19 research outputs found
λ§μ°μ€ λΉκ°μΌλ‘ μ λ¬λ μ½λ λΌ ν‘μ κ³Ό λ°μ€λ¬μ€ μλΈνΈλ¦¬μ€ ν¬μμ λ©΄μ μ‘°μ μμ©
νμλ
Όλ¬Έ (μμ¬)-- μμΈλνκ΅ λνμ : λμλͺ
곡νλΆ, 2014. 2. μ€μ² ν¬.In the respiratory system, chemokines, cytokines and antimicrobial peptides (AMPs) play important roles for regulation of immune response. AMPs can protect the foreign molecules and chemokines can recruit the leukocytes that can remove the pathogen. Cytokines can enhance the effect of AMPs and chemokines and activate various immune cells.
The mucosal adjuvant has been studied by many researchers. Cholera toxin (CT), lipopolysaccharide (LPS) and Bacillus subtilis spore were, also, examined for the development of mucosal adjuvant. However, the effects of these adjuvants have not been understood completely through the administration of intranasal route in the lung and bronchoalveolar lavage fluid (BALF).
In the present study, the effect of the mucosal adjuvants, CT, B. subtilis spore and LPS, was examined by the analysis on the expression of effector molecules and migration of leukocytes in the lung. The adjuvants, CT, B. subtilis spore or LPS, were administered through the intranasal route to mice maintained at SPF facility. Then lung, BALF and serum were taken from the mice at 6, 12, 24 and 72 hr and analyzed mRNA and protein levels of effector molecules. Furthermore, the migration of cells into BALF was examined through analysis of the surface marker using flow cytometer.
The results showed that mRNA of CCL2, CCL4 and CXCL10 were induced by spore or LPS in the lung. However, there are no differences on the mRNA expression of AMPs between the adjuvants. Spore and LPS promoted the expression and secretion of CCL2 and CCL4 proteins in the lung and BALF. In analysis of pro-inflammatory cytokines, spore and LPS dramatically induced the secretion of IL-1Ξ², IL-6 and TNF-Ξ± in the lung and BALF. CT induced the increase of IL-6 in the serum. In analysis of surface marker, spore highly promoted the migration of Gr-1+CD11b+ cells at 6 hr and F4/80+CD11b+Gr-1- cells at 72 hr. LPS, also, induced the migration of Gr-1+CD11b+ cells at 12 and 24 hr. In conclusion, B. subtilis spore can induce the chemokine and cytokine expression in the lung and BALF and enhance the migration of neutrophils into BALF.I. Introduction 1
II. Review of Literature 3
1 Immune modulation in the lung 3
1.1 Recruitment of leukocytes in respiratory tract 3
1.2 Mucosal immunization via intranasal administration 3
2 Effector molecules in the lung 4
2.1 Chemokines 4
2.2 Anti-microbial peptides 5
2.3 Cytokines 7
3 The effect of mucosal adjuvant in lung 8
3.1 Cholera toxin 8
3.2 Lipopolysaccharide 9
3.3 Bacillus subtilis spore 10
III. Materials and Methods 12
1. Reagents 12
2. Preparation and isolation of Bacillus subtilis spore 12
3. Approval for animal study 12
4. Isolation of serum, lung and bronchoalveolar lavage fluid (BALF) 13
5. Isolation of total lysate from lung 13
6. Isolation of total RNA from lung 13
7. Reverse transcription polymerase chain reaction 14
8. Real time - polymerase chain reaction 15
9. Analysis of surface marker 16
10. Measurement of chemokines and cytokines production 16
IV. Results and discussion 17
1. The mRNA of chemokines, CXCL10, CCL2 and CCL4, was remarkably increased in the whole lung of mouse treated with B. subtilis spore or LPS during the early phase of immune response 17
2. B. subtilis spore and LPS enhanced the secretion of CCL2 and CCL4 proteins into BALF during the early immune response. 20
3. CCL2 and CCL4 expression were induced by administration of B. subtilis spore and LPS in the lung 21
4. B. subtilis spore and LPS induced IL-1Ξ² expression in the lung 23
5. B. subtilis spore and LPS induced IL-6 and TNF-Ξ± secretion into BALF 24
6. B. subtilis spore and LPS promoted the recruitment of Gr-1+CD11b+ cells into BALF in early phase 27
V. Literature Cited 30
VI. Summary in Korean 41Maste
μμ μ₯ λͺ¨λΈμμ λ©νΈμμ λ μ±μ λν μ λ λ λ° μ°ΈμΉμ ν΄λ μμ©
Thesis(master`s)--μμΈλνκ΅ λνμ :νλκ³Όμ λκ³Όνμ 곡,2005.Maste
λ°°μΉ νλ‘ν μ½μ μν 3μ§ νΈλ¦¬λ₯Ό μ΄μ©ν ELK
νμλ
Όλ¬Έ(μμ¬) --μμΈλνκ΅ λνμ :μ리과νλΆ,2007.Maste
μμ¬μ μμΈνλ₯Ό ν΅ν λ΄λ©΄μμμ μμ§μ νν μ°κ΅¬ : νμ΄λͺ©μ μμ¬λ‘ ν λ³ΈμΈμ μνμ μ€μ¬μΌλ‘
νμλ
Όλ¬Έ(μμ¬)--μμΈλνκ΅ λνμ :λμνκ³Ό,1997.Maste
Langmuir-Blodgett λ°©λ²μ μ΄μ©ν μ¨λκ°μμ± μλΌμ€ν΄ μ μ¬ ν΄λ¦¬ν©νμ΄λμ κ³λ©΄ κ±°λ μ°κ΅¬
νμλ
Όλ¬Έ (μμ¬)-- μμΈλνκ΅ λνμ : λ°μ΄μ€μμ€ν
.μμ¬νλΆ(λ°μ΄μ€μμ¬κ³΅νμ 곡), 2014. 2. νμ§νΈ.λ³Έ μ°κ΅¬μμλ Langmuir-Blodgett(LB) λ°©λ²μ μ΄μ©νμ¬ κ³΅κΈ°-λ¬Ό κ³λ©΄μ ν‘μ°©λ elastin-like polypeptide(ELP) λΆμμ κ±°λμ μ΄ν΄λ³΄μλ€. ELPλ μ¨λ μκ·Ήμ μν μμ μ΄(phase transition) νΉμ±μ λνλμΌλ‘ λ€μν μ¨λ 쑰건μμ 물리μ μλ ₯μ λ°λ₯Έ ELPμ κ³λ©΄ κ±°λμ λΆμνκΈ° μνμ¬ νλ©΄μλ ₯-λ©΄μ λ±μ¨μ (surface pressure-area(Ο-A) isotherm)μ μΈ‘μ νμκ³ νΉμ 쑰건νμμ κ³λ©΄μ νμ±λ λ¨λΆμλ§μ mica κΈ°νμΌλ‘ μ μ¬νμ¬ atomic force microscopy(AFM)μΌλ‘ νλ©΄ ꡬ쑰λ₯Ό μΈ‘μ νμλ€. λͺ¨λ 쑰건μμ λ¨λΆμλ§μ΄ νμ±λ κ²μΌλ‘ 보μ ELP λΆμκ° κ³λ©΄μ μμ μ μΌλ‘ ν‘μ°©λλ€λ κ²μ νμΈνμμΌλ©° νλ©΄μλ ₯-λ©΄μ λ±μ¨μ μ ννμ λ¨λΆμλ§μ νλ©΄ ꡬ쑰μ λ³νλ₯Ό ν λλ‘ μ¨λμ 물리μ μλ ₯μ΄ κ³λ©΄μ ν‘μ°©λ ELP λΆμμ μ΄μ°¨κ΅¬μ‘°μ λΆμ κ° μνΈμμ©μ λ―ΈμΉλ μν₯μ κ³ μ°°νμλ€.μ 1 μ₯ μ λ‘ 1
μ 2 μ₯ λ¬Έν μ°κ΅¬ 3
2.1 Elastin-like polypeptide(ELP)μ νΉμ± 3
2.2 Langmuir-blodgett(LB) λ°©λ²μ κΈ°λ³Έ μ΄λ‘ λ° μμ© 6
2.2.1 LB λ°©λ²μ κ°λ
6
2.2.2 LB λ°©λ²μ μ΄μ©ν κ³λ©΄μμμ λΆμ κ±°λ μ°κ΅¬ 9
μ 3 μ₯ μ¬λ£ λ° λ°©λ² 13
3.1. Elastin-like polypeptide(ELP)μ μ μ‘° λ° λΆμ 13
3.1.1 ELPμ λ°ν λ° μ μ 13
3.1.2 ELPμ νΉμ± νκ° 16
3.2 Langmuir-blodgett(LB) λ°©λ²μ μ΄μ©ν elastin-like polypeptide(ELP)μ κ³λ©΄ κ±°λ λΆμ 17
3.2.1 νλ©΄μλ ₯-λ©΄μ λ±μ¨μ (Ο-A isotherm) μΈ‘μ 17
3.2.2 LB λ°©λ²μ μ΄μ©ν ELP λ¨λΆμλ§ μ μ‘° 17
3.2.3 Atomic force microscopy(AFM)λ₯Ό μ΄μ©ν ELP λ¨λΆμλ§μ νλ©΄ ꡬ쑰 λΆμ 18
μ 4 μ₯ κ²°κ³Ό λ° κ³ μ°° 19
4.1 Elastin-like polypeptide(ELP)μ νΉμ± 19
4.1.1 ELPμ μμ μ΄(phase transition) 19
4.1.2 ELPμ μ΄μ°¨ ꡬ쑰(secondary structure) 19
4.2 Elastin-like polypeptide(ELP)μ κ³λ©΄ κ±°λ 23
4.2.1 ELPμ νλ©΄μλ ₯-λ©΄μ λ±μ¨μ (Ο-A isotherm) λΆμ 23
4.2.2 μ¨λμ λ°λ₯Έ νλ©΄μλ ₯-λ©΄μ λ±μ¨μ (Ο-A isotherm)μ λ³ν 28
4.3 Elastin-like polypeptide(ELP) λ¨λΆμλ§μ νλ©΄ ꡬ쑰 λΆμ 31
4.3.1 μ¨λμ λ°λ₯Έ ELP λ¨λΆμλ§μ νλ©΄ ꡬ쑰 λ³ν 31
4.3.2 νΉμ μ¨λ 쑰건νμμ 물리μ μλ ₯μ λ°λ₯Έ ELP λ¨λΆμ λ§μ νλ©΄ ꡬ쑰 λ³ν 36
4.4 μ¨λμ 물리μ μλ ₯μ λ°λ₯Έ κ³λ©΄μμμ elastin-like polypeptide(ELP) λΆμ ꡬ쑰μ λΆμ κ° μνΈμμ©μ λν λμν 43
4.5 κ³λ©΄μμμ elastin-like polypeptide(ELP) μ΄μ°¨κ΅¬μ‘° 46
μ 5 μ₯ κ²° λ‘ 48
μ°Έκ³ λ¬Έν 50
Abstract 57Maste
Improvement in response speed of piezo actuator using digital PID servo-positional control and FIR filter
νμλ
Όλ¬Έ(μμ¬)--μμΈλνκ΅ λνμ :κΈ°κ³ν곡곡νλΆ,2005.Maste
Design of a SMA Coil Spring Actuator for Application in Micro Robotics
νμλ
Όλ¬Έ (μμ¬)-- μμΈλνκ΅ λνμ : κΈ°κ³ν곡곡νλΆ, 2011.2. μ‘°κ·μ§.Maste
EXPRESSION OF OD314 DURING AMELOBLAST DIFFERENTIATION AND MATURATION
λ²λλͺ¨μΈν¬λ λ²λμ§μ νμ±νκ³ μ μ§νλ μΈν¬λ‘, λ²λμ§μ μ κΈ°κΈ°μ§μ λΆλΉνκ³ λ²λμ§ μνν κ³Όμ μλ κ΄μ¬νλ€. μΉμ λ°μκ³Όμ μμ λ²λλͺ¨μΈν¬μ λΆνλ μμ°¨μ μΈ μνΌ-κ°μ½ μνΈμμ©μ μνμ¬ μ‘°μ λλ, λΆνλ μ±μκ³Όμ μ μ νν κΈ°μ μ μμ§κΉμ§ μ μλ €μ Έ μμ§ μλ€. μ΅κ·Όμ μμλͺ¨μΈν¬μμ μ²μ λ°κ²¬λ OD314κ° μΉμ λ°μκ³Όμ μμ μμμ§μ νμ±νλ μμλͺ¨μΈν¬ λΏ μλλΌ λ²λλͺ¨μΈν¬μλ λ°νλλ€κ³ νμλ€. μ΄μ λ³Έ μ°κ΅¬μμλ μμ₯ νμ
μ μΉμ λ€μν μκΈ°μ λ²λλͺ¨μΈν¬λ₯Ό μ΄μ©νμ¬, νννμ λΆμκ³Ό in-situ hybridizationμ μν OD314 mRNAμ λ°ν κ·Έλ¦¬κ³ OD314 ν체λ₯Ό μ΄μ©ν λ©΄μμ‘°μ§ννμ λΆμμ ν΅νμ¬ OD314μ μ μμ λ²λλͺ¨μΈν¬ λΆνμ μ±μκ³Όμ μμμ μν μ μ°κ΅¬νμ¬ λ€μκ³Ό κ°μ κ²°κ³Όλ₯Ό μ»μλ€. 1. νννμ μΌλ‘ λ²λλͺ¨μΈν¬λ λΆν λ¨κ³μ λ°λΌ λΆλΉ μ λ¨κ³ λ²λλͺ¨μΈν¬, λΆλΉκΈ° λ²λλͺ¨μΈν¬, μ±μκΈ°μ ννλ λ²λλͺ¨μΈν¬μ μ±μκΈ°μ μ£Όλ¦λ λ²λλͺ¨μΈν¬λ‘ ꡬλΆλμλ€. 2. OD314 mRNAλ λΆλΉκΈ°μ λ²λλͺ¨μΈν¬μμλΆν° λ°νλκΈ° μμνμ¬ λ²λλͺ¨μΈν¬κ° μ±μν΄κ° μλ‘ κ·Έ λ°νμ΄ μ¦κ°νμλ€. 3. OD314 λ¨λ°±μ§μ λΆλΉ μ λ¨κ³μ λ²λλͺ¨μΈν¬μμλ λ°νλμ§ μκ³ , λΆλΉκΈ°μ λ²λλͺ¨μΈν¬μμλ μΈν¬μ§μ μ 체μ μΌλ‘ λ°νλμλ€. μ±μκΈ°μ ννλ λ²λλͺ¨μΈν¬μ μ£Όλ¦λ λ²λλͺ¨μΈν¬μμλ μΈν¬μ κ·Όμ¬κ³Ό μμ¬λλ¨μ OD314 λ¨λ°±μ§μ΄ κ°νκ² λ°νλμλ€. μ΄μμ κ²°κ³Όλ₯Ό μ’
ν©νμ¬ OD314λ λ²λλͺ¨μΈν¬μ λΆνμ μ±μκ³Όμ μμ μΈν¬μ§ λ΄λΆμμ νΉμ§μ μΈ μν μ νλ κ²μΌλ‘ μ¬λ£λλ€.
Ameloblasts are responsible for the formation and maintenance of enamel which is an epithelially derived protective covering for teeth. Ameloblast differentiation is controlled by sequential epithelial-mesenchymal interactions. However, little is known about the differentiation and maturation mechanisms. OD314 was firstly identified from odontoblasts by subtraction between odontoblast/pulp cells and osteoblast/dental papilla cells, even though OD314 protein was also expressed in ameloblast during tooth formation. In this study, to better understand the biological function of OD314 during amelogenesis, we examined expression of the OD314 mRNA and protein in various stages of ameloblast differentiation using in-situ hybridization and immunohistochemistry. The results were as follows : 1. The ameloblast showed 4 main morphological and functional stages referred to as the presecretory, secretory, smooth-ended, and ruffle-ended. 2. OD314 mRNA was expressed in secretory ameloblast and increased according to the maturation of the cells. 3. OD314 protein was not expressed in presecretory ameloblast but expressed in secretory ameloblast and maturative ameloblast. OD314 protein was distributed in entire cytoplasm of secretory ameloblast. However, OD314 was localized at the proxiamal and distal portion of the cytoplasm of smooth-ended and ruffle-ended ameloblast. These results suggest that OD314 may play important roles in the ameloblast differentiation and maturation.νκ΅κ³Όνμ¬λ¨ λͺ©μ κΈ°μ΄μ°
H2 Plasma and PMA Effects on PEALD-Al2O3 Films with Different O2 Plasma Exposure Times for CIS Passivation Layers
In this study, the electrical properties of Al2O3 film were analyzed and optimized to improve the properties of the passivation layer of CMOS image sensors (CISs). During Al2O3 deposition processing, the O2 plasma exposure time was adjusted, and H2 plasma treatment as well as post-metallization annealing (PMA) were performed as posttreatments. The flat-band voltage (Vfb) was significantly shifted (ΞVfb = 2.54 V) in the case of the Al2O3 film with a shorter O2 plasma exposure time; however, with a longer O2 plasma exposure time, Vfb was slightly shifted (ΞVfb = 0.61 V) owing to the reduction in the carbon impurity content. Additionally, the as-deposited Al2O3 sample with a shorter O2 plasma exposure time had a larger number of interface traps (interface trap density, Dit = 8.98 Γ 1013 eVβ1Β·cmβ2). However, Dit was reduced to 1.12 Γ 1012 eVβ1Β·cmβ2 by increasing the O2 plasma exposure time and further reduced after PMA. Consequently, we fabricated an Al2O3 film suitable for application as a CIS passivation layer with a reduced number of interface traps. However, the Al2O3 film with increased O2 plasma exposure time deteriorated owing to plasma damage after H2 plasma treatment, which is a method of reducing carbon impurity content. This deterioration was validated using the CβV hump and breakdown characteristics.11Ysciescopu