• Journal of Preventive Medicine and Public Health
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• v.51 no.3
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• pp.163-168
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• 2018

Objectives: Due to their developmental characteristics, adolescents have a higher probability than other age groups of experiencing injuries caused by accidents, violence, and intentional self-harm. The severity and characteristics of injuries vary by the intentionality and mechanism of injury; therefore, there is a need for a national-level estimate of the scale and the severity of injuries in adolescents that takes these factors into account. Methods: By using data from the Emergency Department-based Injury In-depth Surveillance Data, National Emergency Department Information System, the Korean National Hospital Discharge In-depth Injury Survey, and cause of death statistics, we calculated the emergency department (ED) visit rate, hospitalization rate, and death rate of injuries per 100 000 adolescents for each injury mechanism. The calculated rates were used to generate the injury pyramid ratio (ratio of death rate to hospitalization rate to ED visit rate) to visualize the scale and the severity of the injury. Results: The mortality rate in adolescents due to injury was 10/100 000; the corresponding rates for hospitalization and ED visits were 1623 and 4923, respectively, resulting in an injury pyramid ratio with the general pyramid form, with a 1:162:492 ratio of deaths to hospitalizations to ED visits. The mortality rate due to suicide/intentional self-harm was 5/100 000, while 35 were hospitalized for this reason and 74 made ED visits. The pyramid ratio of 1:7:15 for intentional self-harm/suicide showed a steep pyramidal form, indicating considerable lethality. The mortality rate due to motor vehicle collisions (MVCs) was 3/100 000; 586 were hospitalized for this reason, while 1023 made ED visits. The pyramid ratio of 1:195:341 for MVCs showed a gradual pyramid form, indicating that the lethality was low and the scale of injury was high. Conclusions: The main categories of injuries in adolescents were visualized in pyramid form, contributing to an understanding of the scale of each injury by mechanism in terms of levels of death, hospitalization, and ED visits. These findings will be helpful for understanding how to prioritize injuries in adolescents.

• BMB Reports
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• v.35 no.1
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• pp.67-86
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• 2002

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of $Ca^{2+}$ and $Na^+$ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

• Journal of Trauma and Injury
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• v.21 no.2
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• pp.78-84
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• 2008

Purpose: Recently, the incidence of blast injury has been on the increase worldwide. The purpose of this study was to evaluate and analyze blast injuries in South Korea. Methods: This was a retrospective multi-center study of blast injuries in three tertiary military centers. The medical records of patients with blast injuries from January 2003 to December 2007 were reviewed. The injury severity was evaluated according to the Injury Severity Score (ISS), the Revised Trauma Score (RTS), and the Trauma Score and the Injury Severity Score (TRISS). Results: This study revealed epidemiological data of blast injury in the three tertiary military hospital. A total of 94 cases of blast injury had occurred. Various body regions were involved. The most frequently injured site was the upper extremity (52.1%). The mechanisms for the blast injuries were primary (41.5%), secondary (74.5%), tertiary (7.4%), and quaternary (29.8%). The mean injury-to-hospital arrival time was $3.2{\pm}1.7hour$. The rate of admission was 88.3%, and the rate of ICU admission was 32.5%. Thirty-six (36) cases required an emergency operation. Most were performed by an Orthopedist (55.6%), an Ophthalmologist (19.4%), or a general surgeon (13.9%). The mortality rate from blast injury was 4.3%. Conclusion: This was the first paper to present data on the type of injury, the site of injury, the cause of death, and the mortality from blast injury in South Korea. Chest injury, brain injury, tertiary injury mechanisms, $ISS{\geq_-}16$, and a Maximal Abbreviated Injury Scale Score $(ABI){\geq_-}4$ were significantly associated with death.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.2
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• pp.173-183
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• 2020

An in vitro model for ischemia/reperfusion injury has not been well-established. We hypothesized that this failure may be caused by serum deprivation, the use of glutamine-containing media, and absence of acidosis. Cell viability of H9c2 cells was significantly decreased by serum deprivation. In this condition, reperfusion damage was not observed even after simulating severe ischemia. However, when cells were cultured under 10% dialyzed FBS, cell viability was less affected compared to cells cultured under serum deprivation and reperfusion damage was observed after hypoxia for 24 h. Reperfusion damage after glucose or glutamine deprivation under hypoxia was not significantly different from that after hypoxia only. However, with both glucose and glutamine deprivation, reperfusion damage was significantly increased. After hypoxia with lactic acidosis, reperfusion damage was comparable with that after hypoxia with glucose and glutamine deprivation. Although high-passage H9c2 cells were more resistant to reperfusion damage than low-passage cells, reperfusion damage was observed especially after hypoxia and acidosis with glucose and glutamine deprivation. Cell death induced by reperfusion after hypoxia with acidosis was not prevented by apoptosis, autophagy, or necroptosis inhibitors, but significantly decreased by ferrostatin-1, a ferroptosis inhibitor, and deferoxamine, an iron chelator. These data suggested that in our SIR model, cell death due to reperfusion injury is likely to occur via ferroptosis, which is related with ischemia/reperfusion-induced cell death in vivo. In conclusion, we established an optimal reperfusion injury model, in which ferroptotic cell death occurred by hypoxia and acidosis with or without glucose/glutamine deprivation under 10% dialyzed FBS.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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• pp.139-145
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• 2009

The purpose of this study was to evaluate the effects of the water extract of Samultang (SMT), a Chinese herb, on apoptotic cell death by $H_2O_2$-induced oxidative stress in SK-N-M C cells. A nuclear fragmentation was observed via fluorescence imaging 12 h after exposure to 30 ${\mu}M$ $H_2O_2$ and DNA laddering was detected via agarose electrophoresis gel. In addition, increases in sub-G1 phase and cleavage of the PARP protein were observed. However, treatment with SMT for 2 h prior to $H_2O_2$ exposure significantly reduced apoptotic cell death induced by incubation with 30 ${\mu}M$ $H_2O_2$ in SK-N-MC cells. Pre-incubation with water extract of SMT for 2 h prevented the $H_2O_2$-induced decrease in mitochondrial transmembrane potential. SMT also attenuated the increase in caspase-3 activity and the breakdown of PARP protein caused by $H_2O_2$-induced oxidative stress. These results suggest that the water extract of SMT provides inhibition of apoptotic cell death against oxidative injury in SK-N-MC cells.

• Molecules and Cells
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• v.37 no.4
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• pp.345-355
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• 2014

Mitigating secondary delayed neuronal injury has been a therapeutic strategy for minimizing neurological symptoms after several types of brain injury. Interestingly, secondary neuronal loss appeared to be closely related to functional loss and/or death of astrocytes. In the brain damage induced by agonists of two glutamate receptors, N-ethyl-D-aspartic acid (NMDA) and kainic acid (KA), NMDA induced neuronal death within 3 h, but did not increase further thereafter. However, in the KA-injected brain, neuronal death was not obviously detectable even at injection sites at 3 h, but extensively increased to encompass the entire hemisphere at 7 days. Brain inflammation, a possible cause of secondary neuronal damage, showed little differences between the two models. Importantly, however, astrocyte behavior was completely different. In the NMDA-injected cortex, the loss of glial fibrillary acidic protein-expressing ($GFAP^+$) astrocytes was confined to the injection site until 7 days after the injection, and astrocytes around the damage sites showed extensive gliosis and appeared to isolate the damage sites. In contrast, in the KA-injected brain, $GFAP^+$ astrocytes, like neurons, slowly, but progressively, disappeared across the entire hemisphere. Other markers of astrocytes, including $S100{\beta}$, glutamate transporter EAAT2, the potassium channel Kir4.1 and glutamine synthase, showed patterns similar to that of GFAP in both NMDA- and KA-injected cortexes. More importantly, astrocyte disappearance and/or functional loss preceded neuronal death in the KA-injected brain. Taken together, these results suggest that loss of astrocyte support to neurons may be a critical cause of delayed neuronal death in the injured brain.

• Journal of Veterinary Clinics
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• v.18 no.4
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• pp.358-362
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• 2001

Brain dead (BD) patients remain the largest source of solid organs for transplantation. BD has shown to decrease graft function and survival in rodent models. The aim of this study was to evaluate how brain death affects graft viability in the donor and kidney tolerance to cold preservation as assessed by survival in a canine transplantation. 13 Beagle dogs were used for the study. Brain death was induced by the sudden inflation of a subdural balloon catheter with continuous monitoring of arterial blood pressure and eletroencephalographic activity (n=3). Sixteen hours after conformation of brain death, kidney graft were retrieved (n=6). Non-BD donors served as controls (n=4). All kidneys were flushed with University of Wisconsin (UW) solution and preserved for 24 hours at 4$^{\circ}C$ before transplantation. Recipient survival rates, serum creatinine level were analyzed. Brain death induced the well-known Cushing reaction with a severe increase in blood pressure and tachycardia. Thereafter, cardiac function returned progressively to baseline within 8 hours and remained stable until the end of the experiment. All of dogs in both group transplanted were survived until 7 days (100%), and the kidneys showed functional early rejection at 8.3$\pm$0.5 days and 8.5$\pm$0.5 days after transplantation, in BD and allograft group, respectively. BD kidneys were functionally similar to control kidneys for 7 days after transplantated. Brain death has no deleterious effect on preservation injury and survival of dog kidney transplantation, although it induces changes in hemodynamic parameters. This study reveals that kidneys from BD donors do not exhibit more ischemia reperfusion injury, and support good early function and survival.

• Journal of Environmental Health Sciences
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• v.49 no.3
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• pp.149-158
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• 2023

Background: Injury is one of the major health problems in South Korea. Few studies have evaluated both intentional and unintentional injury when investigating the association between exposure to air pollutants and injury. Objectives: We aimed to explore the association between short-term exposure to ambient air pollution and years of life lost (YLLs) due to injury. Methods: Data on daily YLLs for 2002~2019 were obtained from the the Death Statistics Database of the Korean National Statistical Office. This study estimated short-term exposure to particulate matter with an aerodynamic diameter of <10 ㎛ (PM₁₀), particulate matter with an aerodynamic diameter of <2.5 ㎛ (PM_2.5), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), and ozone (O₃). This time series study was conducted using a generalized additive model (GAM) assuming a Gaussian distribution. We also evaluated a delayed effect of ambient air pollution by constructing a lag structure up to seven days. The best-fitting lag was selected based on smallest generalized cross validation (GCV) value. To explore effect modification by intentionality of injury (i.e., intentional injury [self-harm, assault] and unintentional injury), we conducted stratified subgroup analyses. Additionally, we stratified unintentional injury by mechanism (traffic accident, fall, etc.). Results: During the study period, the average daily YLLs due to injury was 307.5 years. In the intentional injury, YLLs due to self-harm and assault showed positive association with air pollutants. In the unintentional injury, YLLs due to fall, electric current, fire and poisoning showed positive association with air pollutants, whereas YLLs due to traffic accident, mechanical force and drowning/submersion showed negative associations with air pollutants. Conclusions: Injury is recognized as preventable, and effective strategies to create a safe society are important. Therefore, we need to establish strategies to prevent injury and consider air pollutants in this regard.

• Journal of Chest Surgery
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• v.27 no.3
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• pp.255-258
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• 1994

I have experienced with 6 cases traumatic injury of diaphragm from May 1991 to October 1993 at the Youngdong Hospital in Tonghae. This cases included 4 penetrating injuries and 2 nonpenetrating injuries. Associated injuries occurred 4 cases and 2 cases occurred stomach herniation. All cases, operative treatment were done. Result of this treatment cases were good. Complications included 1 early death and only 1 wound infection. Cause of death was related to associated injury.

• Journal of Preventive Medicine and Public Health
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• v.29 no.2 s.53
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• pp.227-238
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• 1996

This study was conducted to evaluate the accuracy of the official death registry in rural area. The base data used for the study was 379 deaths registered during the period of 1993 and 1994 in 4 rural townships of Chonnam province. The interview survey for cause-of-death was performed on the next of kin and/or neighbor. Additional medical informations were collected from hospitals and medical insurance associations for the purpose of verification. The underlying cause-of-death of 278 cases presumed by the survey was compared to the cause on official death registry. There was a prominent disagreement of cause-of-death between the survey data and the registry data(agreement rate: $38.9\sim44.6%$, according to disease classification method). These results may be caused by extremely low rates of physicians' certification, which were mostly confined to the poisoning and injury. Symptoms, signs, and ill defined conditions on death registry could be classified into circulatory disease(32.3%), neoplasm(21.2%), digestive disease(7.1%), injury and poisoning(7.1%) and so on. These results suggest that careful attention and verification be required on utilization of death registry data in rural area.