In this study, effect of mixing ratio of -carrageenan and glucomannan on quality characteristics of jelly incorporated with omija concentrate were analyzed. Through previous studies, the concentration of the gelling agent was fixed at 1.5% of the weight of the jelly. As a control, omija concentrate jelly using a single gelling agent was prepared. The texture of the jelly using glucomannan alone could not be measured because it was difficult to maintain its shape. The texture was changed according to the mixing ratio of -carrageenan and glucomannan. When -carrageenan was mixed with glucomannan, the water holding capacity was increased. Jelly prepared in mixing 2:1 ratio of -carrageenan and glucomannan was observed to have the highest hardness, springiness, gumminess, cohesiveness, and chewiness. Also, in order to manufacture omija jelly that maintains high water retention for a long period of time, it is optimal to mix -carrageenan and glucomannan at a ratio of 1:2.

본 연구는 아유르베다 마사지와 상담의 효과를 까파 체질의 단일사례를 중심으로 연구 하였다. 아유르베다 마사지의 효과와 상담의 효과를 융합한다면 어떤 결과가 나올지 연구 해 볼 필요성이 있다고 본다. 본 연구의 목적은 신체적, 심리적, 영적 문제를 가지고 있는 사람들을 돕는 기초자료가 되고자 한다. 연구참여자는 S시 거주의 여성(30세)으로 까파 체 질이다. 마사지와 상담 장소는 본 연구자의 연구소에서 이루어 졌으며, 기간은 2022년 1월 5일부터 4월 29일까지 주 1회 12회기를 하였다. 회기마다 30분 상담, 마사지 90분, 상담 30 분 총 2시간 30분간 실시하였다. 비만과 피부발진을 가지고 있는 폭식증 환자로서 본 연구 에 동의하고 참여하였다. 연구결과, 참여자의 경우 심리적 문제가 신체화되어 나타났기 때 문에, 심리적 문제를 먼저 다룰 필요성이 있었다. 아유르베다 마사지를 받으면서 아주 부드 러운 터치에서 충분한 사랑을 받는 것을 느꼈다. 연구자가 참여자의 가정과 직장에서 받는 스트레스를 경청해 주고, 공감해주면서 치료가 되었다.

L-ascorbic acid (L-AA; vitamin C) induces apoptosis in cancer cells. This study aimed to elucidate the molecular mechanisms of L-AA-induced apoptosis in human laryngeal epidermoid carcinoma Hep-2 cells. L-AA suppressed the viability of Hep-2 cells and induced apoptosis, as shown by the cleavage and condensation of nuclear chromatin and increased number of Annexin V-positive cells. L-AA decreased Bcl-2 protein expression but upregulated Bax protein levels. In addition, cytochrome c release from the mitochondria into the cytosol and activation of caspase-9, -8, and -3 were enhanced by L-AA treatment. Furthermore, apoptosis-inducing factor (AIF) and endonuclease G (EndoG) were translocated into the nucleus during apoptosis of L-AA-treated Hep-2 cells. L-AA effectively inhibited the constitutive nuclear factor-κB (NF-κB) activation and attenuated the nuclear expression of the p65 subunit of NF-κB. Interestingly, L-AA treatment of Hep-2 cells markedly activated Akt and mitogen-activated protein kinase (MAPK; extracellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase [JNK]) and and LY294002 (Akt inhibitor), SB203580 (p38 inhibitor) or SP600125 (a JNK inhibitor) decreased the levels of Annexin V-positive cells. These results suggested that L-AA induces the apoptosis of Hep-2 cells via the nuclear translocation of AIF and EndoG by modulating the Bcl- 2 family and MAPK/Akt signaling pathways.

The fruit of Chaenomeles sinensis (Thouin) Koehne (Chaenomelis Fructus) known as “Mo-Gua” in Korea has been commonly used in traditional medicine to treat inflammatory diseases, such as sore throat. However, its effect on bone metabolism has not been elucidated yet. Here, we examined the effect of Chaenomelis Fructus ethanol extract (CFE) on receptor activator of nuclear factor (NF)-κB ligand (RANKL)-mediated osteoclast differentiation and formation. CF-E considerably inhibited osteoclast differentiation and tartrate-resistant acid phosphatase-positive multinuclear cell formation from bone marrow-derived macrophages and osteoclast precursor cells in a dose-dependent manner. In addition, the formation of actin rings and resorption pits were significantly suppressed in CF-E-treated osteoclasts as compared with the findings in non-treated control cells. Consistent with these phenotypic inhibitory results, the expressions of osteoclast differentiation marker genes (Acp5, Atp6v0d2 , Oscar, CtsK, and Tm7sf4) and Nfatc1 , a pivotal transcription factor for osteoclastogenesis, were markedly decreased by CF-E treatment. The inhibitory effect of CF-E on RANKL-induced osteoclastogenesis was associated with the suppression of NFATc1 expression, not by regulation of mitogen-activated protein kinases and NF-κB activation but by the inactivation of phospholipase C gamma 1 and 2. These results indicate that CF-E has an inhibitory effect on osteoclast differentiation and formation, and they suggest the possibility of CF-E as a traditional therapeutic agent against bone-resorptive diseases, such as osteoporosis, rheumatoid arthritis, and periodontitis.

The transcription factor nuclear factor-kB (NF-kB) plays an important role in regulating cell growth, apoptosis, and metastatic functions. Constitutive activation of NF-KB has been observed in various cancers; however, molecular mechanisms resulting in such activation remain elusive. Numerous evidences showed that over expression of TGase 2 might be linked with constitutive activation of NF-KB. To understand the pathways responsible for constitutive activation of NF-kB is important for rational design of NF-kB inhibitors for cancer therapy. Human salivary gland adenocarcinoma has been most aggressive solid tumors. Current therapy does not significantly improve survival rates. Thus, to investigate new therapeutic modalities against this adenocarcinoma is necessary. The purpose of this study was to study a constitutive activation of NF-kB with the expression of TG2 in SGT cell line origianted from human salivary gland adenocarcinoma by TGase 2 activity, RT-PCR and immunoslot blotting method. SGT cell line showed the highest TGase 2 activity and NF-kB activation than any other cell line. All the cell lines showed increased NF-kB mRNA activation after A231027 treatment than that of control. In immunoslot blotting, SGT cell line showed NF-kB activation correlated with TGase 2 expression after A231027 and BSA. It suggested that there might be a direct correlation between TGase 2 expression and NF-kB activation in SGT cell line.

53 years old female showed repeated ulceration of labial gingival mucosa at upper and lower anterior teeth, which was a partly desquamated and erythematous lesion. The lesion was slightly extended into vestibule and buccal mucosa in oral cavity, but the similar lesion was not found in other organs by medical inspection. The incisional biopsy including the border of the ulcerated mucosa and normal mucosa showed a severely inflamed mucosa, of which epithelium was gradually detached from the underlying conective tissue, so that it was diagnosed as a mucous membrane pemphigoid (MMP) pathologically. The epithelium was thinned, almost lost its rete pegs, and the basement membrane was completely distorted by the epithelial detachement. The inflammatory cell infiltration was mainly composed of small round cells and plasma cells. Immunohistochemistry was performed to know the expression of pathogenetic proteins using antisera of Igk, E-cadherin, laminin a5, elafin, and eIF5A. The basement membrane at the epithelial detachment was condensely positive for Igk, and the involved epithelium became atrophic but showed consistently positive reaction of matrix proteins and protein translation factor, i.e., E-cadherin, laminin a5, elafin, and eIF5A similar to the adjacent normal mucosa continuous to the MMP lesion. The Igk was also diffusely deposited on the basement membrane of nearby normal mucosa. Many plasma cells infiltrated around the lesion were strongly positive for Igk in their cytoplasms. Therefore, we suggest that the MMP be characterized by the deposition of Igk on the basement membrane of the detached epithelium in the absence of no other pathognomic changes of molecular events.

Heme oxygenase-l (HO-l) exhibits cyt oprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts‘ However‘ therole of HO- l in cancer cells exposed to nicotine has not previously been descnbed We investigated the effects of nicotine on HO-l protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human ora l keratinocyte cells using the MTT assay and Western blotting. We al so examined the involvement of t he phosphoinosit ide-3-0H- kinase (PI3K), mitogen-acti vated protein kinase (MAPK) , and nucJear factor-κ B (NF-κ B) signaling pathways in nicotine-induced cytotoxicity and HO- l levels in IHOK and HN12 cell s‘ Nicotine induced HO- l pro ducti on and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotox icity and accumulation of HO- l were greater in JJ-IOK cells than in HN12 cells Molecular inhibitors of the ERK, p38 MAP kinase, PI3K, and NF-κ B signaling pathways blocked the cytotoxic effects and induction of J-IO-l expression by nicotine. Treatmen t with an t ioxida nts (bil irubin, N-acetyl cysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregula tion of J-IO- l, the effects of which were more pronounced in II-IOK cells than in HN12 cells Collecti vely, these results suggest that J-IO- l plays a principal role in the protective response to nicotine in oral cancel and immortalized keratinocytes. Moreover, the addition of exogenous antioxidants may help to protect oral epithelial cells as chemopreventive agents against nicotine-induced oxidative stress.

Heme oxygenase-l (HO-l) exhibits cyt oprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts‘ However‘ therole of HO- l in cancer cells exposed to nicotine has not previously been descnbed We investigated the effects of nicotine on HO-l protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human ora l keratinocyte cells using the MTT assay and Western blotting. We al so examined the involvement of t he phosphoinosit ide-3-0H- kinase (PI3K), mitogen-acti vated protein kinase (MAPK) , and nucJear factor-κ B (NF-κ B) signaling pathways in nicotine-induced cytotoxicity and HO- l levels in IHOK and HN12 cell s‘ Nicotine induced HO- l pro ducti on and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotox icity and accumulation of HO- l were greater in JJ-IOK cells than in HN12 cells Molecular inhibitors of the ERK, p38 MAP kinase, PI3K, and NF-κ B signaling pathways blocked the cytotoxic effects and induction of J-IO-l expression by nicotine. Treatmen t with an t ioxida nts (bil irubin, N-acetyl cysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregula tion of J-IO- l, the effects of which were more pronounced in II-IOK cells than in HN12 cells Collecti vely, these results suggest that J-IO- l plays a principal role in the protective response to nicotine in oral cancel and immortalized keratinocytes. Moreover, the addition of exogenous antioxidants may help to protect oral epithelial cells as chemopreventive agents against nicotine-induced oxidative stress.

Kappa represents decay parameter about 3~4km under seismic stations. This study estimated domestic kappa characteristics. The korean peninsula kappa showed high value in gyeongsang basin be known as sedimentary rock local as a result of this study.