• Journal of Acupuncture Research
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• v.32 no.1
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• pp.79-88
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• 2015

Objectives : The purpose of this research was to investigate the cytotoxic effect of Natural Killer(NK)-92 cell and Snake Venom, and to elucidate its mechanism on human lung carcinoma cell A549. Methods : In order to figure out whether Snake Venom enhances the cytotoxic effect of NK-92 cell in A549 cell, Cell Viability Assay was conducted. Also, in order to observe the changes of Caspase-3 and Caspase-8, both of which are proteinases that advance apoptosis, and the changes of TNRF and DR3, which are Death Receptors of the extrinsic pathway of apoptosis, Western Blot Analysis was conducted. By conducting RT-PCR analysis, we have tried to confirm Perforin, Granzyme B, and GADPH, all of which are cytotoxic-related proteins. Lastly, in order to observe the effect of Snake Venom on NO formation within human lung carcinoma cells, NO determination was conducted. Results : 1. After conducting Cell Viability Assay, Snake Venom enhanced the cytotoxic effect of NK-92 cell and inhibited the growth of A549. 2. Western Blot Analysis caused proteinases Caspase-3 and Caspase-8, which advance apoptosis, to increase in the combined treatment group, but not in treatment groups that focused only on either Snake Venom or NK-92 cell in A549 lung carcinoma cells. 3. Western Blot Analysis caused an expression of TNFR2 and DR3, both of which are Death Receptors of the apoptosis extrinsic pathway, in the combined treatment group, but not intreatment groups that focused only on either Snake Venom or NK-92 cell in A549 human lung carcinoma cells. 4. After conducting NO determination, NO formation within A549 cell showed no significant changes in both treatment groups that focused NK-92 cell and combined treatment group. 5. After conducting RT-PCR, the expression of Granzyme B and Perforin, which are cytotoxic-related proteins within A549 human lung carcinoma cells, showed growth in the combined treatment group, but not the treatment group that focused only on NK-92 cell. Conclusion : It has been indicated that, when it comes to the A549 cell, Snake Venom enhances the increase of Death Receptor expression and continuous apoptosis reaction, leading to the enhancement of the cancer cell cytotoxic effect of the NK-92 cell. It is expected that Snake Venom can be used with the NK-92 cell for further lung cancer treatment.

• The Journal of Korean Medicine
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• v.25 no.2
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• pp.138-150
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• 2004

Objectives : Alzheimer's disease (AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the biggest problem in public health service. Although a variety of oriental prescriptions, including Sesim-tang, have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet been fully elucidated. The present study investigated the effects of Sesim-tang on apoptotic cell death induced by CT105 (carboxy terminal 105 amino acid peptide fragment of APP) overexpression in SK-N-SH neuroblastoma cell lines. Methods: We studied the regenerative and inhibitory effects on Alzheimer's disease in CT105-induced SK-N-SH cell lines by Sesim-tang water extract. We examined for cell morphological pattern, DNA fragmentation, LDH activity assay, zymography assay, and immunohistochemistric analysis. Additionally, we investigated the association between the CT105 and neurite degeneration caused by CT105-induced apoptotic response in neurone cells. Results: Findings from our experiments have shown that Sesim-tang inhibits the synthesis or activities of CT105, which has neurotoxicities and apoptotic activities in the cell line. In addition, pretreatment with Sesim-tang ($>50\mu\textrm{g}/ml$ for 12 hours) partially prevented CT105-induced cytotoxicity in SK-N-SH cell lines. SK-N-SH cell lines overexpressed with CT105 exhibited remarkable apoptotic cell damage. Based on morphological observations by phase-contrast microscope and LDH activity measurements in the culture media, the CT105-induced cell death was significantly inhibited by Sesim-tang water extract. Sesim-tang was found to reduce the expression of APP and caspase-3 induced by CT105 in SK-N-SH cell lines and in rat hippocampus. Conclusions: As the result of this study, in the Sesim-tang group, apoptosis in the nervous system is inhibited, the repair against the degeneration of SK-N-SH cell lines by CT105 expression is promoted. Hence, Sesim-tang may be beneficial for the treatment of AD.

• Journal of the korean veterinary medical association
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• v.21 no.8
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• pp.456-462
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• 1985

It was carried out to a general review of relation between bovine mastitis and somatic cell count in milk. The results were summarized as follows; 1. The term 'Somatic' means derived from body. Since both leukocytes and epithelial cell are body cell, tota

• Transactions of the Korean hydrogen and new energy society
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• v.24 no.6
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• pp.480-486
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• 2013

In this study, tubular SOFC unit cell with advanced anode current collector was fabricated to improve the cell performance. First, we prepared two types of single cells having the same manufacture processes such as the same electrolyte, electrode coating condition and sintering processes. And then to compare the developed single cell performance with conventional cells, we changed the anode current collecting methods. From the impedance analysis and I-V curve analysis, the cell performance of advanced cell is much higher than that of conventional cell.

• BMB Reports
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• v.47 no.8
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• pp.424-432
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• 2014

The defining feature of Parkinson's disease is a progressive and selective demise of dopaminergic neurons. A recent report on Parkinson's disease animal model demonstrates that poly (ADP-ribose) (PAR) dependent cell death, also named parthanatos, is accountable for selective dopaminergic neuronal loss. Parthanatos is a programmed necrotic cell death, characterized by PARP1 activation, apoptosis inducing factor (AIF) nuclear translocation, and large scale DNA fragmentation. Besides cell death regulation via interaction with AIF, PAR molecule mediates diverse cellular processes including genomic stability, cell division, transcription, epigenetic regulation, and stress granule formation. In this review, we will discuss the roles of PARP1 activation and PAR molecules in the pathological processes of Parkinson's disease. Potential interaction between PAR molecule and Parkinson's disease protein interactome are briefly introduced. Finally, we suggest promising points of therapeutic intervention in the pathological PAR signaling cascade to halt progression in Parkinson's disease.

• Proceedings of the Korean Society of Precision Engineering Conference
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• 2004.10a
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• pp.1215-1220
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• 2004

Cell adhesion to any material surface is considered to be fundamental and important phenomenon in the fields of tissue engineering. Cell adhesion molecules, mechanism, and attachment force have been studied and described a lot. However, the effects of mechanical stimuli on the adhesive forces still have been left much to be investigated. In this study, to investigate the changes in cell adhesive force due to resting time period during the intermittent hydrostatic pressurizing (IHP), cells were cultured under the IHP with various resting times. Then the cell adhesive forces were measured quantitatively utilizing a cell detachment test system and immunofluorescent staining was performed using fluorescent microscopy. In the results, immediately after mechanical stimuli (150 minutes after seeding) and one hour later (210 minutes after seeding), the average adhesive force of experimental group 5 (resting time: 15min) compared with that of control group at same culture time was increased significantly (p<0.05). The results indicated that IHP can contribute in improving cell adhesive force and some of time intervals were required for the expression of cell response.

• Toxicological Research
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• v.18 no.4
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• pp.411-416
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• 2002

Apoptosis, or programmed cell death, is a genetically regulated pathway that is altered in many cancers. Overexpression of bcl-2 leads to resistance to apoptosis and promotes tumorigenesis. To determine the effect of bcl-2 antisense treatment in human lung cancer cell lines, a 20 mer full phosphorothioate oligonucleotide (ODN) targeted at the coding region of the bcl-2 mRNA was synthesized. Western blot analyses were used to examine bcl-2 protein level in five human non-small cell lung cancer (NSCLC) cell lines (NCI-H226, SK-MES-1 NCI-H358, NCI-H522 and NCI-Hl 299) and four human small cell lung cancer (SCLC) cell lines (NCI-H69, NCI-H4l7, HCC-2108 and SW2). Three out of five NSCLC (NCI-H226, SK-MES-1 and NCI-Hl 299) and all of SCLC cell lines expressed Bcl-2 protein. Treatment of these cell with antisense ODN for 48 hours reduced their viability and Bcl-2 protein level. As a conclusion, bcl-2 antisense treatment appears reduction of the Bcl-2 protein levels and cytotoxic effect including apoptosis in human lung cancer cell lines.

• BMB Reports
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• v.49 no.10
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• pp.527-528
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• 2016

In embryonic stem cells (ESCs), cell cycle regulation is deeply connected to pluripotency. Especially, core transcription factors (CTFs) which are essential to maintaining the pluripotency transcription programs should be reset during M/G1 transition. However, it remains unknown about how CTFs are governed during cell cycle progression. Here, we describe that the regulation of Oct4 by Aurora kinase b (Aurkb)/protein phosphatase 1 (PP1) axis during the cell cycle is important for resetting Oct4 to pluripotency and cell cycle related target genes in determining the identity of ESCs. Aurkb starts to phosphorylate Oct4(S229) at the onset of G2/M phase, inducing the dissociation of Oct4 from chromatin, whereas PP1 binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition, which resets Oct4-driven transcription for pluripotency and the cell cycle. Furthermore, Aurkb phosphormimetic and PP1 binding-deficient mutations in Oct4 disrupt the pluripotent cell cycle, lead to the loss of pluripotency in ESCs, and decrease the efficiency of somatic cell reprogramming. Based on our findings, we suggest that the cell cycle is directly linked to pluripotency programs in ESCs.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.21 no.6
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• pp.1480-1489
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• 1996

In ATM networks there are two methods in traffic control as schemes advancing the quality of service. One is reactive control after congestion and the other which is generally recommended, is preventive control before congestion, including connection admission control on call leel and usage parameter control, network parameter control, priority control and congestion control on cell level. In particular, usage parameter control is required for restricting the peak cell rate of bursy tracffic to the parameter negotiated at call set-up phase since the peak cell rate significantly influences the network quality of service. The scheme for progressing quality of service by usage parameter control is themethod using VSA(Virtual Scheduling Algorlithm) recommended ITU-T. The method using VSSA(Virtual Scheduling Suggested Algorlithm) in this paper is suggested by considering cell delay variation and token rate of leaky bucket, compared VSA and VSANT(Virtual Scheduling Algolithm with No Tolerance) with VSSA which polices violated cell probability of conformed peak cell rate and intentionally excessive peak cell rate. VSSA method using IPP(Interruped Poisson Process) model of input traffic source showed more quality of service than VSA and VSANT methods as usage parameter control because the suggested method reduced the violated cell probability of contformed peak cell rate and intentionally excessive peak cell rate.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3987-3989
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• 2013

This is a commentary on what a cancer cell is and why cancer cells metastasize. Normal cell get transformed to a cancer cell, with excessive production of free radicals that mutate the DNA of a normal cell. The immortality and malignant stage of transformed cell is maintained by higher GSH levels. With the faster rate of proliferation, when the cancer cell finds the place of origin is not conducive to its further growth, cancer cell chooses to take the metastatic course. We argue that if we can stop the exit of cancer cell from place of origin, cancer spread can be stopped or even cured.