• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.5
• /
• pp.515-521
• /
• 1997

Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ($NF-_{\kappa}B$) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha($TNF{\alpha}$) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.

• The Korean Journal of Physiology and Pharmacology
• /
• v.15 no.6
• /
• pp.353-361
• /
• 2011

In this study, cyanidin-3-glucoside (C3G) fraction extracted from the mulberry fruit (Morus alba L.) was investigated for its neuroprotective effects against oxygen-glucose deprivation (OGD) and glutamate-induced cell death in rat primary cortical neurons. Cell membrane damage and mitochondrial function were assessed by LDH release and MTT reduction assays, respectively. A time-course study of OGD-induced cell death of primary cortical neurons at 7 days in vitro (DIV) indicated that neuronal death was OGD duration-dependent. It was also demonstrated that OGD for 3.5 h resulted in approximately 50% cell death, as determined by the LDH release assay. Treatments with mulberry C3G fraction prevented membrane damage and preserved the mitochondrial function of the primary cortical neurons exposed to OGD for 3.5 h in a concentration-dependent manner. Glutamate-induced cell death was more pronounced in DIV-9 and DIV-11 cells than that in DIV-7 neurons, and an application of $50{\mu}M$ glutamate was shown to induce approximately 40% cell death in DIV-9 neurons. Interestingly, treatment with mulberry C3G fraction did not provide a protective effect against glutamate-induced cell death in primary cortical neurons. On the other hand, treatment with mulberry C3G fraction maintained the mitochondrial membrane potential (MMP) in primary cortical neurons exposed to OGD as assessed by the intensity of rhodamine-123 fluorescence. These results therefore suggest that the neuroprotective effects of mulberry C3G fraction are mediated by the maintenance of the MMP and mitochondrial function but not by attenuating glutamate-induced excitotoxicity in rat primary cortical neurons.

• The Korean Journal of Applied Statistics
• /
• v.24 no.5
• /
• pp.769-789
• /
• 2011

The life table is a statistical model for life expectancy and reflects mortality experiences exposed to a particular group of people. The following three issues are prerequisite for constructing the life table : a selection of how to estimate the death probability from observed death rates, a graduation method to smooth irregularity of the death probabilities, and an extension method of the death probabilities for oldest-old ages. To construct the life table that is fittest to Korean mortality experiences, we examine five estimation methods such as Chiang's and Greville's for the death probability, three graduation techniques including Beer's and Greville's formulae, and twelve mathematical functions for the extension of death probabilities for oldest-old ages. We also propose a method to resolve the cross-over problem arising from construction the life table.

• Journal of Korean Academy of Fundamentals of Nursing
• /
• v.12 no.1
• /
• pp.91-100
• /
• 2005

Purpose: This research used quantitative research to identify differences in death consciousness between pre and post education. The study was also designed to further understanding of the effects of nursing education by using a qualitative analysis to examine hospice education experience. Method: This study a one group pre-post test design. Results: 1 The mean score for the students' death consciousness before the hospice education averaged $2.15{\pm}\;.33$, a medium level for death Consciousness. The Score after education was $2.25{\pm}\;.36$, that is, there was higher score for death consciousness after education. 2. The result of classification, giving their names and categorizing the experience of being in a coffin shown to be self-reflection, regret, recognition to death, death as discontinuation of life, the last closing from everything, death as a sad and cruel event, death as another world, specialist intuition of nursing. Conclusion: This research provided an opportunity for nursing students to consider death earnestly and realistically through hospice nursing education. We also discovered affirmative changes in the students' viewpoint of death, students who in future clinical practice may work with elders. We also found increases in motives to develop ability to present effective aid to dying patients.

• Journal of forensic and investigative science
• /
• v.3 no.1
• /
• pp.43-49
• /
• 2008

This study was conducted to analyze the current problems in completing death certificates and to identify the correct method for completing death certificates. Total 298 death certificates in A hospital from January to December in 2005 were reviewed. There was only 88 death certificates (29.5%) without an error. The frequency of the major errors were 8.7% in 'mechanism of death listed instead of cause of death', 9.4% in 'competing causes', and 11.4% in 'improper sequencing'. The frequency of minor errors were 99.3% in 'absence of time intervals', 19.5% in 'repetition of same cause', 18.8% in "more than 2 causes listed in same space". Errors were common in the completion of death certificates in the middle sized hospital setting. It is very important to complete death certificate accurately in practice. Education in undergraduate course and persistent training in internship and residency program will be needed.

• Biotechnology and Bioprocess Engineering:BBE
• /
• v.5 no.1
• /
• pp.40-43
• /
• 2000

Pyrrolidinedithiocarbamate (PDTC) and N-Acetylcysteine (NAC) are metal and nonmetal-chelating antioxidant which can induce rat and human smooth muscle cell death. When the smooth muscle cells from mouse aorta (MASMC) that we successfully cultured recently was exposed to PDTC and NAC in a normal serum state, the cells were induced to death by these compounds. However, PDTC did not induce the cell death in a serum depleted medium. This data suggests that certain factors in the serum may mediate the cytotoxic effect of PDTC. The metal chelator, Ca-EDTA blocked PDTC-induced cell death, but Cu-, Fe-, and Zn-EDTA did not block the PDTC-induced cell death. This data indicated that copper, iron, and zinc in the serum may lead to the cytotoxic effect of PDTC. Investigation of the intracellular zinc level in PDTC-induced smooth muscle cell death using the zinc probe dye N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide shows that only the muscle-containing layers of the arteries have higher level of zinc. As expected, PDTC increased the intracellular fluorescence level of the zinc. In agreement with these results, the addition of an exogenous metal, zinc, induced the vascular aortic smooth muscle cell death which led to an increased intracellular zinc level. We concluded that PDTC induced mouse aortic smooth muscle cell death required not only zinc level but also intracellular copper and iron level. The mechanism of this antioxidant to induce vascular smooth muscle cell death may provide a new strategy to prevent their proliferation in arteriosclerotic lesions.

• International Journal of Oral Biology
• /
• v.34 no.2
• /
• pp.97-103
• /
• 2009

L-trans-pyrrolidine-2,4-dicarboxylate (PDC) is a potent inhibitor of glutamate transporters. In our current study, we investigated whether the neuronal death induced by PDC involves mechanisms other than excitotoxicity in mixed mouse cortical cultures. Cortical cultures at 13-14 days in vitro were used and cell death was assessed by measuring the lactate dehydrogenase efflux into bathing media. Glutamate and PDC both induced neuronal death in a concentration-dependent manner but the neurotoxic effects of glutamate were found to be more potent than those of PDC. Treatment with 10, 100 and 200 ${\mu}$M PDC equally potentiated 50 ${\mu}$M glutamate-induced neuronal death. The neuronal death induced by 75 ${\mu}$M glutamate was almost abolished by treatment with the NMDA antagonists, MK-801 and AP-5, but was unaffected by NBQX (an AMPA antagonist), trolox (antioxidant), BDNF or ZVAD-FMK (a pan-caspase inhibitor). However, the neuronal death induced by 200 ${\mu}$M PDC was partially but significantly attenuated by single treatments with MK-801, AP-5, trolox, BDNF or ZVAD-FMK but not NBQX. Combined treatments with MK-801 plus trolox, MK-801 plus ZVAD-FMK or MK-801 plus BDNF almost abolished neuronal death, whereas combined treatments with trolox plus ZVADFMK, trolox plus BDNF or ZVAD-FMK plus BDNF did not enhance the inhibitory action of any single treatment with these drugs. These results demonstrate that the neuronal death induced by PDC involves not only in the excitotoxicity induced by the accumulation of glutamate but also the oxidative stress induced by free radical generation. This suggests that apoptotic neuronal death plays a role in PDCinduced oxidative neuronal injury.

• The Journal of the Korea Contents Association
• /
• v.12 no.7
• /
• pp.215-222
• /
• 2012

The purpose of this study was to examine the impact of education for welldying on the death anxiety and death reception of care workers who were most closely linked to death among workers who were engaged in senior welfare. It's basically meant to let care workers have a good understanding of death, death process and death-related factors to help elderly people close their life in a comfortable manner. The subjects in this study were the care workers who worked in J nursing home in the region of Gwangju. They received education in nine sessions, once a week, and the collected data were analyzed by the statistical package 15.0. The statistical analysis methods used in this study were reliability analysis, descriptive statistics analysis, t-test and ANOVA. The findings of the study were as follows: First, the welldying program participants showed a decrease in death anxiety. Second, the welldying program participants became more receptive to death.

• Journal of Ginseng Research
• /
• v.30 no.1
• /
• pp.1-7
• /
• 2006

Ceramide has been involved in celt death and acted as a lipid mediator of stress responses. Elevation of ceramide level was reported to occur in oxidative stress and lead to cell death in many cell types. This study was undertaken to elucidate a protective role of ginsenoside Rgl in cell death induced by oxidative stress. When LLC-PK1 cells were treated with $H_2O_2$ at a concentration of $400{\mu}M$ for 5 hr, cell death was observed and a released LDH activity indicative of cytotoxicity was Increased. $H_2O_2$ exposure to LLC-PK1 cells was shown to elevate the content of total ceramide by approximately 200% compared to control cells. Ceramide level was hypothesized to be a key to a reversal of cell death to survival. Ginsenoside Rgl at the concentrations ranging from 12.5 to $250{\mu}M$ protected LLC-PK1 cells from cell death induced by $H_2O_2\;at\;400{\mu}M$ for 5 hr, and decreased the ceramide level relative to $H_2O_2$. Ginsenoside Rgl inhibited neutral human ceramidase by 71% of controls, while sphingomyelinase was not inhibited. These results suggest that ginsenoside Rgl show the protection against cell death via the modulation of ceramide metabolism, and ceramide may be a promising therapeutic target for human diseases related to cell death.

• Korean Journal of Veterinary Research
• /
• v.44 no.3
• /
• pp.373-378
• /
• 2004

To help the interpretation of causes of death, it is critical that the background incidence of factors contributing to death be recorded and archived. Information was gathered from the control groups of 19 rat carcinogenicity studies. All cases of death occurring within the 2-year period were reviewed. Out of 1124 males and 1084 females, 720 male (64.1%) and 689 female (63.6%) decedents were recorded. There was no difference in the probability of survival between two sexes. Analysis of factors contributing to death revealed that 400 males (48.7%) had neoplastic changes, 189 males (23.0%) had non-neoplastic lesions, and 232 males (28.3%) died from unknown causes. In females, these figures were 627 (76.4%), 62 (7.6%) and 132 (16.0%), for neoplastic, non-neoplastic and unknown findings, respectively. It could be suggested that the risk of death by non-neoplastic reasons was higher in the males than in the females, whereas females were more likely to be affected by tumours. In the neoplastic causes of death, pituitary tumours were the most common in both sexes, followed by mammary tumours in females, and haemopoietic tumours in males. In non-neoplastic cause of death, renal diseases were the most common in both sexes, followed by skin diseases and cardiovascular diseases in males, and skin diseases and poditis in males. A relatively large number of animals (28.3% in males and 16.0% in females) were found dead, without any significant clinical or histologically identifiable cause. Most of the animals with pituitary tumours were killed in extremis and the proportion of females (70.1%) being greater than males (46.8%). There were no case which died by accident, and also only minimal incidence which died by bleeding procedures.