• The Journal of Internal Korean Medicine
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• v.40 no.3
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• pp.425-442
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• 2019

Objectives: This study aimed to reveal the pharmacological properties of the newly prescribed herbal mixture, Chenmadansamgamibokhap-tang(CDBT), against hypoxia-induced neuronal cell injury (especially mouse hippocampal neuronal cell line, HT-22 cells) and their corresponding mechanisms. Methods: A cell-based in vitro experiment, in which a hypoxia condition induced neuronal cell death, was performed. Various concentrations of the CDBT were pre-treated to the HT-22 cells for 4 h before 18 h in the hypoxia chamber. The glial cell BV-2 cells were stimulated with $IFN{\gamma}$ and LSP to produce inflammatory cytokines and reactive oxygen species. When the neuronal HT-22 cells were treated with this culture solution, the drug efficacy against neuronal cell death was examined. Results: CDBT showed cytotoxicity in the normal condition of HT-22 cells at a dose of $125{\mu}g/mL$ and showed a protective effect against hypoxia-induced neuronal cell death at a dose of $31.3{\mu}g/mL$. CDBT prevented hypoxia-induced neuronal cell death in a dose-dependent manner in the HT-22 cells by regulating $HIF1{\alpha}$ and cell death signaling. CDBT prevented neuronal cell death signals and DNA fragmentation due to the hypoxia condition. CDBT significantly reduced cellular oxidation, cell death signals, and caspase-3 activities due to microglial cell activations. Moreover, CDBT significantly ameliorated LPS-induced BV-2 cell activation and evoked cellular oxidation through the recovery of redox homeostasis. Conclusions: CDBT cam be considered as a vital therapeutic agent against neuronal cell deaths. Further studies are required to reveal the other functions of CDBT in vivo or in the clinical field.

• Journal of Trauma and Injury
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• v.18 no.2
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• pp.119-126
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• 2005

Background: Blunt thoracic trauma in children has a high morbidity and mortality. In this study, we assessed the significance of the injury pattern, mechanism and initial status in emergency department on severity and prognosis in pediatric blunt thoracic trauma patients. Method: We retrospectively reviewed medical records and chest X-ray and CT images of 111 pediatric blunt thoracic trauma patients from October 2000 to June 2005. Data recorded age, gender, season, injury mechanism, injury pattern, associated injury, length of hospital stay and cause of death. Result: Of all 111 patients, 68 patients were injured by motor vehicle accidents, 30 were falls, 5 were motorcycle accidents, 3 were sports accidents and 5 were miscellaneous. In thoracic trauma, single injury of lung contusion were 35 patients and 32 patients had multiple thoracic injuries. Hospital stay in school age group were longer than preschool age group. The causes of death were brain injury in 9, respiratory distress in 4, and hypovolemic shock in 2 patients. Emergently transfused and mechanically ventilated patients had higher mortality rates than other patients. Patients required emergency operation and patients with multiple thoracic injuries had higher mortality rates. Conclusion: In this study, patients with combined injury, emergency transfusion, mechanical ventilation, emergency operation, multiple injuries in chest X-ray had higher mortality rates. Therefore in these pediatric blunt thoracic trauma patients, accurate initial diagnosis and proper management is required.

• BMB Reports
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• v.53 no.6
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• pp.311-316
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• 2020

Cholestasis is a condition in which the bile duct becomes narrowed or clogged by a variety of factors and bile acid is not released smoothly. Bile acid-induced liver injury is facilitated by necrotic cell death, neutrophil infiltration, and inflammation. Metformin, the first-line treatment for type 2 diabetes, is known to reduce not only blood glucose but also inflammatory responses. In this study, we investigated the effects of metformin on liver injury caused by cholestasis with bile acid-induced hepatocyte injury. Static bile acid-induced liver injury is thought to be related to endoplasmic reticulum (ER) stress, inflammatory response, and chemokine expression. Metformin treatment reduced liver injury caused by bile acid, and it suppressed ER stress, inflammation, chemokine expression, and neutrophil infiltration. Similar results were obtained in mouse primary hepatocytes exposed to bile acid. Hepatocytes treated with tauroursodeoxycholic acid, an ER stress inhibitor, showed inhibition of ER stress, as well as reduced levels of inflammation and cell death. These results suggest that metformin may protect against liver injury by suppressing ER stress and inflammation and reducing chemokine expression.

• Proceedings of the PSK Conference
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• 2003.10a
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• pp.104-105
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• 2003

Hypoxic-ischemic (H-I) encephalopathy in the prenatal and perinatal period is a major cause of morbidity and mortality and often results in cognitive impairment, seizures, and motor impairment (cerebral palsy). Many studies of neonatal H-I brain injury have utilized the well characterized Levine model in which unilateral carotid ligation is followed by exposure to hypoxia. (omitted)

• Safety and Health at Work
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• v.1 no.2
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• pp.107-111
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• 2010

This paper provided a brief summary of the current strategic goals, activities, and impacts of the NIOSH (National Institute for Occupational Safety and Health) occupational injury research program. Three primary drivers (injury database, stakeholder input, and staff capacity) were used to define NIOSH research focuses to maximize relevance and impact of the NIOSH injury-prevention-research program. Injury data, strategic goals, program activities, and research impacts were presented with a focus on prevention of four leading causes of workplace injury and death in the US: motor vehicle incidents, falls, workplace violence, and machine and industrial vehicle incidents. This paper showcased selected priority goals, activities, and impacts of the NIOSH injury prevention program. The NIOSH contribution to the overall decrease in fatalities and injuries is reinforced by decreases in specific goal areas. There were also many intermediate outcomes that are on a direct path to preventing injuries, such as new safety regulations and standards, safer technology and products, and improved worker safety training. The outcomes serve as an excellent foundation to stimulate further research and worldwide partnership to address global workplace injury problems.

• Journal of Trauma and Injury
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• v.18 no.2
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• pp.101-106
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• 2005

Purpose: The number of the deceased from free-fall is increasing nowadays. Free-fall comes to a great social problem in that even the survivor will be suffering for cord injury or brain injury, and so on. We analyzed the cases of free-fall patients to find out whether the injury severity is mainly correlated with the height of fall. Methods: We retrospectively investigated the characteristics of patients, who fall from the height above 2m from January 2000 to August 2004. We excluded the patients who transferred to other hospital, transferred from other hospital, and not known the height of fall. 145 patients were evaluated. Variables included in data analysis were age, height of fall, injury severity score (ISS), the being of barrier, and the survival or not. To find out the correlation between height of fall and death, we used receive operating characteristics (ROC) curve analysis. Results: The mean age of patients was $36.5{\pm}19.4$ years old. 110 were male and 35 were female. Mean height of fall was $11.1{\pm}8.5m$. 51 patients (35.2%) were died and 30 patients of them (58.9%) got emergency room on dead body. The mean height of fall is $8.9{\pm}5.8m$ for 94 survivors and $15.2{\pm}11.0m$ for the 51 deceased (p<0.001). The area under the ROC curve was 0.646, which means the height of fall was not adequate factor for predicting for death. At 13.5m, as cut?off value, sensitivity is 52.9%, specificity is 86.2%, positive predictive value is 67.5% and negative predictive value is 77.1%. There were statistical differences in mortality rate and ISS between 'below 13.5m group' and 'above 13.5m group', but there was not statistical difference in head and neck AIS. Conclusion: The height of fall is not adequate factor for prediction of death. So other factors like intoxication or not, the being of barrier or protection device need to be evaluated for predicting of free-fall patient's death.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.2
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• pp.65-71
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• 2003

Increasing evidences suggest that ischemia-induced vascular damage is an integral step in the cascade of the cellular and molecular events initiated by cerebral ischemia. In the present study, employing a mouse brain endothelioma-derived cell line, bEnd.3, and oxygen-glucose deprivation (OGD) as an in vitro stroke model, the role of nuclear factor kappa B (NF-${\kappa}B$) activation during ischemic injury was investigated. OGD was found to activate NF-${\kappa}B$ and to induce bEnd.3 cell death in a time-dependent manner. OGD phosphorylated neither 32 Ser nor 42 Tyr of $I{\kappa}B{\alpha}$. OGD did not change the amount of $I{\kappa}B{\alpha}$. The extents of OGD-induced cell death after 8 h, 10 h, 12 h and 14 h of OGD were 10%, 35%, 60% and 85%, respectively. Reperfusion following OGD did not cause additional cell death, indicating no reperfusion injury after ischemic insult in cerebral endothelial cells. Three known as NF-${\kappa}B$ inhibitors, including pyrrolidine dithiocarbamate (PDTC) plus zinc, aspirin and caffeic acid phenethyl ester (CAPE), inhibited OGD-induced NF-${\kappa}B$ activation and increased OGD-induced bEnd.3 cell death in a dose dependent manner. There were no changes in the protein levels of bcl-2, bax and p53 which are modulated by NF-${\kappa}B$ activity. These results suggest that NF-${\kappa}B$ activation might be a protective mechanism for OGD-induced cell death in bEnd.3.

• Journal of Trauma and Injury
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• v.34 no.4
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• pp.225-232
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• 2021

Purpose: Trauma is the top cause of death in people under 45 years of age. Deaths from severe trauma can have a negative economic impact due to the loss of people belonging to socio-economically active age groups. Therefore, efforts to reduce the mortality rate of trauma patients are essential. The purpose of this study was to investigate preventable mortality in trauma patients and to identify factors and healthcare-related challenges affecting mortality. Ultimately, these findings will help to improve the quality of trauma care. Methods: We analyzed the deaths of 411 severe trauma patients who presented to Gachon University Gil Hospital regional trauma center in South Korea from January 2015 to December 2017, using an expert panel review. Results: The preventable death rate of trauma patients treated at the Gachon University Gil Hospital regional trauma center was 8.0%. Of these, definitely preventable deaths comprised 0.5% and potentially preventable deaths 7.5%. The leading cause of death in trauma patients was traumatic brain injury. Treatment errors most commonly occurred in the intensive care unit (ICU). The most frequent management error was delayed treatment of bleeding. Conclusions: Most errors in the treatment of trauma patients occurred in early stages of the treatment process and in the ICU. By identifying the main causes of preventable death and errors during the course of treatment, our research will help to reduce the preventable death rate. Appropriate trauma care systems and ongoing education are also needed to reduce preventable deaths from trauma.

• Molecules and Cells
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• v.46 no.8
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• pp.496-512
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• 2023

A fructose-enriched diet is thought to contribute to hepatic injury in developing non-alcoholic steatohepatitis (NASH). However, the cellular mechanism of fructose-induced hepatic damage remains poorly understood. This study aimed to determine whether fructose induces cell death in primary hepatocytes, and if so, to establish the underlying cellular mechanisms. Our results revealed that treatment with high fructose concentrations for 48 h induced mitochondria-mediated apoptotic death in mouse primary hepatocytes (MPHs). Endoplasmic reticulum stress responses were involved in fructose-induced death as the levels of phosho-eIF2α, phospho-C-Jun-N-terminal kinase (JNK), and C/EBP homologous protein (CHOP) increased, and a chemical chaperone tauroursodeoxycholic acid (TUDCA) prevented cell death. The impaired oxidation metabolism of fatty acids was also possibly involved in the fructose-induced toxicity as treatment with an AMP-activated kinase (AMPK) activator and a PPAR-α agonist significantly protected against fructose-induced death, while carnitine palmitoyl transferase I inhibitor exacerbated the toxicity. However, uric acid-mediated toxicity was not involved in fructose-induced death as uric acid was not toxic to MPHs, and the inhibition of xanthine oxidase (a key enzyme in uric acid synthesis) did not affect cell death. On the other hand, treatment with inhibitors of the nicotinamide adenine dinucleotide (NAD)⁺-consuming enzyme CD38 or CD38 gene knockdown significantly protected against fructose-induced toxicity in MPHs, and fructose treatment increased CD38 levels. These data suggest that CD38 upregulation plays a role in hepatic injury in the fructose-enriched diet-mediated NASH. Thus, CD38 inhibition may be a promising therapeutic strategy to prevent fructose-enriched diet-mediated NASH.

• Journal of Chest Surgery
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• v.27 no.6
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• pp.483-485
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• 1994

Recently, we experienced one case of penetrating cardiac injury patient by the knife.This patient was treated by emergency operation through left anterolateral thoracotomy under local anesthesia at emergency room. But, the patient was brought about the brain death inspite of normalized function of heart and lung. Now we have a conclusion that was able to recover of heart and lung functions by doctor`s exactly judgement and practice, at least.