• The Journal of Korean Medicine
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• v.30 no.4
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• pp.142-161
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• 2009

Objectives: There are many unknowns surrounding Jeong-Jo's death. To better understand Jeong-Jo's death, we closely inspected his medical records from the 20 days before his death in The Annals of the Chosun Dynasty (朝鮮王朝實錄) and Seungjeongwon Ilgi (承政院日記), Understanding medical treatment before death, we can correctly trace the cause of Jeong-Jo's death. Methods: According to The Annals of the Chosun Dynasty (朝鮮王朝實錄) and Seungjeongwon Ilgi (承政院日記), we examined his medical records between June 14 and June 28 of 1800, as to the change in chief complaint, cold and heat, thirst, syndrome differentiation, the opinions of Jeong-Jo, and the opinions of doctors, The original work, The Annals of the Chosun Dynasty and Seungjeongwon Ilgi were provided by NIKH (The National Institute of Korean History). The Korean translation of The Annals of the Chosun Dynasty was also provided by NIKH. Seungjeongwon Ilgi (original work written in Chinese characters) was directly translated into Korean by the study author. Results: 1. Jeong-Jo's is likely to have died of septicemia caused by an abscess on his back. 2. The cause of Jeong-Jo's death could be stroke due to hypertension, mental stress, and 'Wha (火) disease' Conclusions: The dominant view that Jeong-Jo was murdered by poison is not likely.

• Journal of Sasang Constitutional Medicine
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• v.21 no.1
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• pp.44-52
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• 2009

1. Objectives Jeong-Jo's death has many mistery. So we understand rightly Jeong-Jo's death. we inspect closely medical records of 20 days before death(in The Annals of the Choson Dynasty(朝鮮王朝實錄), Hong Je Jun Se(弘齋全書)， GukSoBoGam(國朝寶鑑). We understand medical treatment before death. It is based on Jeong-Jo's Constitution. So we trace the cause of a Jeong-Jo's death rightly. 2. Methods According to The Annals of the Choson Dynasty(朝鮮王朝實錄), Hong Je Jun Se(弘齋全書) GukSoBoGam(國朝寶鑑). We found out Jeoung-Jo's Sasang constitutional elemet. We point on Jeoung-Jo's nature and emotion, temperament and talent, features and way of speaking, physical appearance, healthy state, ordinary symptom, pathological syndromes and pharmacology. so documentary records was worthy of notice. 3. Results and conclusions 1. Jeong-Jo has prominent cheekbones,flat face. It belong to Tae-eum. 2. Jeong-Jo's physical appearance is mild,around,large. It belong ro Tae-eum. 3. Jeong-Jo's favorite food and herb were belong to Tae-eum interior febrile disease herb. which is Exhale Dispersing Qi 4. So even though Jeoung-Jo is Tae-eum, He had a weak body. It main cause that Smoking, insomnia, heave work, Hwa disease. 5. Jeong-Jo's is Interior febrile disease induced form the liver affected by heat in Tae-eumin

• BMB Reports
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• v.48 no.7
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• pp.395-400
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• 2015

Parkinson's disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP⁺) induced SH-SY5Y neuronal cell death and in a 1-methyl-4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP⁺-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases. [BMB Reports 2015; 48(7): 395-400]

• Radiation Oncology Journal
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• v.21 no.4
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• pp.306-314
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• 2003

Purpose : In our Previous study, we have shown the main cel1 death pattern Induced by irradiation or protein tyrosine kinase (PTK) inhibitors in K562 human myeiogenous leukemic cell line. Death of the cells treated with irradiation alone was characterized by mitotic catastrophe and typical radiation-induced apoptosis was accelerated by herblmycin A (HMA). Both types of cell death were inhibited by genistein. In this study, we investigated the effects of HMA and genistein on cell cycle regulation and its correlation with the alterations of radiation-induced cell death. Materials and Methods: K562 cells In exponential growth phase were used for this study. The cells were Irradiated with 10 Gy using 6 MeV Linac (200-300 cGy/min). Immediately after irradiation, cells were treated with 250 nM of HMA or 25 $\mu$N of genistein. The distributions of cell cycle, the expressions of cell cycle-related protein, the activities of cyclin-dependent kinase, and the yield of senescence and differentiation were analyzed. Results: X-irradiated cells were arrested In the G2 phase of the cell cycle but unlike the p53-positive cells, they were not able to sustain the cell cycle arrest. An accumulation of cells in G2 phase of first ceil-cycle post-treatment and an increase of cyclin Bl were correlated with spontaneous, premature, chromosome condensation and mitotic catastrophe. HMA induced rapid G2 checkpoint abrogation and concomitant p53-independent Gl accumulation. HMA-induced cell cycle modifications correlated with the increase of CDK2 kinase activity, the decrease of the expressions of cyclins I and A and of CDK2 kinase activity, and the enhancement of radiation-induced apoptosis. Genistein maintained cells that were arrested in the G2-phase, decreased the expressions of cyclin Bl and cdc25c and cdc25C kinase activity, increased the expression of pl6, and sustained senescence and megakaryocytic differentiation. Conclusion: The effects of HMA and genistein on the radiation-induced cell death of KS62 cells were closely related to the cell cycle regulatory activities. In this study, we present a unique and reproducible model in which for investigating the mechanisms of various, radiation-induced, cancer cell death patterns. Further evaluation by using this model will provide a potent target for a new strategy of radiotherapy.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.7
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• pp.2993-2999
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• 2014

Saccharina japonica is a family member of Phaeophyceae (brown macro-alga) and extensively cultivated in China, Japan and Korea. Here, the potential anti-cancer effect of n-hexane fraction of S. japonica was evaluated in SK-Hep1 human hepatocellular carcinoma cells. The N-hexane fraction reduced cell viability and increased the numbers of apoptotic cells in a both dose- and time-dependent manner. Apoptosis was activated by both caspase-dependent and independent pathways. The caspase-dependent cell death pathway is mediated by cell surface death receptors and activated caspase-8 amplified the apoptotic signal either through direct activation of downstream caspase-3 or pro-apoptotic proteins (Bad, Bax and Bak) subsequently leading to the release of cytochrome c. On the other hand, caspase-independent apoptosis appeared mediated by disruption of mitochondrial membrane potential and translocation of AIF to the nucleus where they induced chromatin condensation and/or large-scale DNA fragmentation. In addition, the n-hexane fraction induced endoplasmic reticulum (ER)-stress and cell cycle arrest. The results suggested that potential anti-cancer effects of n-hexane extract from S. japonica on SK-Hep1 cells.

• Journal of Ginseng Research
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• v.44 no.1
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• pp.96-104
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• 2020

Objectives: Oleanolic acid, a minor element of ginsenosides, and its derivatives have been shown to have cytotoxicity against some tumor cells. The impact of cytotoxic effect of oleanolic acid 3-acetate on ovarian cancer SKOV3 cells and endometrial cancer HEC-1A cells were examined both in vivo and in vitro to explore the underlying mechanisms. Methods: Cytotoxic effects of oleanolic acid 3-acetate were assessed by cell viability, phosphatidylserine exposure on the cell surface, mitochondrial release of cytochrome C, nuclear translocation of apoptosis-inducing factor, depolarization of mitochondrial transmembrane potential (∆Ψ_m), and generation of reactive oxygen species (ROS). In vivo inhibition of tumor growth was also assessed with xenografts in immunocompromised mice. Results: Oleanolic acid 3-acetate exhibited potent cytotoxicity toward SKOV3 and HEC-1A cells by decreasing cell viability in a concentration-dependent manner. Importantly, oleanolic acid 3-acetate effectively suppressed the growth of SKOV3 cell tumor xenografts in immunocompromised mice. Furthermore, oleanolic acid 3-acetate induced apoptotic cell death as revealed by loss of ∆Ψ_m, release of cytochrome c, and nuclear translocation of apoptosis-inducing factor with a concomitant activation of many proapoptotic cellular components including poly(ADP-ribose) polymerase, Bcl-2, and caspases-8, caspase-3, and caspase-7. Oleanolic acid 3-acetate, however, caused a decrease in ROS production, suggesting the involvement of an ROS-independent pathway in oleanolic acid 3-acetate-induced apoptosis in SKOV3 and HEC-1A cells. Conclusion: These findings support the notion that oleanolic acid 3-acetate could be used as a potent anticancer supplementary agent against ovarian and endometrial cancer. Oleanolic acid 3-acetate exerts its proapoptotic effects through a rather unique molecular mechanism that involves an unconventional ROS-independent but mitochondria-mediated pathway.

• BMB Reports
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• v.49 no.7
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• pp.382-387
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• 2016

Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stress-induced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases.

• Journal of Animal Science and Technology
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• v.58 no.4
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• pp.17.1-17.7
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• 2016

Background: The Sapsaree (Canis familiaris) is a Korean native dog that is very friendly, protective, and loyal to its owner, and is registered as a natural monument in Korea (number: 368). To investigate large-scale gene expression profiles and identify the genes related to exercise-induced stress in the Sapsaree, we performed whole-transcriptome RNA sequencing and analyzed gene expression patterns before and after exercise performance. Results: We identified 525 differentially expressed genes in ten dogs before and after exercise. Gene Ontology classification and KEGG pathway analysis revealed that the genes were mainly involved in metabolic processes, such as programmed cell death, protein metabolic process, phosphatidylinositol signaling system, and cation binding in cytoplasm. The ten Sapsarees could be divided into two groups based on the gene expression patterns before and after exercise. The two groups were significantly different in terms of their basic body type ($p{\leq}0.05$). Seven representative genes with significantly different expression patterns before and after exercise between the two groups were chosen and characterized. Conclusions: Body type had a significant effect on the patterns of differential gene expression induced by exercise. Whole-transcriptome sequencing is a useful method for investigating the biological characteristics of the Sapsaree and the large-scale genomic differences of canines in general.

• Journal of The Korean Dental Society of Anesthesiology
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• v.11 no.2
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• pp.146-152
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• 2011

Background: Elderly patients with progressive dementia including Alzheimer's disease (AD) are more and more often scheduled to undergo general anesthesia for various pathologies including dental problem. But, there is high risk of deterioration of underlying mental diseases and other co-morbidities. So it is important to implement preventive strategies and take adequate measures to minimize negative perioperative events in these patients. Methods: We reviewed the 17 cases of 11 patients with AD who underwent ambulatory general anesthesia for dental treatment at the clinic for the disabled in Seoul National University Dental Hospital. Results: The mean age was 68 (57-81) years. All of them were diagnosed with AD and some had hypertsnsion, bronchiectasis, urinary incontinence. For anesthesia induction, 3 cases (1 patient) was needed physical restraint, but others showed good or moderate cooperation. Drugs used for anesthesia induction was thiopental (11 cases), propofol (3 cases) and sevoflurane (3 cases). All patients received nasotracheal intubation without difficulties. Mean total anesthetic time was 3 hour 44 min ${\pm}$ 60 min and staying time at PACU was 83 ${\pm}$ 34 min. All the patients except one who showed hypertension discharged without any complication. There was no death or long term hospitalization because of severe complications. Conclusions: If general anesthesia is needed, pertinent diagnostic tests and workup about other medical problems, and appropriate anesthetic planning are essential for safety.

• Korean Journal of Environmental Biology
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• v.31 no.4
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• pp.486-492
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• 2013

Recently, a new disease showing symptoms such as epidermal exfoliation and muscular necrosis occurred in cultured Korean catfish. Although the mortality of fishes was low but the economic damages owing to loss of commercial value were severe. The authors isolated the causative agent from diseased fish and observed pathological changes both in naturally and artificially infected fish. The causative bacteria was identified as Aeromonas veronii. Subsequently we observed the daily death and pathological symptoms of artificially infected fish with Aeromonas veronii. Symptoms of artificially infected fish were similar to those of naturally infected fish and all fish died within 7 days after infection. Histopathological changes on the naturally infected fish revealed severe congestion and necrotic degeneration in the liver, spleen and kidney. Some bacterial aggregates with inflammatory degeneration were observed in the heart, and congestion and fibrosis in the lamina propria of digestive tube were predominant. In artificially infected fish, skin erosion and necrotic degeneration of muscle tissue around injected region were particularly manifested. Degeneration of hepatocytes in liver and hyalic degeneration around ellipsoids in spleen were partially observed. However, there were no predominant signs in digestive tube in artificially infected fish.