Associations between periodontal infection and cardiovascular disease have been documented. Porphyromonas gingivalis is a well-established periodontal pathogen, and tissue factor (TF) is a key initiator of the coagulation cascade. In this context, P. gingivalis has been reported to enhance TF expression in human endothelial cells. The present study investigated the underlying mechanisms of TF induction by P. gingivalis in human umbilical vein endothelial cells. P. gingivalis increased TF expression in a dose- and time-dependent manner. Not only live bacteria but also glutaraldehyde-fixed bacteria increased TF expression to the same extent. However, sonicates of P. gingivalis did not induce TF expression. Cytochalasin D and SMIFH2, which are inhibitors of actin polymerization and actin nucleation, respectively, inhibited the TF expression induced by P. gingivalis . Finally, TF production was decreased or increased in the presence of various signaling inhibitors, including mitogen-activated protein kinases. These results suggest that P. gingivalis induces endothelial TF expression by a bacterial internalization-dependent mechanism and through diverse signal transduction mechanisms.

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.

Proteasome inhibitors can improve the efficiency of cancer treatments by inhibiting nuclear factor κB(NF-κB) activation in cancer cells. Lentils are a type of beans of which consumption of such beans is increasing. The purpose of this study was to investigate the effects of lentils extract (LE) on the proteasomal activities, NF-κB activation, and cell cycle in HepG2 human liver cancer cells. LE treatments inhibited proteasomal activities at concentrations of 10, 50, and 100 μg/mL respectively, and repressed NF-κB activation at concentrations of 1, 10, and 100 μg/mL respectively, in HepG2 cells. LE treatments at concentrations of 1, 10, and 100 μg/mL respectively, increased sub-G1 cell population in HepG2 cells, which may be the result of apoptosis. The results suggest that LE inhibited NF-κB activation partially with its proteasome inhibitory activities, and the increase of sub-G1 cell population was induced partially, by inhibition of NF-κB activation in HepG2 cells.

동물의 장기를 인간에게 이식하게 되면 초급성거부반응(Hyperacute rejection, HAR)이 일어난다. 초급성거부반응은 면역계의 구성요소 중 보체(complement)에 의해 일어나는 거부반응으로 돼지의 혈관세포 표면에 있는 Galα(1,3)Gal 당분자에 인간의 항체가 즉각 반응하기 때문에 일어나며, α1,3-galactosyltransferase(α1,3-GT) 유전자는 돼지 혈관세포 표면의 Galα(1,3)Gal 당분자 생성에 관여한다. 따라서 인간에게 돼지의 장기를 이식하기 위해서는 α1,3-galactosyltransferase 유전자를 제거하는 것이 필요한 것으로 알려져 있다. 본 연구실의 이전 연구에서, 시카고 미니돼지 귀체세포에서 상동 재조합(Homologous recombination)을 통해 α1,3-galactosyltransferase 유전자가 제거된 체세포를 개발한 바 있으며, 이 체세포를 통하여 α1,3-GT 유전자가 제거된 돼지도 생산된 바 있다. 본 연구에서는, human serum 처리 시 돼지 세포를 보호해 준다고 보고되고 있는 human complement regulator인 human Decay-accelerating factor(hDAF)와 human α1,2-fucosyltransferase(hHT)유전자를 α1,3-GT 유전자 위치에 gene targeting하여 동시에 hDAF와 hHT가 발현하는 체세포를 개발하였다. Knock-in vector는 hDAF와 hHT 두 유전자가 발현할 수 있도록 IRES로 연결하였으며, α1,3-GT 유전자의 start codon을 이용하여 발현할 수 있도록 구축하였다. 구축한 vector는 electroporation을 통해 미니돼지 체세포에 도입하였으며, PCR 결과, α1,3-GT 유전자 위치에서 상동 재조합이 일어났음을 확인하였다. Positivenegative 선별 방법을 통해 얻은 gene targeting 된 체세포는 RT-PCR에 의해 hDAF와 hHT 유전자의 발현이 확인되었으며, 대조군(NIH minipig)에 비해 α1,3-GT 유전자의 발현이 감소하였다. 또한 이들 세포에 100% human complement serum을 처리하였을 때 knock-in 세포가 대조군에 비해 30% 정도 더 높은 생존율을 보였다. 따라서 개발된 체세포는 이종간 장기이식을 위한 돼지 생산과 함께 이를 이용한 이종간의 장기 이식 시 초급성 거부반응을 억제하는 데 사용될 수 있을 것으로 생각된다.

Since the computer technology has been drastically developed and broadly employed for the design of human machine system, human system interface was somehow digitalized. Actually the operator’'s working environment employing the digital devices are not be

The purpose of this article is to examine the relationship between unsafe behavior, human factor and human error. For the object, several correlation analyses for those three elements were implemented. Several hypotheses for the relationship between them was suggested. The suggested hypotheses were verified by a comprehensive survey received from 132 safety manager of manufacturing industry. The conclusions were proven from the hypotheses verificaiton as belows; 1) The dependent relation items between unsafe behavior and human factor are dress protection tool, machine(equipment) and working rule have a dependent relation. 2) The dependent relation items between human factor and human error are uncommunication, control, slaps, fatigue, education, system, unmonitoring, failure. 3) The dependent relation items between human error and unsfafe behavior are decline and product/working method,failure and uncommunication have a dependent relation.

Through so that accident of semiconductor industry deduces unsafe factor of the person center on unsafe behaviour that incident history and questionnaire and I made starting point that extract very important factor. It served as a momentum that make up base that analyzes factors that happen based on factor that extract factor cause classification for the first factor, the second factor and the third factor and presents model of human error. Factor for whole defines factor component for human factor and to cause analysis 1 stage in human factor and step that wish to do access of problem and it do analysis cause of data of 1 step. Also, see significant difference that analyzes interrelation between leading persons about human mistake in semiconductor industry and connect interrelation of mistake by this. Continuously, dictionary road map to human error theoretical background to basis traditional accidental cause model and modern accident cause model and leading persons. I wish to present model and new model in semiconductor industry by backbone that leading persons of existing scholars who present model of existent human error deduce relation. Finally, I wish to deduce backbone of model of pre-suppression about accident leading person of the person center.