Journal of the Korean Crystal Growth and Crystal Technology
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v.13
no.5
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pp.254-259
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2003
In the fabrication process of transparent conducting thin films of the ATO (antimony-doped tin oxide) on a soda lime glass substrate by a sol-gel dip coating method, the effects of the $SiO_2$ buffer layer formed on the substrate and $N_2$ annealing treatment were investigated by XPS (X-ray photoelectron spectroscopy) analysis. Optical transmittance and electrical resistivity of the 400 nm-thick ATO thin films which were deposited on $SiO_2$ buffer layer/soda lime glass and then annealed under nitrogen atmosphere were 84 % and $5.0\times 10^{-3}\Omega \textrm{cm}$ respectively. The XPS analysis confirmed that a $SiO_2$ buffer layer inhibited Na ion diffusion from the substrate, resulting in prohibiting the formation of a secondary phase such as $Na_2SnO_3$ and SnO and increasing Sb ion concentration and ratio of $Sb^{5+}/Sb^{3+}$ in the film. And it was also found that $N_2$ annealing treatment leads to the reduction of $Sn^{4+}$as well as $Sb^{5+}$ however the reduction of $Sn^{4+}$ is more effective and therefore consequently results in decrease in the electrical resistivity to produce an excellent electrical properties of the film.
The diffusion barrier properties of TiN by using Cu(Mg) alloy film have been investigated. Cu(Mg) alloy film was deposited on air-exposed TiN film. Upon annealing, interfacial MgO of 100 $\AA$ has been formed due to the reaction of Mg with oxygen existed on the surface of TiN. Combined MgO/TiN structure prevented the interdiffusion of Cu and Si up to $800^{\circ}C$. To improve the adhesion of Cu(Mg) alloy film to the TiN, TiN layer was treated by $O_2$ plasma, followed by vacuum annealing at $300^{\circ}C$. It was found that increased oxygen on the surface of TiN film by plasma treatment enhanced segregation of Mg toward the interface, resulting in the formation of dense MgO layer. Improved adhesion characteristics have been formed through this treatment. However, increased power of $O_2$ plasma led to the formation of TiO$_2$ and decreased the Mg content to be segregated to the interface, resulting in the decrease in adhesion property. In addition, the deposition of 50 ${\AA}$ Si on the TiN enhanced the adhesion of Cu(Mg) alloy to TiN without deteriorating the TiN diffusion barrier characteristics.
This study aimed to explore the potential for food-industry application of atmospheric pressure dielectric barrier discharge plasma (atmospheric pressure DBD plasma) as a non-thermal sterilization technology for microorganism. The effects of the key parameters such as power, oxygen ratio, exposure time and distance on Escherichia coli KCCM 21052 sterilization by the atmospheric pressure DBD plasma treatment were investigated. The experimental results revealed that increasing the power, exposure time or oxygen ratio and decreasing the exposure distance led to an improvement in the sterilization efficiency of E. coli. Furthermore, the atmospheric pressure DBD plasma (1.0 kW power, 1.0% (v/v) $O_2$, 5 min exposure time and 20 mm exposure distance) treatment was very effective for the sterilization of food-borne pathogenic bacteria. The sterilization rate of E. coli, Bacillus cereus KCCM 40935, Bacillus subtilis KCCM 12027, Bacillus thuringiensis KCCM 11429 and Bacillus atrophaeus KCCM 11314 were 72.3%, 74.6%, 88.5%, 84.7% and 91.3%, respectively.
Our previous report determined that miR-144 is a key regulator of intestinal epithelial permeability in irritable bowel syndrome with diarrhea (IBS-D) rats. Recent evidence has shown that lactobacilli play an important role in the relief of IBS-D symptoms. However, few studies have addressed the mechanisms by which microRNAs and lactobacilli exert their beneficial effects on intestinal epithelial permeability. Hence, to elucidate whether miRNAs and lactobacilli play roles in intestinal epithelial barrier regulation, we compared miRNA expression levels in intestinal epithelial cells (IECs) under Lactobacillus casei (L. casei LC01) treatment. IECs and L. casei LC01 were co-cultured and then subjected to microRNA microarray assay. qRT-PCR, western blot and ELISA were used to detect the expression of occludin (OCLN) and zonula occludens 1 (ZO1/TJP1). The interaction between miRNAs and L. casei LC01 acting in IECs was investigated through transfection of RNA oligoribonucleotides and pcDNA 3.1 plasmid. The results are as follows: 1) L. casei LC01 decreased the expression of miR-144 and FD4 and promoted OCLN and ZO1 expression in IECs; 2) L. casei LC01 enhanced the barrier function of IECs via downregulation of miR-144 and upregulation of OCLN and ZO1; 3) Under L. casei LC01 treatment, OCLN and ZO1 overexpression could partially eliminate the promoting effect of miR-144 on intestinal permeability in IECs. Our results demonstrate that L. casei LC01 regulates intestinal permeability of IECs through miR-144 targeting of OCLN and ZO1. L. casei LC01 can be a possible therapeutic target for managing dysfunction of the intestinal epithelial barrier.
In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.
To improve surface wettability, each sample was treated by atmospheric pressure plasma (APP) using dielectric barrier discharge (DBD) system. Argon and oxygen gases were used for treatment gas to modify the $TiO_2$ surface by APP with RF power range from 50 to 200 W. Water contact angle was decreased from $20^{\circ}$ to $10^{\circ}$ with argon only. However, water contact angle was decreased from $20^{\circ}$ to < $1^{\circ}$ with mixture of argon and oxygen. Water contact angle with $O_2$ plasma was lower than water contact angle with Ar plasma at the same RF power. It seems to be increasing the polar force of $TiO_2$ surface. Also, analysis result of X-ray photoelectron spectra (XPS) shows the increase of intensity of O1s shoulder peak, resulting in increasing of surface wettability by APP. Moreover, each water contact angle increased according to increase past time. However, contact angle increase with plasma treatment was lower than without plasma treatment. Additionally, the efficiency of $TiO_2$ photocatalyst was improved by plasma surface-treatment through the degradation experiment of phenol.
Objectives Hataedock is an orally administered herbal extract treatment for newborn babies that dispels toxic heat and meconium gathered by the fetus. The purpose of this study was to evaluate whether Hataedock alleviates inflammatory skin damage in AD (Atopic Dermatitis)-induced NC/Nga mice through regulating and maintaining the skin barrier and anti-inflammation effects.Methods We established an AD model in three-week-old NC/Nga mice through the repeated application of DNFB (dinitrochlorobenzene) on days 28, 35, and 42 after Hataedock treatment was orally administered. We identified changes in the skin barrier and anti-inflammation effects through the histological and immunohistochemical changes of TNF- α, NF-κB p65, iNOS, COX-2, and apoptotic bodies.Results Skin damage and angiogenesis were mitigated in the HT (Hataedock) group. Damage to the intercellular space of the stratum corneum as well as hyperplasia, edema, the infiltration of lymphocytes, and the increase of capillaries decreased in the HT group. Our results suggest that Hataedock treatment significantly down-regulated levels of TNF- α by 38% (p<0.001) and of NF-κB p65 by 70% (p<0.001). But Hataedock up-regulated apoptosis by 183% in dermatitis-induced skin.Conclusions These results suggest that Hataedock alleviates AD through diminishing the various inflammatory cytokines in skin lesions that are involved in the initial steps of AD development. It might have potential applications for the prevention and treatment of atopic dermatitis.
Kim, Nam-Hyuk;Kim, Seong-Oh;Song, Je-Seon;Son, Heung-Kyu;Choi, Byung-Jai;Lee, Jae-Ho;Choi, Hyung-Jun
Journal of the korean academy of Pediatric Dentistry
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v.37
no.1
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pp.109-116
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2010
Impaction is defined as a cessation of the eruption of a tooth caused by a clinically or radiographically detectable physical barrier in the eruption path or by an ectopic position of the tooth. The reasons for impaction of the maxillary central incisor are supernumerary tooth, odontoma, ectopic position of tooth germ, dilacerated tooth and so force. Impacted tooth cause space loss due to proximal movement of adjacent tooth, malocclusion, root resorption of adjacent tooth, cyst formation, so careful observation and early detection is important and exact treatment should be applied to prevent these results. The treatment options of impacted tooth include induction an eruption through extraction of deciduous tooth or surgical exposure, reposition of impacted tooth by surgical method or orthodontic treatment. Orthodontic traction is recommended when an eruption does not happen after removal of barrier or surgical exposure, when eruption path is too transpositioned to be corrected spontaneously so eruption does not expected. In these cases, traction of impacted maxillary central incisor was carried out using orthodontic method with closed eruption technique and it showed good clinical results so we report these cases.
Dental implant may be immediately placed in postextraction socket which has alveolar bone defect. The purpose of this study was to compare the bone regeneration and bone quality around defects adjacent to implants that were placed into extraction sockets according to EFEB, GTAM barrier and GTAM barrier with DFDB. Mandibular P2, P3 and P4 were extracted bilaterally in dogs, and buccal defects were created about 4mm in depth and 3.3mm in width. Screwed pure titanium implants, 3.8mm in diameter and 10mm in length, were placed into the extraction sockets. The experimental groups were divided into four groups : the G group was covered with a GTAM barrier on the defective area, the D+G group was filled with DFEB and covered with a GTAM barrier, the D group was filled with DFDB only and the control group was sutured without any special treatment on the defective area. The experimental animals were killed after 12 weeks and specimens were prepared for light microscopic evaluation and fluorescent dyes were administered daily for 2 weeks after implantation, and injected on the 4th and 11th week for fluorescent microscopic examination to observe new bone formation and bone remodeling. The new Bone height of the buccal defect was measured and compared with the another for bone gain and the removal torque for the implant was measured for the comparison of bone density and bone-implant osseointegration. Results obtained were as follows : 1. Experimental groups showed bone regeneration in oder from D+G, G, D group and control. D+G and G group was significantly from D group and control(P<0.01). 2. In the defective area of control the regenerated alveolar bone showed poorly developed lamellated structure and fibrous tissue intervention into the bone-implant interface but the others showed well developed lamellated structure and osseointegration. 3. All implant groups showed no significaant difference in the removal torque for implant(P>0.05) These results suggest that immediate implants placed in defective sockets were successfully osseointegrated and utilizing placed in defective sockets were successfully osseointegrated and utilizing not only the combination of GTAM and DFDB but also only the GTAM was favorable for the predictable regeneration of the defective area.
Shin, Su Bin;Jang, Seok Ju;Lee, Na Gyeong;Choi, Byung Tae;Shin, Hwa Kyoung
Journal of Life Science
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v.32
no.7
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pp.550-566
/
2022
Stroke is among the leading causes of death and long-term physical and cognitive disabilities worldwide, affecting an estimated 15 million people annually. The pathophysiological process of stroke is complicated by multiple and coordinated events. The breakdown of the blood-brain barrier (BBB) in people with stroke can significantly contribute to the development of ischemic brain injury. Therefore, BBB disruption is recognized as a hallmark of stroke; thus, it is important to develop novel therapeutic strategies that can protect against BBB dysfunction in ischemic stroke. Traditional medicines are composed of natural products, which represent a promising source of new ingredients for the development of conventional medicines. Indeed, several studies have shown the effectiveness of Korean medicine on stroke, highlighting the value of Korean medicinal treatment for ischemic stroke. This review summarizes the current information and underlying mechanisms regarding the ameliorating effects of the formula, decoction, herbs, and active components of traditional Korean medicine on cerebral ischemia-induced BBB disruption. These traditional medicines were shown to have protective effects on the BBB in many cellular and animal ischemia models of stroke, and experiments in various animal species, such as mice and rats. In addition, they showed brain-protective effects by protecting the BBB through the regulation of tight junction proteins and matrix metalloproteinase-9, reducing edema, neuroinflammation, and neuronal cell death. We hope that this review will help promote further investigation into the neuroprotective effects of traditional Korean medicines and stimulate the performance of clinical trials on Korean herbal medicine-derived drugs in patients with stroke.
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