• IMMUNE NETWORK
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• v.8 no.2
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• pp.39-45
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• 2008

Background: Down regulation of major histocompatibility complex class II transactivator (CIITA) has been identified as a major factor of immunosuppression in sepsis and the level of CIITA expression inversely correlates with the degree of severity. However, it has not been fully elucidated whether the lower expression of CIITA is a cause of disease process or a just associated sign. Here we determined whether the CIITA deficiency decreased survival rate using murine sepsis model. Methods: Major histocompatibility complex class II (MHC-II) deficient, CIITA deficient and wild type B6 mice were subjected to cecal ligation puncture (CLP) surgery. CIITA and recombination activation gene (RAG)-1 double deficient mice were generated to test the role of lymphocytes in CIITA-associated sepsis progression. Results: Sepsis mortality was enhanced in CIITA deficient mice, not by impaired bacterial clearance resulted from CD4 T cell depletion, but hyper-inflammatory response such as excessive release of a pro-inflammatory cytokine, high-mobility group box 1 (HMGB1). Conclusion: Our results demonstrate that CIITA deficiency affects the course of sepsis via the unexpected function of CIITA, regulation of cytokine release.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.129-136
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• 1992

As it has been reported that the depolarization-induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus and various lines of evidence indicate the involvement of adenylate cyclase system in $A_1-adenosine$ post-receptor mechanism in hippocampus, it was attempted to delineate the role of adenylate cyclase system in the $A_1-receptor-mediated$ control of ACh release in this study. Slices from rat hippocampus were incubated with $[^3H]-choline$ and the release of the labelled products was evoked by electrical stimulation $(3\;Hz,\;5\;Vcm^{-1},\;2\;ms,\;rectangular\;pulses)$, and the influence of various agents on the evoked tritium-outflow was investigated. $N^6-cyclopentyladenosine$ (CPA), a specific $A_1-adenosine$ receptor agonist, in concentrations ranging from 0.1 to $10\;{\mu}M$, decreased the $[^3H]-ACh$ release in a dose-dependent manner without the changes of basal rate of release. 8-cyclopentyl-1,3-dipropylxanthine $(DPCPX,\;1{\sim}10\;{\mu}M)$, a selective $A_1-receptor$ antagonist, increased the $[^3H]-ACh$ release in a dose-related fashion with slight increase of basal tritium-release. And the CPA effects were significantly inhibited by DPCPX $(2\;{\mu}M)$ pretreatment and the dose-response curve produced by CPA was shifted to the right. The responses to N-ethylmaleimide $(NEM,\;10\;&\;30\;{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the CPA effect were completely abolished by NEM pretreatment. Forskolin, a specific adenylate cyclase activator, in concentrations ranging from 0.3 to $10\;{\mu}M$, increased the evoked ACh-release in a dose-dependent manner and the CPA effects were inhibited by forskolin. These results indicate that the $A_1-adenosine$ heteroreceptor plays an important role in ACh-release via nucleotide-binding protein Gi in the rat hippocampus and that the adenylate cyclase system might be participated in this process.

• The Korea Journal of Herbology
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• v.22 no.1
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• pp.35-40
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• 2007

Objectives : This in vitro research was conducted to investigate the effect of the Ginseng Radix plus Crataegi Fructus. on the cytokine protein release and Nitric oxide release in releted to Alzheimer's disease. Methods : Specifically, the effects of the Ginseng Radix plus Crataegi Fructus extract on $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ of BV2 microglia cell line treated with lipopolysacchride. Results: The Ginseng Radix plus Crataegi Fructus extract suppressed the production of inflammatory cytokine protein $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ and in BV2 microglia cell line treated with lipopolysacchride. Conclusion: These results suggest that the Ginseng Radix plus Crataegi Fructus extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the Gin-CHF extract for Alzheimer's disease is suggested for future research.

• Textile Coloration and Finishing
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• v.24 no.1
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• pp.27-32
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• 2012

Generally, hair treatments by complementary actions to give a sense of activity are permanent setting, dyeing, and bleaching, etc. In this study, we investigated the wave formation ability and hair damage occuring in permanent setting and bleaching process. The wave formation ability was evaluated by the differences of length and curl diameter after permanent setting. And the hair damage was also evaluated by the protein release ability and SEM of hair. The bleached hair immediately after permanent setting treatment has better wave formation ability, but much more damaged than the bleached hair after rinsing thoroughly with warm water. It was considered that the chain of hair keratin broke down easily by the bleaching action in the existence of permanent setting agents.

• Macromolecular Research
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• v.17 no.7
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• pp.464-468
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• 2009

Gelatin nanoparticles derived from bovine or porcine have been developed as various types of drug delivery system, and they need to be cross-linked to maintain their physicochemical properties in aqueous environments. Although gelatin is a widely used material in pharmaceutical industries, the safety issue of animal-origin gelatins, such as transmissible mad cow disease and anaphylaxis, remains to be solved. The purpose of this study was to prepare type A gelatin (GA) nanoparticles by modified, two-step, desolvation method and compare the toxicity of the resulting GA nanoparticles with recombinant human gelatin (rHG) nanoparticles. The GA nanoparticles were characterized, and drug loading and release pattern were measured. FITC-BSA, a model protein, was efficiently loaded in the nanoparticles and then released in a biphasic and sustained release pattern without an initial burst. In particular, the cell viability of the GA nanoparticles was less than that of the rHG nanoparticles. This finding suggests that rHG nanoparticles should be considered as an alternative to animal-origin gelatin nanoparticles in order to minimize the safety problems.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.316.2-316.2
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• 2002

Manassantin B classified into dineolignans have been isolated from Saururus chinensis Manassantin B was found to induce apoptosis in human promyelocytic leukaemia HL -60 cells with characteristic apoptotic features like increase of nucleosomalladder. apoptotic body ormation. flipping of membrane phosphatidylserine. Manassantin B induced FAS and FAS ligand expression, and activated caspase 8 which cleaved bid to tbid in cytosol. The release of cytochrome c to sytosol was accompanied with decrease of bcl-2 protein and incresase of tbid and bax protein in mitochondria. Released xytochrome c activated caspase 9 and-3. but these effects were completely attenuated by the treatment of broad caspses ingibitor. Z-VAD fmk. These results indicate that manassatin B induce apoptosis through upregulation of FAS. caspase family and mitochondria-related proteins.

• Journal of Integrative Natural Science
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• v.11 no.1
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• pp.9-13
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• 2018

KiSS1-derived peptide receptor, a GPCR protein, binds with the hormone Kisspeptin plays a major role in the neuroendocrine regulation of reproduction. It is important in the onset of puberty and triggers the release of gonadotrophin-releasing hormone. It is a potential drug target for the disorders related to GnRH, hence, analysing the structural features of the receptor becomes important. The three dimensional of the receptor modelled in a previous study was utilised. In this study, we have analysed the protein - protein interaction of the receptor with Kisspeptin 10 and 15. The study revealed the important residues which are involved in the interaction. The result of this study could be helpful in understanding the mechanism of Kiss1 receptor activation and the pathophysiology of the disorders related to the receptor.

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.150.2-151
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• 2000

• Journal of Microbiology
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• v.44 no.1
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• pp.11-22
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• 2006

Escherichia coli protein Rho is required for the factor-dependent transcription termination by an RNA polymerase and is essential for the viability of the cell. It is a homohexameric protein that recognizes and binds preferably to C-rich sites in the transcribed RNA. Once bound to RNA, it utilizes RNA-dependent ATPase activity and subsequently ATPase-dependent helicase activity to unwind RNA-DNA hybrids and release RNA from a transcribing elongation complex. Studies over the past few decades have highlighted Rho as a molecule and have revealed much of its mechanistic properties. The recently solved crystal structure could explain many of its physiological functions in terms of its structure. Despite all these efforts, many of the fundamental questions pertaining to Rho recognition sites, differential ATPase activity in response to different RNAs, translocation of Rho along the nascent transcript, interactions with elongation complex and finally unwinding and release of RNA remain obscure. In the present review we have attempted to summarize 'the knowns' and 'the unknowns' of the Rho protein revealed by the recent developments in this field. An attempt has also been made to understand the physiology of Rho in the light of its phylogeny.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.6
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• pp.319-325
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• 2002

The induction of interleukin-6 (IL-6) using combined proinflammatory agents $(LPS/IFN-{\gamma}\;or\;TNF-{\alpha}/IFN-{\gamma})$ was studied in relation to p38 mitogen-activated protein kinase (MAPK) and $NF-{\kappa}B$ transcriptional factor in primary neonatal cardiomyocytes. When added to cultures of cardiomyocytes, the combined agents $(LPS/IFN-[\gamma}\;or\;TNF-{\alpha}/IFN-{\gamma})$ had stimulatory effect on the production of IL-6 and the elevation was significantly reduced by SB203580, a specific p38 MAPK inhibitor. SB203580 inhibited protein production and gene expression of IL-6 in a concentration-dependent manner. In this study, $IFN-{\gamma}$ enhancement of $TNF-{\alpha}-induced\;NF-{\kappa}B$ binding affinity as well as p38 MAP kinase activation was observed. However, a specific inhibitor of p38 MAPK, SB203580, had no effect on $TNF-{\alpha}/IFN-{\gamma}\;or\;LPS/IFN-{\gamma}-induced\;NF-{\kappa}B$ activation. This study strongly suggests that these pathways about $TNF-{\alpha}/IFN-{\gamma}$ or $LPS/IFN-{\gamma}-activated$ IL-6 release can be primarily dissociated in primary neonatal cardiomyocytes.