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구형 고분자수지로 활성탄제조 시 비표면적과 비용적의 조절
서수길 ( Soo-gil Seo ),이강춘 ( Gang-choon Lee ) 한국환경기술학회 2014 한국환경기술학회지 Vol.15 No.6
본 연구는 탄소원으로 polystyrene-DVB 공중합으로 제조된 양이온교환수지를 활성탄제조 시 탄소원으로 사용하여 활성탄의 주요물성인 비표면적과 비용적에 미치는 운전인자의 영향이 실험적으로 연구되었다. 제조된 활성탄의 비표면적과 비용적은 탄화온도, 수증기주입량, 활성화온도 그리고 활성화시간이 증가함에 따라 증가하였다. 그러나 제조된 활성탄의 양은 수증기주입량, 활성화온도 그리고 활성화시간이 증가에 반비례하였다. 활성탄의 수율을 고려하면서 비표면적과 비용적을 조절하기 위하여 수증기주입량 0.1 g/min이하, 활성화온도 950℃이하, 활성화시간 80 min이하의 운전조건이 적합하다. Using a cation exchange resin of polystyrene-DVB copolymer as a carbon source for the production of activated carbon, the effects of operating parameters on the physical properties of activated carbon such as specific surface area and specific volume were experimentally studied. Specific surface area and specific volume of activated product increased with carbonization temperature, steam feed rate, activation temperature, and activation time. However the amount of product was inversely proportional to steam feed rate, activation temperature, and activation time. Considering the yield of produced activated carbon, the steam feed rate of 0.1 g/min and under, the activation temperature of 950℃ and under, and the activation time of 80 min and under are recommended as the operating range for controlling the physical properties of activated carbon.
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트립토판 대사체 3-hydroxyanthranilic acid 의 TRAIL-유도 활성 T 세포 사멸 효과
Su-Kil Seo(서수길) 한국생명과학회 2011 생명과학회지 Vol.21 No.2
Indoleamine 2,3-dioxygenase (IDO)에 의한 트립토판 대사체의 생성은 T 세포에 강력한 억제효과를 미치지만 여전히 그 작용기전에 대한 연구보고는 미비한 실정이다. 본 연구자는 트립토판 대사체 3-HAA가 선택적으로 활성 T 세포의 사멸을 촉진시키는 효과가 있음을 확인하였고, 이는 세포주기 억제와는 관련이 없었다. 3-HAA처리 시 활성 T 세포에서 TRAIL과 그의 수용체의 발현이 현저히 증가하고, 이들 상호작용을 차단하였을 때 3-HAA-매개 활성 T 세포사멸 효과가 유의하게 낮아졌다. 본 연구를 통해 트립토판 대사체 3-HAA의 선택적 T세포 억제 효과가 TRAIL-유도 세포사멸과 관련됨을 알 수 있다. Generation of tryptophan-derived metabolites by indoleamine 2,3-dioxygenase (IDO) is a potent immunoregulatory mechanism in T cell responses. However, the mechanism remains unclear. We showed that 3-hydroxyanthranilic acid (3-HAA), the most potent metabolite, selectively induced apoptosis in activated T cells, but not in resting T cells. This was not associated with cell cycle arrest. We found that TRAIL expression was selectively induced in activated T cells by treatment of 3-HAA. Blockade of the TRAIL: DR4/DR5 pathway significantly inhibited 3-HAA-mediated T cell death. Our data suggest that TRAIL-induced apoptosis is involved in the mechanism of 3-HAA-mediated T cell death.
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Expression and Function of TLR2 on CD4 Versus CD8 T Cells
이선미,주영돈,서수길 대한면역학회 2009 Immune Network Vol.9 No.4
Background: Toll-like receptors (TLRs) play a fundamental role in innate immunity through their capacity to recognize pathogen-associated molecular patterns. Also, TLRs that are expressed in T cells are reported to function as co-stimulatory receptors. However, the functional capacity of TLRs on CD4 T and CD8 T cells has not been directly compared. Here we compared CD4 and CD8 T cell responses to TLR2 ligand plus TCR-mediated stimulation. Methods: TLR2 expression was analyzed on T cell subsets under naïve and alloantigen- primed conditions. We analyzed the effects of TLR2 co-stimulation on proliferation and survival of T cell subsets in vitro when stimulated with soluble anti-CD3 in the presence or absence of synthetic ligand Pam3CSK4. Results: TLR2 expression on CD8 T cells was induced following activation; this expression was much higher than on CD4 T cells. Thus, the molecule was constitutively expressed on Listeriaspecific memory CD8 T cells. Based on these expression levels, proliferation and survival were markedly elevated in CD8 T cells in response to the TLR2 co-stimulation by Pam3CSK4 compared with those in CD4 T cells. Conclusion: Our data show that TLR2 co-stimulation is more responsible for proliferation and survival of CD8 T cells than for that of CD4 T cells. Background: Toll-like receptors (TLRs) play a fundamental role in innate immunity through their capacity to recognize pathogen-associated molecular patterns. Also, TLRs that are expressed in T cells are reported to function as co-stimulatory receptors. However, the functional capacity of TLRs on CD4 T and CD8 T cells has not been directly compared. Here we compared CD4 and CD8 T cell responses to TLR2 ligand plus TCR-mediated stimulation. Methods: TLR2 expression was analyzed on T cell subsets under naïve and alloantigen- primed conditions. We analyzed the effects of TLR2 co-stimulation on proliferation and survival of T cell subsets in vitro when stimulated with soluble anti-CD3 in the presence or absence of synthetic ligand Pam3CSK4. Results: TLR2 expression on CD8 T cells was induced following activation; this expression was much higher than on CD4 T cells. Thus, the molecule was constitutively expressed on Listeriaspecific memory CD8 T cells. Based on these expression levels, proliferation and survival were markedly elevated in CD8 T cells in response to the TLR2 co-stimulation by Pam3CSK4 compared with those in CD4 T cells. Conclusion: Our data show that TLR2 co-stimulation is more responsible for proliferation and survival of CD8 T cells than for that of CD4 T cells.
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Acquired factor VIII deficiency after consuming the dried gallbladder of a cobra, Naja naja
Hyun Ju Kim,이원식,Young Jin Lee,Hyun Soo Jun,서수길,주영돈 대한혈액학회 2010 Blood Research Vol.45 No.3
Acquired factor VIII deficiency is very rare, often fatal. It is associated with pregnancy, autoimmune diseases, malignancy, and drugs, although no underlying cause is found in 50%. A 49-year-old male was referred with right shoulder bruising. The coagulation test showed a prolonged activated partial thromboplastin time. The factor VIII level was less than 1%, and the factor VIII inhibitor antibody titer was 246 Bethesda units/mL. The findings were compatible with acquired factor VIII deficiency. He had consumed the dried gallbladder of a cobra, Naja naja, for two weeks, it contained venom. After the initial treatment with factor VIII, he did not take supplemental coagulation factor VIII. The patient was readmitted with left forearm swelling. He lost consciousness suddenly and brain computed tomography (CT) revealed a subdural hematoma. Despite administering recombinant factor VII, his bleeding was not controlled and he died.
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