• The Journal of the Convergence on Culture Technology
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• v.3 no.4
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• pp.27-33
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• 2017

Epicurus and Lucretius expressed that death is neither evil to the living nor the dead. On the contrary, our everyday perception of death is that death is evil. Such everyday perception might seem in lack of introspection and blind but our living environment and form of life are strongly supporting this perception. This paper argues that there is reasonable cause for believing death is evil. In order to justify this argue, this paper critically supports Thomas Nagel's 'Deprivation Theory', which identifies the cause of death being in evil in the deprivation of life. This paper investigates the main substances of 'Deprivation Theory, suggests the related problems and therefore reconstitutes the main arguments of 'Deprivation Theory, resulting in the investigation of the following facts; that we cannot avoid the fate of death, but that our existence is headed towards the future, and that as independent individuals we have infinite possibilities of life. Death is natural to humanity as species, but as independent individuals death deprives us from possible life and future. Therefore, death we encounter in our living environment and form of life is evil. As species, we can agree with Epicurus and Lecretius' view, but as independent individuals we cannot share them.

• BMB Reports
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• v.34 no.3
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• pp.189-193
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• 2001

Curcumin a yellow pigment from Curcuma Tonga, has been known to possess antioxidative and anticarcinogenic properties, as well as to induce apoptosis in some cancer cells. There have been, however, several contradictory reports that hypothesized curcumin (a hydrophobic molecule) can bind a membrane Gpid bilayer and induce nonspecific cytotoxicity in some cell lines. Why curcumin shows these contradictory effects is unknown. In A-431 cells, growth inhibition by curcumin is due mostly to the specific inhibition of the intrinsic tyrosine kinase activity of the epidermal growth factor receptor, as reported earlier by Korutla et al. Thus, we assumed that the cell death of A-431 by curcumin might be due to the specific induction of apoptosis. In this paper we clearly show that curcumin induces apoptosis in A-431 cells. The cureumin-induced cell death of A-431 exhibited various apoptotic features, including DNA fragmentation and nuclear condensation. Furthermore, the curcumin-induced apoptosis of A-431 cells involved activation of caspase-3-like cysteine protease. Involvement of caspase-3 was further confirmed by using a caspase-3 specific inhibitor, DEVD-CHO. In another study, decreased nitric oxide (NO) production was also shown in A-431 cells treated with curcumin, which seems to be the result of the inhibition of the iNOS expression by curcumin, as in other cell lines. However, 24 h after treatment of curcumin there was increased NO production in A-431 cells. This observation has not yet been clearly explained. We assumed that the increased NO production may be related to denitrosylation of the enzyme catalytic site in caspase-3 when activated. Taken together, this study shows that the cell death of A-431 by curcumin is due to the induction of apoptosis, which involves caspase-3 activation.

• Journal of Environmental Science International
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• v.30 no.7
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• pp.573-584
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• 2021

To analyze the effects of PM₁₀ and PM_2.5 on daily mortality cases, the relations of death counts from natural causes, respiratory diseases, and cardiovascular diseases with PM₁₀ and PM_2.5 concentrations were applied to the generalized additive model (GAM) in this study. From the coefficients of the GAM model, the excessive mortality risks due to an increase of 10 ㎍/m³ in daily mean PM₁₀ and PM_2.5 for each cause were calculated. The excessive risks of deaths from natural causes, respiratory diseases, and cardiovascular diseases were 0.64%, 1.69%, and 1.16%, respectively, owing to PM₁₀ increase and 0.42%, 2.80%, and 0.91%, respectively, owing to PM_2.5 increase. Our result showed that particulate matter posed a greater risk of death from respiratory diseases and is consistent with the cases in Europe and China. The regional distribution of excessive risk of death is 0.24%-0.81%, 0.34%-2.6%, and 0.62%-1.94% from natural causes, respiratory diseases, and cardiovascular diseases, respectively, owing to PM₁₀ increase, and 0.14%-1.02%, 1.07%-3.92%, and 0.22%-1.73% from natural causes, respiratory diseases, and cardiovascular diseases, respectively, owing to PM_2.5 increase. Our results represented a different aspect from the regional concentration distributions. Thus, we saw that the concentration distributions of air pollutants differ from the affected areas and identified the need for a policy to reduce damage rather than reduce concentrations.

• Journal of Life Science
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• v.20 no.4
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• pp.519-527
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• 2010

Paclitaxel is known as a potent inhibitor of microtubule depolymerization. It leads to mitotic arrest and cell death by stabilizing the spindle in various cell types. Here, we investigated the effects of paclitaxel on the proliferation and cell death of rabbit articular chondrocytes. Paclitaxel inhibited proliferation in a dose- and time- dependent manner, determined by MTT assay in rabbit articular chondrocytes. We also established paclitaxel-induced G2/M arrest by fluorescent activated cell sorter (FACS) analysis. Paclitaxel increased expression of cyclin B, p53 and p21, while reducing expression of cdc2 and cdc25C in chondrocytes, as detected by Western blot analysis. Interestingly, paclitaxel showed the mitotic catastrophe that leads to abnormal nucleus division and cell death without DNA fragmentation through activation of caspase. Cell death by mitotic catastrophe in cells treated with paclitaxel was suppressed by inhibiting G1/S arrest with 2 mM thymidine. These results demonstrate that paclitaxel induces cell death via mitotic catastrophe without activation of casepase in rabbit articular chondrocytes.

• The Korean Society of Law and Medicine
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• v.10 no.1
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• pp.263-305
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• 2009

Is it lawful to withhold or withdraw life-sustaining treatment applied to a patient in a terminal condition or permanent unconscious condition? In Korea, there are no such laws or regulations which control affairs related to the withholding or withdrawal life-support treatment and active euthanasia as the Natural Death Act or the Death with Dignity Act in the U. S. A. And in addition there has had no precedent of Supreme Court. Recently Supreme Court has pronounced a historical judgment on a terminal care case. The court allowed the withdrawal of life-sustaining treatment from a patient in a permanent unconscious state. Fundamentally the court judged that the continuation of that medical treatment would infringe dignity and value of a patient as a human being. And the court required some legal grounds to consider such withdrawal or withholding of medical care lawful. The legal grounds are as follow. First, the patient is in a incurable and irreversible condition and already entered a stage of death. Second, the patient executed a directive, in advance, directing the withholding or withdrawal of life-support treatment in a incurable and irreversible condition or in a terminal condition. Otherwise, at least, the patient's will would be presumed through his/her character, view of value, philosophy, religious faith and career etc. I regard if a patient is in a incurable and irreversible condition or in a terminal condition, the medical contract between a patient and a doctor would be terminated because of the actual impossibility of achievement of it's purpose. So I think the discontinuation of life-sustaining care would be legally allowed without depending on the patient's own will.

• The Korean Journal of Legal Medicine
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• v.42 no.4
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• pp.111-125
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• 2018

Statistical analysis was performed on national forensic autopsy data collected in the Republic of Korea, with the exception of Ulsan, during 2017. A total of 8,777 cases were categorized based on the region; information was provided by the Police Agency and the Coast Guard regarding sex, age, manner of death, and cause of death. Analysis of the manner of death revealed that 3,971 cases (45.2%) were unnatural deaths, 3,679 cases (41.9%) were natural deaths, and 1,127 cases (12.8%) were unknown deaths. Among the unnatural deaths, the majority of the cases (1,740 cases, 43.8%) were accidents, 1,316 cases (33.1%) were suicide, 385 cases (9.7%) were homicide, and 530 cases (13.3%) were undetermined deaths. Among the unnatural deaths, the majority of the cases (1,575 cases, 39.7%) were trauma, followed by 793 cases (20.0%) of poisoning and 689 cases (17.4%) of asphyxia. Falling down was the major cause of death by trauma (737 cases, 46.8%). As a result of the classification of asphyxia based on previous study, strangulation was the major cause, with 538 cases (78.1%). Among the natural deaths, heart disease was the major cause (1,790 cases, 48.7%), followed by vascular disease (697 cases, 18.9%).

• The Korean Journal of Ecology
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• v.18 no.1
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• pp.179-188
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• 1995

Death patterns of gap-makers and changes of environmental factors in gaps formed by disturbance were studied in Pinus densiflora forests of Youngwol, Mt, Mansu, Mt. Songni, Uljin, and Mt, Obong in Korea. Death pattern of gap-makers showed that standing deat type was the most frequent in all the study areas. Longevity of Pinus densiflora was about 140 years, which was about half of that of the temperate deciduous broad-leaved trees. size of gaps were distributed from $20m^2$ to $235m^2$, more than 80% of those were gaps created by death of two or more trees. Relative light intensity and water content of soil in gap area were higher than those in non-gap area and those in the central part of gap were the highest.

• Proceedings of the Korean Environmental Sciences Society Conference
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• 2020.10a
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• pp.218-218
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• 2020

Astaxanthin, a natural antioxidant carotenoid, has been thought to provide health benefits by decreasing the risk of oxidative stress?related diseases. In the present study, we investigated the effect of an astaxanthin during the autophagic cell death induced by bisphenol A (BPA) which is known major environmental pollutants. We found that astaxanthin significantly blocked the autophagic cell death via inhibition of intracellular Reactive Oxygen Species (ROS) in normal human dermal fibroblasts. Astaxanthin significantly inhibited the phosphorylation mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) responsible for the expression of LC3-II and Beclin-1 in BPA-treated normal human dermal fibroblasts. We suggest that astaxanthin blocks autophagic cell death induced by BPA via the inhibition of ROS-mediated signaling events in human dermal fibroblasts.

• BMB Reports
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• v.51 no.8
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• pp.400-405
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• 2018

Chronic stress induces neuronal cell death, which can cause nervous system disorders including Parkinson's disease and Alzheimer's disease. In this study, we evaluated the neuroprotective effects of Clematis terniflora extract (CTE) against corticosterone-induced apoptosis in rat pheochromocytoma (PC12) cells, and also investigated the underlying molecular mechanisms. At concentrations of 300 and $500{\mu}g/ml$, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by $200{\mu}M$ corticosterone. CTE decreased the expression levels of endoplasmic reticulum (ER) stress proteins GRP78, GADD153, and mitochondrial damage-related protein BAD, suggesting that it downregulates ER stress evoked by corticosterone. Furthermore, our results suggested that these protective effects were mediated by the upregulation of p-AKT and p-ERK1/2, which are involved in cell survival signaling. Collectively, our results indicate that CTE can lessen neural damage caused by chronic stress.

• Journal of Plant Biotechnology
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• v.37 no.1
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• pp.57-66
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• 2010

Programmed cell death systems are important for an active type of cell deaths. Among them, a type of programmed cell death, autophagy is activated in cancer cells in response to multiple stresses and has been demonstrated to promote tumor cell survival and drug resistance. Thus, in the area of cancer, over the time frame form around the 1940s to date, of the 155 small molecules, 73% are other than "synthetic", with 47% actually being either "natural products" or "directly derived therefrom". Autophagy has multiple physiological functions in multicellular organisms, including protein degradation and organelle turnover. Genes and proteins that constitute the basic machinery of the autophagic process were first identified in the yeast system and some of their mammalian orthologues have been characterized as well. Numerous oncogenes, including Akt1, Bcl-2, NF1, PDPK1, class I PI3K, PTEN, and Ras and oncosuppressors, inculuding Bec-1, Bif-1, DAPK-1, p53 and UVRAG suppress or promote the autophagy pathway. Regulation of autophagy in tumors is governed by similar principles of the normal cells, only in a much more complicated manner, given the frequently observed abnormal PI3K activation in cancer and the multitude of interactions between the PI3K/AKT/mTOR pathway and other cell signaling cascades, often also deregulated in tumor cells. Autophagy induction by some anticancer agents underlines the potential utility of its induction as a new cancer treatment modality of development for natural medicines.