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Tae Jin Kang

Publications and source records attributed to Tae Jin Kang.

9 recordsLinked to original sources
PubMed2006

In situ compatibilizer-reinforced interface between a flexible polymer (a functionalized polypropylene) and a rodlike polymer (a thermotropic liquid crystalline polymer).

We present an investigation of the interfacial reinforcement between a flexible folded-chain polymer (functionalized polypropylene-maleic anhydride-grafted polypropylene, MAPP) and a rodlike polymer (a themotropic liquid crystalline polymer, TCLP - poly(ester amide)). Fracture toughness was measured using an asymmetric double-cantilever beam test (ADCB). High fracture toughness at the bonding temperature of 200 degrees C indicates that a chemical reaction has occurred at the interface to provide a strong interaction between MAPP and TLCP. Despite the higher modulus of TLCP, the fracture was propagated in the TLCP phase because of inherent TLCP domain structure. An analysis on the locus of failure revealed that at constant bonding temperature the fracture toughness between MAPP and TLCP was influenced not only by the bonding temperature but also by the bonding time. The fracture toughness increased with the bonding temperature until 200 degrees C was reached and then decreased at higher bonding temperature. The fracture toughness increased with annealing time until it reached a plateau value. We ascribe the dependence of the fracture toughness on the bonding time to the progressive occurrence of two different failure mechanisms, adhesive failure and cohesive failure. The adhesive strength increased with bonding temperature whereas the cohesive strength decreased because of weaker adhesion between TLCP crystalline domains. The dependence of fracture toughness on bonding time was explained in terms of the TLCP crystalline domain structure.

Journal Article↗
PubMed2006

A role for Stat1 in the regulation of lipopolysaccharide-induced interleukin-1beta expression.

Because the induction of interleukin-1beta (IL-1beta) is critical to antibacterial host defenses and its excessive generation is a prominent component of sepsis, regulation of this proinflammatory cytokine is a critical factor in the immune response to lipopolysaccharide (LPS). We previously showed that LPS-induced IL-1beta expression was regulated by a Stat1-dependent, nitric oxide (NO)-mediated mechanism. Subsequent in vivo studies showed that whereas Stat1 had a role in the downregulation of IL-1beta expression, it had a more significant effect on its initial induction. Although both interferon-beta (IFN-beta) and IFN-gamma activate Stat1, the early appearance of IFN-beta in the circulation after LPS administration suggested its pivotal role in Stat1-mediated IL-1beta expression in vivo. Further in vitro analysis of peritoneal macrophages from IFN-beta (/), Stat1(/), and caspase-1(/) mice and their wild-type controls following LPS stimulation demonstrated that IL-1beta mRNA was expressed in these mice but not in macrophages from MyD88(/) mice. Despite the presence of IL-1beta mRNA, IL-1beta protein was markedly reduced in the absence of Stat1 activation in macrophages derived from IFN-beta (/) and Stat1(/) mice or in the absence of caspase-1 activity, which itself was dependent on Stat1 activation. These studies support the hypothesis that the expression of IL-1beta requires both the MyD88-dependent induction of IL-1beta mRNA and pro-IL-1beta as well as the MyD88-independent, Stat1-mediated processing of that gene product into active cytokine.

Animals↗
PubMed2006

Importance of nitric oxide synthase in the control of infection by Bacillus anthracis.

The spore-forming, gram-positive bacterium Bacillus anthracis, the causative agent of anthrax, has achieved notoriety due to its use as a bioterror agent. In the environment, B. anthracis exists as a dormant endospore. Upon infection, germination of endospores occurs during their internalization within the phagocyte, and the ability to survive exposure to antibacterial killing mechanisms, such as O2*-, NO*, and H2O2, is a key initial event in the infective process. Macrophages generate NO* from the oxidative metabolism of L-arginine, using an isoform of nitric oxide synthase (NOS 2). Exposure of murine macrophages (RAW264.7 cells) to B. anthracis endospores up-regulated the expression of NOS 2 12 h after exposure, and production of NO* was comparable to that achieved following other bacterial infections. Spore-killing assays demonstrated a NO*-dependent bactericidal response that was significantly decreased in the presence of the NOS 2 inhibitor L-N6-(1-iminoethyl)lysine and in L-arginine-depleted media. Interestingly, we also found that B. anthracis bacilli and endospores exhibited arginase activity, possibly competing with host NOS 2 for its substrate, L-arginine. As macrophage-generated NO* is an important pathway in microbial killing, the ability of endospores of B. anthracis to regulate production of this free radical has important implications in the control of B. anthracis-mediated infection.

Animals↗
PubMed2006

Automated defect detection system using wavelet packet frame and Gaussian mixture model.

This paper proposes an approach for automated defect detection in homogeneous textiles using texture analysis. The texture features are extracted by the wavelet packet frame decomposition followed by the Karhunen-Loève transform. The texture feature vector for each pixel is used as an input to a Gaussian mixture model that determines whether or not each pixel is defective. The parameters of the Gaussian mixture model are estimated with nondefective textile images in supervised defect detection. An approach for unsupervised defect detection is also presented that can identify the heterogeneous subblocks on the basis of the Kullback-Leibler divergence between two Gaussian mixtures. The proposed method was evaluated on 25 different homogeneous textile image pairs, one of each pair with a defect and the other with no defect, and was compared with existing methods using texture analysis. The experimental results yielded visually good segmentation and an excellent detection rate with a low false alarm rate for both supervised and unsupervised defect detection. This confirms the validity of the proposed approach for automated defect detection and localization.

Journal Article↗
PubMed2005

Mutations in genes related to drug resistance in Mycobacterium leprae isolates from leprosy patients in Korea.

OBJECTIVE: Identification of the presence and drug resistance of Mycobacterium leprae is key to the diagnosis and treatment of leprosy in non-endemic country like Korea. The aim of this study was to screen the drug target DNA such as folP, rpoB, gyr, and 23S rRNA of drug resistance strain of M. leprae. PATIENTS AND METHODS: Sequences of those genes were analyzed for the 104 bacterial index positive cases out of 171 leprosy patients in Korea using touchdown PCR, single stranded conformational polymorphism. RESULTS: Twenty (19.2%) cases have shown the mutations in folP gene of dapsone-resistant M. leprae in which three (2.89%) cases were mutations in two genes, folP and rpoB, of multidrugs resistant strains to dapsone and rifampin, and two (1.92%) cases in folP and gyr genes of resistance to dapsone and oflaxacin, respectively. Besides double mutation for folP gene was one case (0.96%) and for rpoB gene one case, respectively. There was no mutant isolates in 23S rRNA gene against clarithromycin. CONCLUSIONS: This result should leads to a better understanding of the status of multidrug resistant leprosy in Korea and may assist in the rapid diagnosis of drug resistant M. leprae and the choice of the appropriate treatment regimens.

Adult↗
PubMed2005

Murine macrophages kill the vegetative form of Bacillus anthracis.

Anti-protective antigen antibody was reported to enhance macrophage killing of ingested Bacillus anthracis spores, but it was unclear whether the antibody-mediated macrophage killing mechanism was directed against the spore itself or the vegetative form emerging from the ingested and germinating spore. To address this question, we compared the killing of germination-proficient (gp) and germination-deficient (DeltagerH) Sterne 34F2 strain spores by murine peritoneal macrophages. While macrophages similarly ingested both spores, only gp Sterne was killed at 5 h (0.37 log kill). Pretreatment of macrophages with gamma interferon (IFN-gamma) or opsonization with immunoglobulin G (IgG) isolated from a subject immunized with an anthrax vaccine enhanced the killing of Sterne to 0.49 and 0.73 log, respectively, but the combination of IFN-gamma and IgG was no better than either treatment alone. Under no condition was there killing of DeltagerH spores. To examine the ability of the exosporium to protect spores from macrophages, we compared the macrophage-mediated killing of nonsonicated (exosporium+) and sonicated (exosporium-) Sterne 34F2 spores. More sonicated spores than nonsonicated spores were killed at 5 h (0.98 versus 0.37 log kill, respectively). Pretreatment with IFN-gamma increased the sonicated spore killing to 1.39 log. However, the opsonization with IgG was no better than no treatment or pretreatment with IFN-gamma. We conclude that macrophages appear unable to kill the spore form of B. anthracis and that the exosporium may play a role in the protection of spores from macrophages.

Animals↗
PubMed2004

Differential production of interleukin-10 and interleukin-12 in mononuclear cells from leprosy patients with a Toll-like receptor 2 mutation.

Toll-like receptor 2 (TLR2) is a key mediator of the immune response to mycobacterial infections, and mutations in TLR2 have been shown to confer susceptibility to infection with mycobacteria. This study investigated the profiles of cytokines, such as interferon (IFN)-gamma, interleukin (IL)-10, IL-12 and tumour necrosis factor (TNF)-alpha in response to Mycobacterium leprae in peripheral blood mononuclear cells (PBMC) with the TLR2 mutation Arg677Trp, a recently reported polymorphism that is associated with lepromatous leprosy. In leprosy patients with the TLR2 mutation, production of IL-2, IL-12, IFN-gamma, and TNF-alpha by M. leprae-stimulated PBMC were significantly decreased compared with that in groups with wild-type TLR2. However, the cells from patients with the TLR2 mutation showed significantly increased production of IL-10. There was no significant difference in IL-4 production between the mutant and wild-type during stimulation. Thus, these results suggest that the TLR2 signal pathway plays a critical role in the alteration of cytokine profiles in PBMC from leprosy patients and the TLR2 mutation Arg677Trp provides a mechanism for the poor cellular immune response associated with lepromatous leprosy.

Adult↗
PubMed2002

A polymorphism in the toll-like receptor 2 is associated with IL-12 production from monocyte in lepromatous leprosy.

Toll-like receptor 2 (TLR2) is critical in the immune response to mycobacterial infections, and the mutations in the TLR2 have been shown to confer the susceptibility to infection with mycobacteria. We previously reported the detection of TLR2 Arg677Trp mutation in lepromatous leprosy. Here, the events triggered by TLR2 in response to cell lysate of Mycobacterium leprae(MLL), the causative agent of leprosy, were investigated. Upon stimulation with MLL, monocytes produced TNF-alpha and Interleukin-12 (IL-12), which play a role in the innate immune response to infection. Anti-TLR2 mAb blocked greater than 50% of the MLL-induced production of IL-12. We also performed the functional study on TLR2 by measurement of IL-12 production in serum and monocytes from leprosy patients with TLR2 mutation (Arg677Trp). The monocytes obtained from patients with the TLR2 mutation, in comparison to the wild-type TLR2, is significantly less responsive to MLL. It was also confirmed that patients with TLR2 mutation showed significantly lower serum levels of IL-12, in comparing with TLR2 wild-type. Our results reveal that innate immune response of monocytes against M. lepraeis mediated by TLR2, and suggest that the mutation in the intracellular domain of TLR2 gene is associated with IL-12 production in lepromatous leprosy.

Amino Acid Sequence↗