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In this study, the composition of traditional Korean Dancheong pigments existing in national-designated wooden architectural heritages was analyzed, and the current status of pigments according to the raw material characteristics used was statistically examined. As for the red pigment, Seokganju, Yeondan, Jusa had a high share, and natural and artificial inorganic pigments had a high usage rate. As for yellow pigments, organic pigments(estimated Deunghwang), Hhwangto, and gold showed a high share. In the case of organic pigments and gold, Yeonbaek was used as a based pigment to increase color development. As for the green pigment, Hayeob, Noerok, Samrok showed a high share. The Hayeob and Neorok are identified as a single raw material, but it can be seen that the Samrok is made by mixing copper oxides such as moolooite and lead-based white raw materials. Blue pigments have a lower share of pigments compared to other colors. As for the blue pigment, Guncheong, Hoecheong, and Seokcheong showed a high market share, and natural and artificial inorganic pigments accounted for the majority. In particular, it is characteristic that the use of expensive pigments such as Seokcheong and Guncheong is concentrated on the Palace Dancheong. White and black pigments have a low share in Dancheong coloring, but the white and black lines play a very important role in the perfection of Dancheong. It can be seen that the white pigment has a high share of Baekto(white clay) and Yeonbaek, and is used not only for coloring but also as a based pigment for color pigments. Most of the black pigment is made up of more than 95% organic raw material containing carbon as its main component, and it shows various aspects depending on the lower pigment layer. Through this, it was confirmed based on on-site analysis data of wooden architectural heritage that the color pigment used in Dancheong had a higher percentage of use of inorganic pigments and that the use rate of natural inorganic pigments was higher than that of artificial synthetic pigments in inorganic pigments.

Myeloid subclusters

Cytotoxic T cell (CTL) subclusters

Endothelial subclusters

Major cell lineages in the single-cell atlas

PC subclusters

Clinicopathological information of five patients with diffuse-type gastric cancer.

Functional enrichment analysis of fibroblast subclusters

T cell subclusters

Purpose:Histologic features of diffuse-type gastric cancer indicate that the tumor microenvironment (TME) may substantially impact tumor invasiveness. However, cellular components and molecular features associated with cancer invasiveness in the TME of diffuse-type gastric cancers are poorly understood.Experimental Design:We performed single-cell RNA-sequencing (scRNA-seq) using tissue samples from superficial and deep invasive layers of cancerous and paired normal tissues freshly harvested from five patients with diffuse-type gastric cancer. The scRNA-seq results were validated by immunohistochemistry (IHC) and duplex in situ hybridization (ISH) in formalin-fixed paraffin-embedded tissues.Results:Seven major cell types were identified. Fibroblasts, endothelial cells, and myeloid cells were categorized as being enriched in the deep layers. Cell type–specific clustering further revealed that the superficial-to-deep layer transition is associated with enrichment in inflammatory endothelial cells and fibroblasts with upregulated CCL2 transcripts. IHC and duplex ISH revealed the distribution of the major cell types and CCL2-expressing endothelial cells and fibroblasts, indicating tumor invasion. Elevation of CCL2 levels along the superficial-to-deep layer axis revealed the immunosuppressive immune cell subtypes that may contribute to tumor cell aggressiveness in the deep invasive layers of diffuse-type gastric cancer. The analyses of public datasets revealed the high-level coexpression of stromal cell–specific genes and that CCL2 correlated with poor survival outcomes in patients with gastric cancer.Conclusions:This study reveals the spatial reprogramming of the TME that may underlie invasive tumor potential in diffuse-type gastric cancer. This TME profiling across tumor layers suggests new targets, such as CCL2, that can modify the TME to inhibit tumor progression in diffuse-type gastric cancer.See related commentary by Huang and Brekken, p. 6284

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Purpose: Histologic features of diffuse-type gastric cancer indicate that the tumor microenvironment (TME) may substantially impact tumor invasiveness. However, cellular components and molecular features associated with cancer invasiveness in the TME of diffuse-type gastric cancers are poorly understood. Experimental Design: We performed single-cell RNA-sequencing (scRNA-seq) using tissue samples from superficial and deep invasive layers of cancerous and paired normal tissues freshly harvested from five patients with diffuse-type gastric cancer. The scRNA-seq results were validated by immunohistochemistry (IHC) and duplex in situ hybridization (ISH) in formalin-fixed paraffin-embedded tissues. Results: Seven major cell types were identified. Fibroblasts, endothelial cells, and myeloid cells were categorized as being enriched in the deep layers. Cell type–specific clustering further revealed that the superficial-to-deep layer transition is associated with enrichment in inflammatory endothelial cells and fibroblasts with upregulated CCL2 transcripts. IHC and duplex ISH revealed the distribution of the major cell types and CCL2-expressing endothelial cells and fibroblasts, indicating tumor invasion. Elevation of CCL2 levels along the superficial-to-deep layer axis revealed the immunosuppressive immune cell subtypes that may contribute to tumor cell aggressiveness in the deep invasive layers of diffuse-type gastric cancer. The analyses of public datasets revealed the high-level coexpression of stromal cell–specific genes and that CCL2 correlated with poor survival outcomes in patients with gastric cancer. Conclusions: This study reveals the spatial reprogramming of the TME that may underlie invasive tumor potential in diffuse-type gastric cancer. This TME profiling across tumor layers suggests new targets, such as CCL2, that can modify the TME to inhibit tumor progression in diffuse-type gastric cancer. See related commentary by Huang and Brekken, p. 6284

One paper fragment and three pigments were excavated from earthenware found in the Hoeamsa Temple site (Historic Site No. 128), which is presumed to have been constructed in the 12th century. This study identifies the types and characteristics of the paper and pigments through methods such as fiber identification, pigment component analysis, and crystal structure analysis. Using the Graff 'C' staining method, the paper fragment is identified as paper-mulberry bast fiber (B. kazinoki Siebold), and according to radiocarbon dating results, the paper is believed to be from the Joseon Dynasty, between 1460 and 1640, which is when the Hoeamsa temple was believed to have been rebuilt. The green pigment consists of cerussite, malachite, and ataccamite, while quartz, muscovite, and illite were detected in the white pigment, and quartz, hematite, illite, and kaolinite were detected in the red pigment. The L* value ranged from 41.59 to 79.05. The white pigment showed the highest brightness value at 79.05, while the green pigment was measured at 58.20 and the red pigment at 41.59. The a* value ranged from -2.25 to 22.75: the a* value of the red pigment was the highest at 22.75, the green pigment was the lowest at -2.25. The b* value ranged from 7.44 to 26.26: the b*value of the red pigment was the highest at 26.26 and the white pigment was the lowest at 7.44.These scientific data identified the raw materials of paper used during the Joseon Dynasty. In addition, the data can be used for repair and restoration of ancient dancheong (traditional Korean decorative coloring on wooden buildings and artifacts) by analyzing the composition of pigments and identifying the characteristics of crystal structure.

Mutation signatures represent unique sequence footprints of somatic mutations resulting from specific DNA mutagenic and repair processes; however, their causal associations and potential utility for genome research remain largely unknown. In this study, we performed PanCancer-scale correlative analyses to identify the genomic features associated with tumor mutation burdens (TMB) and individual mutation signatures. We observed that TMB was correlated with tumor purity, ploidy, and the level of aneuploidy, as well as with the expression of cell proliferation-related genes representing genomic covariates in evaluating TMB. Correlative analyses of mutation signature levels with genes belonging to DNA damage-repair processes revealed that deficiencies of NHEJ1 and ALKBH3 may elevate TMB levels in cancer genomes accompanying APOBEC overactivity and DNA mismatch repair deficiency, respectively. We further employed a strategy to identify feature-driven, de novo mutation signatures and demonstrated they can be reconstructed using known causal features such as APOBEC overexpression, MLH1 underexpression, POLE mutations, and the level of homologous recombination deficiency. We further demonstrated, that tumor hypoxia-related mutation signatures are similar to those associated with APOBEC suggesting that APOBEC-related mutagenic activity mediates hypoxia-related mutational consequences in cancer genomes, and also, that mutation signatures can be further used to predict hypoxic tumors. Taken together, our study advances mutation signature-level mechanistic insights in cancer genomes, extending categories of cancer-relevant mutation signatures and their potential biological implications.Author summaryMutation signature analysis is powerful in deciphering the causative mutagenic events and their contributions in individual cancer genomes, but the causal relationship of individual mutation signatures are still largely unknown. PanCancer-scaled correlative analysis revealed mutation resource candidates in cancer genomes such as NHEJ1 and ALKBH3 deficiencies that may facilitate the accumulation of mutations in the setting of APOBEC overactivity and DNA mismatch repair deficiency, respectively. A feature-driven mutation discovery approach was employed to identify the mutation signatures representing homologous recombination deficiency and tumor hypoxia, the extent of which may serve as mutation-based phenotypic measures, previously estimated by DNA copy number alterations and mRNA expression signatures, respectively. Our study advances our understanding into the mechanistic insights of mutation signatures and proposes a method to utilize somatic mutations as a molecular proxy in terms of mutation signatures.

Retroviral vectors show long-term gene expression in gene therapy through the integration of transgenes into the human cell genome. Murine leukemia virus (MLV), a well-studied gammaretrovirus, has been often used as a representative retroviral vector. However, frequent integrations of MLV-based vectors into transcriptional start sites (TSSs) could lead to the activation of oncogenes by enhancer effects of the genetic components within the vectors. Therefore, the MLV integration preference for TSSs limits its wider use in clinical applications. To reduce the integration preference of MLV-based vectors, we attempted to perturb the structure of the viral integrase that plays a key role in determining integration sites. For this goal, we inserted histones and leucine zippers, having DNA-binding property, into internal sites of MLV integrase. This integrase engineering yielded multiple mutant vectors that showed significantly different integration patterns compared with that of wild-type vector. Some mutant vectors did not prefer the key regulatory genomic domains of human cells, TSSs. Moreover, a couple of engineered vectors did not integrate into the genomic sites near the TSSs of oncogenes. Overall, this study suggests that structural perturbation of integrase is a simple way to develop safer MLV-based retroviral vectors for use in clinical applications.

This study were conducted the particle-size analysis on 57 blue pigments to understand the step distribution characteristics of blue pigments made out of Azurite by using Malvern's Mastersizer 2000. As the result, most of the conventional blue pigments in Korea, Japan, and Chinese showed good granularity step separation except for few, and the smaller the particle, the more the Span value increased and the wider the granularity distribution range. On the basis of Friedman and Sanders's Grain size, most of the pigments were sand size to silt size. 72.2% of B-100 was clay size and 2.5% of A-14 was gravel size. Even the same components can differ by the grain size directly affecting the important property such as color formation, oil absorption, specific gravity, usability, etc. so the information about the granularity distribution would be used for basic data to deal with natural pigments.

문화재 복원을 비롯한 회화용으로 많이 사용되는 녹색 안료 중 천연 무기안료인 석록과 뇌록의 물리적 특성규명을 위하여 본 연구를 수행하였다. 석록은 Malachite가 주 구성광물이고, 뇌록은 Celadonite가 주 구성광물이다. 본 연구를 위하여 K社의 A등급 석록, B등급 석록, 소성석록의 물리적 특성을 평가하였으며, 이와 비교하기 위하여J社의 송엽녹청, 소녹청을 평가하였다. 뇌록은 K社의 뇌록을 평가하였다. 석록 및 송엽녹청의 소성 여부는 색도를 제외한 다른 물리적 특성에 큰 영향을 미치지 않는 것으로 판단되며, K社의 석록과 소성석록과의 색차가 J社의 송엽녹청과소녹청의 색차보다 훨씬 높았다. K社는 녹색도 +a*가 J社보다 가로로 넓게 분포하여 녹색의 다양한 색표현이 가능하다. 뇌록은 색도, 비중, 흡유량 등의 물리적 특성이 석록과는 많은 차이를 보였다. 뇌록의 색도는 a*가 0에 가까이 분포하여석록에 비하여 무채색에 더 가까웠고, 비중은 석록에 비해 작고, 흡유량은 2배 정도 컸다. 또한 뇌록과 암녹은 비록 구성물질에 차이가 있어도 물리적 특성이 비슷하여 대체하여 사용 가능 할 것으로 보인다. 본 연구결과를 통하여 천연안료의물리적 특성을 규명하여 품질기준을 확립하고, 문화재 보존, 복원의 선택적 사용에 대한 기초적인 자료로 활용되길기대한다.

This study was conducted to investigate the effect of the strengthening treatment of methyl cellulose (MC) on properties and aging characteristics of the dewaxed papers during humid heating aging. Beeswax-treated Hanji was dewaxed by the supercritical fluid extraction method, and subsequently the strengthening treatment was performed with MCs having three different viscosities. MC was first applied by dipping a dewaxed paper into a MC solution whose concentration was controlled from 0.5% to 1.5%. After the strengthened papers were artificially aged at 80℃ and 65% RH, the changes in optical and mechanical properties of the samples were evaluated. The results show that viscosity and especially pick-up of MC influenced the strengthening efficiency and aging characteristics of de-waxed paper. Strength was increased with the MC coating weight; in addition, strength-ening with MC improved preservability of the dewaxed paper. The optimum conditions for the strengthening with MC was found to be the coating ratio of 4% with 1500 cP MC.Keywords: Methyl cellulose, viscosity, coating weight, strengthening, dewaxed paper, aging characteristics

Di-(2-ethylhexyl)-phthalate (DEHP), the most widely utilized industrial plastizer and a ubiquitous environmental contaminant, can act on peroxisome proliferators-activated nuclear hormone receptor family (PPAR) isoforms. To understand the contribution of sphingolipid metabolism to DEHP-induced hepatotoxicity, effect of DEHP exposure on activities of sphingolipid metabolic enzymes in rat liver was investigated. DEHP (250, 500 or 750 mg/kg) was administered to the rats through oral gavage daily for 28 days. The activities of acidic and alkaline ceramidases were slightly increased in 250 mg/kg DEHP-administered rat livers and significantly elevated in 500 mg/kg DEHP-administered ones, although the level of 750 mg/kg DEHP-administered ones was not increased. Neutral ceramidase, acidic and neutral sphingomyelinases, sphingomyeline synthase and ceramide syhthase were not changed at all by DEHP exposure. Therefore, acidic and alkaline ceramidases might play important roles in DEHP-induced hepatotoxicity.

The objective of the present study was to examine the role of selenium in the metabolism of Aβ and in Aβ-induced neuronal death. Selenium treatment significantly reduced Aβ40, Aβ42, and sAPPβ production by reducing Aβ producing β-secretase and γ-secretase activities. The lipid peroxidation product 4-Hydroxynonenal (HNE)-induced transcription of β-secretase (BACE1) was blocked by selenium. Finally, our data show that selenium protects against HNE and Aβ-mediated toxicity in primary cultured neurons. The present study suggests that selenium may be able to salvage the neuronal degeneration of Alzheimer's disease, thereby limiting β-amyloid production and neuronal death.

B7-H1 (also known as CD274 and PD-L1) is a cosignalling molecule regulating T-cell immunity positively or negatively in vivo. However, little is known about the role of endogenous B7-H1 in bacterial infection. We found that B7-H1 expression was up-regulated in various cell populations including CD4+ and CD8+ T cells, natural killer (NK) cells and macrophages following Listeria monocytogenes infection. Administration of the antagonistic B7-H1 monoclonal antibody resulted in a significant increase in mortality in mice infected with a lethal dose of L. monocytogenes compared with mice given the control immunoglobulin. In vivo blockade of B7-H1 greatly inhibited the production of tumour necrosis factor (TNF)-alpha and nitric oxide, key effector molecules responsible for intracellular killing by macrophages. B7-H1 blockade also suppressed the expression of granzyme B and interferon (IFN)-gamma by NK cells. Interestingly, blocking of endogenous B7-H1 selectively inhibited CD8+ T cells rather than CD4+ T cells in response to L. monocytogenes infection, as evidenced by the reduction of IFN-gamma production and the expression of effector surface markers including CD62L(int/low) and CD44(high) in CD8+ T cells from mice given anti-B7-H1 monoclonal antibody. In addition, we found that the proliferation of listeriolysin-O (LLO)-specific and IFN-gamma-producing L. monocytogenes-reactive CD8+ T cells was significantly decreased not only in the effector phase but also in the memory phase in the presence of anti-B7-H1 antibody. Our findings thus suggest that endogenous B7-H1 can provide positive costimulatory signals for innate and adaptive immunity leading to protection against intracellular bacterial infection.

The co-signaling molecule B7-H1 (CD274) functions as both a co-inhibitor through programmed death-1 (PD-1) receptor and a co-stimulator via an as-yet-unidentified receptor on T cells. We investigated the physiological role of endogenous B7-H1 in the pathogenesis of herpetic stromal keratitis (HSK) caused by herpes simplex virus type 1 (HSV-1). Following HSV-1 infection of the cornea of mice, B7-H1 expression was up-regulated in the CD11b+ macrophage population in the draining lymph nodes (dLN) and in the inflamed cornea. In addition, HSV-1 infection significantly increased PD-1 expression on CD4+ T cells in the dLN and inflamed cornea. The administration of antagonistic B7-H1 monoclonal antibody resulted in the proliferation of HSV-specific CD4+ T cells that secreted interferon (INF)-γ, and inhibited the apoptosis of HSV-specific CD4+ T cells, which exaggerated HSK. These results strongly suggest that the B7-H1 may be involved in suppression of the development of HSK.

To investigate a potential molecular basis for a link between diabetes and atherosclerosis, experiments were performed to determine the role of NAD(P)H oxidase in the enhanced proliferative capacity of vascular smooth muscle cells (VSMC) from OLETF rat, an animal model of type 2 diabetes. An enhanced proliferative response to 10% fetal bovine serum with an increased cell cycle progression from G 1 to S phase as well as an augmented superoxide generation with an increased NAD(P)H oxidase activity were observed in diabetic versus control VSMC. Both the enhanced proliferation and superoxide generation in diabetic VSMC were significantly attenuated not only by diphenyleneiodonium (10 μM) and apocynin (100 μM), NAD(P)H oxidase inhibitors but also by protein tyrosine kinase inhibitors such as genistein (100 μM) and AG 112 (100 μM). Furthermore, the enhanced NAD(P)H oxidase activity in diabetic VSMC was significantly attenuated by genistein and AG112, but not by daidzein (100 μM), a genistein analogue devoid of protein tyrosine kinase inhibitory properties. Based on these results, it is suggested that the enhanced proliferative capacity of diabetic VSMC is closely related to the activation of NAD(P)H oxidase that is induced through activation of protein tyrosine kinase.

Chronic alcohol consumption contributes to numerous diseases, including cancers, cardiovascular diseases, and liver cirrhosis. Epidemiological studies have shown that excessive alcohol consumption is a risk factor for dementia. Along this line, Alzheimer's disease (AD) is the most common form of dementia and is caused by the accumulation of amyloid-β (Aβ plaques in neurons. In this study, we hypothesized that chronic ethanol consumption is associated with pathological processing of APP in AD. To investigate the relationship between chronic alcohol consumption and Aβ production, brain samples from rats fed an alcohol liquid diet for 5 weeks were analyzed. We show that the expression levels of APP, BACE1, and immature nicastrin were increased in the cerebellum, hippocampus, and striatum of the alcohol-fed group compared to the control group. Total nicastrin and PS1 levels were induced in the hippocampus of alcohol-fed rats. These data suggest that the altered expression of APP and Aβ-producing enzymes possibly contributes to the chronic alcohol consumption-mediated pathogenesis of AD.

The objective of the present study was to examine the role of selenium in the metabolism of A beta and in A beta-induced neuronal death. Selenium treatment significantly reduced A beta 40, A beta 42, and sAPP beta production by reducing A beta producing beta-secretase and gamma-secretase activities. The lipid peroxidation product 4-Hydroxynonenal (HNE)-induced transcription of beta-secretase (BACE1) was blocked by selenium. Finally, our data show that selenium protects against HNE and A beta-mediated toxicity in primary cultured neurons. The present study suggests that selenium may be able to salvage the neuronal degeneration of Alzheimer's disease, thereby limiting beta-amyloid production and neuronal death.

Presenilins are the catalytic subunit of the large gamma-secretase complex, that promotes intramembranous proteolysis of the beta-amyloid precursor protein (APP), resulting in the production of beta-amyloid (A beta). Mutant presenilin causes early-onset familial Alzheimer's disease (FAD), is related to abnormal Ca(2+) signaling, and render cells vulnerable to cell death. In the present study, we demonstrated that Ca(2+)-mediated cell death is functionally associated with gamma-secretase activity. We found that gamma-secretase activity was elevated during Ca(2+)-mediated cell death. Using selective gamma-secretase inhibitors, we examined the role of gamma-secretase in cell death triggered by increased intracellular Ca(2+). Indeed, treatment with the selective gamma-secretase inhibitors, compound E, DAPT, or L-685.458 significantly decreased Ca(2+)-triggered cell death with that of the controls, but did not affect staurosporin or tunicamycin-mediated cell death. These results implicate the role of gamma-secretase activity in Ca(2+)-mediated cell death.

The establishment of a chronic hepatitis C (CHC) infection is associated with defective HCV-specific T cell responses. Recent studies suggest that negative T cell regulators such as programmed death 1 (PD-1) contribute to the impairment of virus-specific T cell functions in chronic viral infections. However, the implication of peripheral monocytes from CHC patients in the inhibition of HCV-specific T cell responses is only partially defined. In this study, we found that B7-H1, a ligand of PD-1, was significantly up-regulated on monocytes of CHC patients. Proliferation of T cells in response to anti-CD3 antibody was directly suppressed by B7-H1+CD14+ monocytes, and this suppression was reversed by addition of antagonistic B7-H1 mAb. Furthermore, blocking of monocyte-associated B7-H1 (moB7-H1) significantly enhanced the frequency of IFN-γ-producing, HCV-specific CD4+ and CD8+ effector T cells and the production of Th1 cytokines, such as IL-2 but not Th2 cytokines, including IL-4 and IL-10. Upon B7-H1 blockade, production of perforin was also increased in CD8+ T cells stimulated with HCV peptides. Our findings suggest that moB7-H1 inhibits HCV-specific CD4+ and CD8+ T lymphocyte proliferation and suppresses Th1 cytokine production and perforin secretion. Blockade of the B7-H1 pathway thus represents an attractive approach in the treatment of chronic HCV infection.

To correlate clinical outcomes with the expression of interleukin-2 receptor alpha (CD25) positive cells during induction chemotherapy (IC) in adult patients with acute myeloid leukaemia (AML), we investigated the prognostic importance of subsets of peripheral blood (PB) CD45+CD25+ cells. Seventy-five patients with newly diagnosed AML received the same initial IC; and serial PB samples were taken. The gated CD45/CD25 cell populations were used to compare the intensity of immunophenotypic signals based on the treatment timeline. Patients who responded poorly to IC demonstrated exceptionally higher levels of PB CD45+CD25+ cells by percentage (p = 0.003) or by absolute count (p = 0.046) on the seventh day (D + 7) of initial IC. In addition, patients in complete remission (CR) (n = 61) demonstrated relatively lower levels of steady PB CD45+CD25+ after standard IC. These results suggest that the expression of CD25 can be used to predict the response to IC during an early period of treatment. Copyright © 2007 John Wiley & Sons, Ltd.

To investigate the mechanisms that contribute to the acceleration of atherosclerosis in diabetes, the role of NAD(P)H oxidase in the enhanced proliferative capacity of diabetic vascular smooth muscle cells (VSMC) was studied. VSMC from streptozotocin (STZ)-induced diabetic rat aorta had increased proliferative capacity and generated higher levels of superoxide in comparison with cells from control rats. Both the enhanced proliferation and superoxide generation in diabetic VSMC were significantly attenuated not only by tiron (1mM), a superoxide scavenger but also by diphenyleneiodonium (DPI; 10microM), an NAD(P)H oxidase inhibitor. Both the activity of NAD(P)H oxidase and p22phox expression were significantly increased in diabetic VSMC. Furthermore, inhibition of p22phox expression by transfection of antisense p22phox oligonucleotides into diabetic VSMC resulted in a decrease in superoxide generation, which was accompanied by a significant attenuation of cell proliferation. Based on these results, it is suggested that diabetes-associated increase in NAD(P)H oxidase activity via enhanced expression of p22phox contributes to augmented VSMC proliferation in diabetic rats.

Hemiplegia cruciata (HC) manifests as paralysis of the ipsilateral arm and contralateral leg. Herein, we report a 64-year-old man with weakness of the right leg and of the left arm after multiple sclerosis (MS). His brain and spine magnetic resonance imaging show a lower medulla lesion, which is extended to posterior part of C1 spine through cervicomedullary junction. HC usually results from stroke or trauma, but it is rare as presenting symptom of MS. (Korean J Clin Neurophysiol 2014;16:39-41)

The Annals of Joseon Dynasty, which recorded governmental affairs for 472 years (AD 1392-1863) dur-ing the Joseon dynasty is an representative paper cultural heritage in Korea. Being recognised their au-thenticity and values they were designated as the No 151 national treasure of Korea in 1973 and registered as 'The Memories of the World' by UNESCO in 1997. Unusually, some volumes of the Annals were treated by beeswax for the permanent preservation. However, the examinations on the deterioration of the beeswax-treated volumes had been exposed the serious damage than the untreated volumes. In particular, the larger amount of beeswax were worst in deterioration condition.In order to solve these problems, NRICH(National Research Institute of Cultural Heritage) of Korea launched the investigation study for the conservation of beeswax-treated volumes of the Annals. Now then, the five study areas have been set up; 1) to understand the damaged condition of the Annals; 2) to analyse the raw materials and produc tion techniques; 3) to test the degradation degree using the duplica-tion samples for understanding the aging factors and mechanism; 4) to develop the conservation techni-ques through dewaxing and thereafter strengthening the base paper of Hanji; 5) to develop the long-term storage technique using inert gases. On the basis of outcomes from this study, NRICH will plan to estab-lish the systematic conservation and management plan for the beeswax-treated volumes of the Annals in future.

In this study, to understand the aging factor and mechanism in different partitions of the beeswax-treated volumes, the duplicated beeswax-treated volume was artificially aged at 80 of temperature and 65% of relative humidity and then a physical and optical properties of an aged volumes was analyzed. Also, the degraded components of the beeswax samples isolated from different partitions of aged volumes was measured using a gas chromatography / mass spectroscopy (GC/MS). In results, the surface of beeswax-treated volume which is primarily affected by a main aging factors such as light, oxygen, moisture was more deteriorated than the inside of that volume. However, unlike inside of the book volume which was made from paper, the inside of beeswax-treated volume wax was also considerably deteriorated. The inside of the beeswax-treated volume is largely unaffected by the oxygen and humidity during aging due to the water repellency and the air permeation resistance of beeswax. Therefore, it is confirmed that aging factors and mechanisms in the inside of the volume are different from thats of the outside of the volume. This fact was also verified by the results of GC/MS analysis of an beeswax samples which was sampled from different partitions of aged volumes. As result as GC/MS analysis of the beeswax extracted from the outside of the aged volume, the low molecular compounds with a carbon length of C9-C20 (fatty acid, etc) were increased and the compounds with a carbon length of above C34 (ester, etc) were also increased.

Background: The prevalent natural killer (NK) cells induce alloreaction against leukemic cells during post-transplant. NK cell alloreactivity depends on the compatibility of killer cell immunoglobulin-like receptors (KIR) epitopes for graft-versus-host disease. Genotypic expressions of inhibitory or activating KIR in patients with acute myelogenous leukemia (AML) and their HLA-matched sibling donors, as a model for Korean KIR haplotype diversity and NK alloreactivity, were investigated. Methods: Ninety-two patients in complete remission and their 76 HLA-matched sibling donors were enrolled in this study. All the patients were scheduled to receive allogeneic hematopoietic stem cell transplantations (HSCT). KIR PCR-SSP typing was performed for 19 different kinds of KIR genes and pseudogenes. The PCR data representing the KIR genotypes from both the patients and donors were compared. Results: We found 43 Korean KIR haplotypes. Thirty-three variable haplotypes for the AML patients, in addition to 25 haplotypes for the normal HSCT donors, were demonstrated. Of note, the expressions of specific genes such as 2DL2 (P=0.026), 2DS2 (P=0.042), and 2DS4 (P=0.037) revealed remarkable differences between the patients and the normal donors. Korean HLA-identical sibling pairs showed 38% KIR matches in terms of the gene content and allelic polymorphism. Although the KIR gene content was the same between the patients and the donors, 40% of those matched pairs of patients and donors showed allelic polymorphism, specifically in the context of 2DL5 and 2DS4 genes. Conclusion: These results indicate that the expressions of donor inhibitory and activating repertoire of KIR genotypes, even in the HLA-matched sibling setting, are unique parameters to be considered when we perform allogeneic sibling HSCT.