됨을 뒷받침한다. 이러한 transpeptidation 결과는 product 저해실험에 의한 결과에 기초한 것과는 반대로 L-S-pNF가 해리되기전에 Nle-A-L-OMe가 먼저 한다는 것을 보여준다. 그리고, electrospray mass spectrum 으로부터 위에서 검출된 새로운 펩티드에 해당하는 peak (MW 636.1)을 얻었는데, 이는 새 펩티드의 생성을 확실히 증명하는 증거이다. 한편, Nle-A-L-OMe 생성에 대한 solvent isotope effect는 1.736$\pm$0.121이며 L-S-pNF는 2.28$\pm$0.184 그리고 L-S-pNF-L-L의 생성에는 inverse isotope effect로서 0.576$\pm$0.045였는데, 이는 상기 생성물 해리 순서를 확인시켜 준다. D$_{2}$에서 transpeptidation은 더 빠르기 때문에 isotopically-sensitive단계는 Nle-A-L-OMe해리후에 존재하는 것을 알 수 있다. 본 실험결과는, Rebholz and Northrop$^{1)}$ 및 Cho등의 $^{2)} iso-mechanism이론의 타당성을 제시한다.

• 생명과학회지
• /
• 제31권12호
• /
• pp.1110-1119
• /
• 2021

본 연구의 목적은 LPS가 처리된 RAW 264.7 대식세포에서의 염증 반응이 미세먼지(PM_2.5)에 의해 더욱 증가될 수 있는지를 조사하는 것이다. 이를 위하여 LPS와 미세먼지(PM_2.5)가 단독으로 처리되거나 LPS가 존재하는 조건에서 미세먼지(PM_2.5)가 처리된 RAW 264.7 세포에서 염증 매개변수와 ROS의 생성 정도 및 염증 조절 유전자들의 발현 수준을 조사하였다. 본 연구의 결과에 의하면 세포 독성이 없는 범위에서 LPS가 처리된 세포에서 미세먼지(PM_2.5)는 염증성 매개 인자(NO 및 PGE₂) 및 cytokine (IL-6 및 IL-1β)의 생성 수준이 각각의 단독 처리군에 비하여 매우 증가되었으며. 이는 이들의 생성에 관여하는 유전자들의 전사 및 번역 수준에서의 발현 증가와 연관성이 있었다. 또한, LPS가 처리된 RAW 264.7 세포에 미세먼지(PM_2.5)가 노출되었을 때, 핵에서 NF-κB의 발현이 더욱 증가하였고, 세포질에서는 NF-κB 뿐만 아니라 IκB-α의 발현이 감소되었다. 이러한 결과는 LPS와 미세먼지(PM_2.5)의 단독 처리에 비하여 동시 처리된 경우 NF-κB 신호계의 활성이 더욱 증가하여 염증성 유전자들의 전사 활성촉진에 기여하였음을 의미한다. 나아가 LPS가 처리된 RAW 264.7 세포에서 미세먼지(PM_2.5)에 의해 ROS 생성이 크게 증가되었지만 NF-κB 억제제는 ROS의 생성을 감소시키지 못하였다. 그러나, ROS 생성을 인위적으로 억제하였을 경우, 미세먼지(PM_2.5)에 의해 증가된 염증 매개 인자의 발현 및 생성과 NF-κB의 활성화가 모두 감소되었다. 따라서, 본 연구의 결과는 LPS가 처리된 RAW 264.7 세포에서 미세먼지(PM_2.5)에 의해 유도된 NF-κB 매개 염증반응의 증가는 ROS 생성 의존적 현상임을 시사한다.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• 제32권2호
• /
• pp.94-100
• /
• 2006

Purpose: This study was done to confirm the role of NF-$\kappa$B in cisplatin-induced apoptosis of oral squamous cell carcinoma. Materials and Methods: Five cell lines originated from different oral cancer patients were tested for the apoptosis by the treatment of cisplatin. These cells showed different degree of cisplatin-resistance and the order is OSCC-2>OSCC-3>OSCC-5> OSCC-1>OSCC-4. OSCC-2 and OSCC-4 cells were assayed for the apoptosis by measuring DNA fragmentation and TUNEL staining after cisplatin treatment. While OSCC-4 cells showed apoptosis, OSCC-2 cells showed no or very slight apoptosis by cisplatin treatment. Next, It was determined whether NF-$\kappa$B activation is required in mediating cisplatin-induced apoptosis of OSCC-4. Result: The result was that elevated NF-$\kappa$B activity mediated cisplatin-induced apoptosis. Conclusion: In conclusion, these findings suggest that NF-$\kappa$B activation is essential to cisplatin-induced apoptosis and it may be involved in cisplatin resistance in OSCC cells.

• 동의생리병리학회지
• /
• 제17권5호
• /
• pp.1251-1256
• /
• 2003

To determine the effect of Zibachunggan-tang(ZCT) on the process of lipopolysaccharide (LPS)-induced nuclear factor-kBp65 (NF-kBp65) activation, and LPS-induced expression of pro-inflammatory proteins including tumor necrosis factor-α (TNF-α), nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in HepG2 cell. Immunoblot analysis showed that the level of nucleic NF-kBp65 was rapidly up-regulated and cytosolic inhibitory I-kBα was down-regulated by LPS challenge. While ZCT inhibited an increase of NF-kBp65 and degradation of I-kBα in HepG2 cell. Beside LPS-induced expression of a group of genes, such as TNF-α, inducible iNOS and COX-2, are repressed by ZCT. It may be concluded that ZCT attenuates the progress of LPS-induced inflammation by reduction of NF-kBp65 activation. The ZCT would be useful as a therapeutic agent for endotoxin-induced liver disease.