• Clinical and Experimental Pediatrics
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• v.57 no.3
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• pp.135-139
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• 2014

Purpose: Adult Korean patients on chronic dialysis have a 9-year survival rate of 50%, with cardiovascular problems being the most significant cause of death. The 2011 annual report of the North American Pediatric Renal Trials and Collaborative Studies group reported 3-year survival rates of 93.4% and relatively poorer survival in younger patients. Methods: In this study, we have reviewed data from Korean Pediatric Chronic Kidney Disease Registry from 2002 to 2010 to assess survival rates and causes of death in Korean children on chronic dialysis. Results: The overall estimated patient survival rates were 98.4%, 94.4%, and 92.1% at 1, 3, and 5 years, respectively. No significant difference was observed in survival rates between patients on peritoneal dialysis and those on hemodialysis. Patients for whom dialysis was initiated before 2 years of age (n=40) had significantly lower survival rates than those for whom dialysis was initiated at 6-11 years of age (n=140). In all, 26 patients had died; the mortality rate was 19.9 per 1,000 patient years. The most common causes of death were infections and comorbidities such as malignancy and central nervous system (CNS) or liver diseases. Conclusion: The outcomes observed in this study were better than those observed in adults and comparable to those observed in pediatric studies in other countries. To improve the outcomes of children on chronic dialysis, it is necessary to prevent dialysis-related complications such as infection, congestive heart failure, or CNS hemorrhage and best control treatable comorbidities.

• Journal of Preventive Medicine and Public Health
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• v.46 no.5
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• pp.261-270
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• 2013

Objectives: This study investigated the socio-demographic characteristics and medical causes of death among meteorological disaster casualties and compared them with deaths from all causes. Methods: Based on the death data provided by the National Statistical Office from 2000 to 2011, the authors analyzed the gender, age, and region of 709 casualties whose external causes were recorded as natural events (X330-X389). Exact matching was applied to compare between deaths from meteorological disasters and all deaths. Results: The total number of deaths for last 12 years was 2 728 505. After exact matching, 642 casualties of meteorological disasters were matched to 6815 all-cause deaths, which were defined as general deaths. The mean age of the meteorological disaster casualties was 51.56, which was lower than that of the general deaths by 17.02 (p<0.001). As for the gender ratio, 62.34% of the meteorological event casualties were male. While 54.09% of the matched all-cause deaths occurred at a medical institution, only 7.6% of casualties from meteorological events did. As for occupation, the rate of those working in agriculture, forestry, and fishery jobs was twice as high in the casualties from meteorological disasters as that in the general deaths (p<0.001). Meteorological disaster-related injuries like drowning were more prevalent in the casualties of meteorological events (57.48%). The rate of amputation and crushing injury in deaths from meteorological disasters was three times as high as in the general deaths Conclusions: The new information gained on the particular characteristics contributing to casualties from meteorological events will be useful for developing prevention policies.

• 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.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.97-107
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• 2014

The placenta is a temporary fetomaternal organ capable of supporting fetal growth and development during pregnancy. In particular, abnormal development and dysfunction of the placenta due to cha nges in the proliferation, differentiation, cell death, and invasion of trophoblasts induce several gynecological diseases as well as abnormal fetal development. Autophagy is a catalytic process that maintains cellular structures by recycling building blocks derived from damaged microorganelles or proteins resulting from digestion in lysosomes. Additionally, autophagy is necessary to maintain homeostasis during cellular growth, development, and differentiation, and to protect cells from nutritional deficiencies or factors related to metabolism inhibition. Induced autophagy by various environmental factors has a dual role: it facilitates cellular survival in normal conditions, but the cascade of cellular death is accelerated by over-activated autophagy. Therefore, cellular death by autophagy has been known as programmed cell death type II. Autophagy causes or inhibits cellular death via the other mechanism, apoptosis, which is programmed cell death type I. Recently, it has been reported that autophagy increases in placenta-related obstetrical diseases such as preeclampsia and intrauterine growth retardation, although the mechanisms are still unclear. In particular, abnormal autophagic mechanisms prevent trophoblast invasion and inhibit trophoblast functions. Therefore, the objectives of this review are to examine the characteristics and functions of autophagy and to investigate the role of autophagy in the placenta and the trophoblast as a regulator of cell death.

• BMB Reports
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• v.56 no.3
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• pp.166-171
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• 2023

Monocytes are peripheral leukocytes that function in innate immunity. Excessive triglyceride (TG) accumulation causes monocyte death and thus can compromise innate immunity. However, the mechanisms by which TG mediates monocyte death remain unclear to date. Thus, this study aimed to elucidate the mechanisms by which TG induces monocyte death. Results showed that TG induced monocyte death by activating caspase-3/7 and promoting poly (ADP-ribose) polymerase (PARP) cleavage. In addition, TG induced DNA damage and activated the ataxia telangiectasia mutated (ATM)/checkpoint kinase 2 and ATM-and Rad3-related (ATR)/checkpoint kinase 1 pathways, leading to the cell death. Furthermore, TG-induced DNA damage and monocyte death were mediated by caspase-2 and -8, and caspase-8 acted as an upstream molecule of caspase-2. Taken together, these results suggest that TG-induced monocyte death is mediated via the caspase-8/caspase-2/DNA damage/executioner caspase/PARP pathways.

• Journal of Korea Game Society
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• v.16 no.1
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• pp.33-42
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• 2016

The Purpose of this study is to analyze the mechanism of permanent death and playing aspects in Rogue-like games. The death in digital game is not only punishment of failure, but reward for player's growth. However the mechanism of permanent death which does not allow to resurrect is critical penalty for players and causes play-cycle with high anxiety. In the mechanism of permanent death, players do critical play to evade the death. But when they replay the game they modify their unethical choices to build alternative game world. Through the mechanism of permanent death which demands critical and alternative play, it could be possible to find the way to design games with serious choice.

• The Korean Journal of Applied Statistics
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• v.20 no.3
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• pp.449-458
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• 2007

Bipolar disorder, also known as manic-depressive illness, is a brain disorder that causes unusual shifts in person's mood, energy, and ability to function. Compared with manic episode, the depression episode causes more serious results such as restless, loss of interest or pleasure, or thoughts of death or suicide and the cure rate of depression episode is lower than that of manic episode. Furthermore, a long term use of antidepressants in bipolar patients may result in manic episode. Our interest is to investigate the effect of antidepressant on switch of moods of bipolar patients and to estimate the transition probabilities of switch between moods, depression and (hypo) manic. In this study, three approaches are applied in terms of multi state model. Parametric model is applied using left censoring data and nonparametric model is implemented under illness-death model with counting process. In order to estimate the effect of covariates, a multiplicative model is used. These all methods have similar results.

• BMB Reports
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• v.50 no.10
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• pp.510-515
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• 2017

Triglyceride (TG) accumulation causes macrophage cell death, which affects the development of atherosclerosis. Here, we examined whether caspase-2 is implicated in TG-induced macrophage cell death. We found that caspase-2 activity is increased in TG-treated THP-1 macrophages, and that inhibition of caspase-2 activity drastically inhibits TG-induced cell death. We previously reported that TG-induced macrophage cell death is triggered by caspase-1, and thus investigated the relationship between caspase-2 and caspase-1 in TG-induced macrophage cell death. Inhibition of caspase-2 activity decreased caspase-1 activity in TG-treated macrophages. However, caspase-1 inhibition did not affect caspase-2 activity, suggesting that caspase-2 is upstream of caspase-1. Furthermore, we found that TG induces activation of caspase-3, -7, -8, and -9, as well as cleavage of PARP. Inhibition of caspase-2 and -1 decreased TG-induced caspase-3, -7, -8, and -9 activation and PARP cleavage. Taken together, these results suggest that TG-induced macrophage cell death is mediated via the caspase-2/caspase-1/apoptotic caspases/PARP pathways.

• The Journal of the Korean life insurance medical association
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• v.3 no.1
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• pp.269-273
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• 1986

We have examined 5,304 cases of claims by death that had occured for recent three years from January, 1983 to November, 1985 in Dae han kyoyuk Ins. Co. As a result, we came to following conclusions: 1. The total numbers of the deaths are increased for three years, but the deaths, classifying by medical examinations are decreased. 2. The great part of the death were due to Accident death(27.7%), occupied Number 1, malignant neoplasm(23.9%) Number 2 and Circulatory system disease(23.9%), which were the main canses of death in the insured people. 3. With age, section ranging from 30-39 years of death cases took extremely large portions by 35.2%. 4. For the period elapsed, the deaths within 2 years to ander 3 years, 18.6%, above 6 years, 18.6%, thus the period elapsed was longer more and more as years go. 5. By the deaths of malignant neoplasm, hepatoma in male and gastric cancer in female were important causes of death.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.16
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• pp.7261-7266
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• 2015

Breast cancer, the most common cancer in the women, is the leading cause of death. Necrotic signaling pathways will enable targeted therapeutic agents to eliminate apoptosis-resistant cancer cells. In the present study, the effect of shikonin on the induction of cell necroptosis or apoptosis was evaluated using the T-47D breast cancer cell line. The cell death modes, caspase-3 and 8 activities and the levels of reactive oxygen species (ROS) were assessed. Cell death mainly occurred through necroptosis. In the presence of Nec-1, caspase-3 mediated apoptosis was apparent in the shikonin treated cells. Shikonin stimulates ROS generation in the mitochondria of T-47D cells, which causes necroptosis or apoptosis. Induction of necroptosis, as a backup-programmed cell death pathway via ROS stimulation, offers a new strategy for the treatment of breast cancer.