• Journal of Preventive Medicine and Public Health
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• 제46권5호
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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.

• Clinical and Experimental Reproductive Medicine
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• 제41권3호
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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.

• 한국환경과학회지
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• 제30권7호
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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.

• BMB Reports
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• 제56권3호
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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.

• 한국게임학회 논문지
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• 제16권1호
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• pp.33-42
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• 2016

본 연구의 목적은 로그라이크 게임에서 파생된 영속적 죽음의 매커니즘을 고찰하고 해당 매커니즘이 가져오는 독특한 플레이 양식을 고찰하는 데 있다. 이를 위해 게임에서의 일반적인 죽음의 과정과 영속적 죽음의 과정을 비교 분석했으며 이후 영속적 죽음의 과정이 게임의 플레이와 리플레이에 미치는 결과를 살펴보았다. 영속적 죽음은 캐릭터의 부활 가능성이 없다는 점에서 극도의 긴장을 유발하는 플레이 사이클을 구축한다. 이러한 치명적 패널티는 플레이어로 하여금 죽음을 유예하기 위한 선택적 플레이를 야기하지만 이후 플레이어의 숙련된 스킬을 바탕으로 자신의 선택을 수정하고 대안적 세계를 구축해 나가는 리플레이로 이어진다. 신중한 선택과 대안적 플레이를 요하는 영속적 죽음의 매커니즘을 통해 진지한 고민을 담을 수 있는 게임의 새로운 가능성을 모색할 수 있을 것이다.

• 응용통계연구
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• 제20권3호
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• pp.449-458
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• 2007

양극성 장애 (bipolar disorder)는 조증 삽화 (manic episode)와 우울증 삽화 (depression episode)를 반복적으로 경험하는 기분장애이다. 양극성 장애환자에게 우울증은 조증보다 심각한 결과를 가져오며, 치료의 효과를 측정하기도 어렵다고 알려져 있다. 본 연구의 목적은 우울증(depression) 상태에 있는 환자들을 대상으로 항우울제를 사용하여 정상 (normal) 상태로 전환했을 때, 약물의 장기 사용으로 일어날 수 있는 조증 (mania)과 같은 부작용을 통제하고자 한다. 이를 위해 정상 상태에서 조증으로 전환하는데 소요되는 시간의 분포를 추정한다. 본 연구에서는 세 가지 방법, 모수적, 비모수적 그리고 준모수적 방법을 차례대로 적용하였다. 특히 기분 전환의 흐름을 파악하기 위해 3단계 모형을 사용하였다. 예를 들어, Illness-Death 모형하에서 기분 전환의 발생시점에 대한 분포를 추정하기 위해 계수 과정에 의해 기분 전환에 대한 과정을 모형화하였다.

• BMB Reports
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• 제50권10호
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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.

• 보험의학회지
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• 제3권1호
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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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• 제16권16호
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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.

• Journal of Preventive Medicine and Public Health
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• 제37권4호
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• pp.345-352
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• 2004

Objectives : Previous studies showed that death certification by physicians was an important predictor to improve the quality of death certificate data in South Korea. This study was conducted to examine the proportion of death certificates issued by physicians and associated factors in South Korea from 1990 to 2002. Methods : Data from 3,110,883 death certificates issued between 1990 and 2002, available to the public from the National Statistical Office of Korea, were used to calculate the proportion of death certificates issued by physicians and to examine associated factors with logistic regression analysis. Results : The overall proportion of death certificates issued by physicians increased from 44.6% in 1990 to 77.6% in 2002 (mean: 63.5%). However, the proportion was greatly influenced by the deceased's age. In 2002, more than 90% of the deceased aged 51 or less were certified by physicians. A higher proportion was found among deceased who had tertiary education (college or higher) living in more developed urban areas. Conclusion : The information regarding the cause of death for younger, well-educated deceased in urban areas of South Korea may show a higher level of accuracy. Epidemiologic research using information on causes of death may well benefit from the continually increasing proportion of death certificates issued by physicians in the future in South Korea.