• Proceedings of the Ginseng society Conference
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• 1984.09a
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• pp.83-88
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• 1984

It is now well established that the rodenticide Vacor (N-3-pyridyl-mehtyl-N'-p-nitropheny-lurea) causes a hyperglycemia in human and rats. It is also reported that there are some components (DPG-3) in ginseng radix which cause hypoglycemic effect on alloxan diabetic mice. In the present study, attempts were made to demonstrate in Vacor-poisoned rats the hypo-glycemic activity of red ginseng component(RGC), which was extracted by Kimura's DPG-3 extraction procedure and found to be effective for lowering a hyperglycemia in alloxan-diabetic rats. Vacor in a dose of $LD_{50}$ (10mg/kg) produced a glucose intolerance with a paradoxical moderate increase in blood immunoreactive insulin and derangement in glucose metabolism of epididymal adipocytes in rats. Although RGC (20mg/kg, i.p.) did not exert any significant influence on a hyperglycemia induced by large lethal doses (25mg/kg) of Vacor ingestion, it improved the LDso Vacor-induced glucose intolerance and caused a further increase in blood insulin levels in Vacor-poisoned rats. The administration of RGC (20mg/kg, i.p.) normalized Vacor-induced depression of glucose metabolism and lipogenesis in the epididymal adipocytes with an improvement of reduced responses to insulin of adipocytes from Vacor-poisoned rats. These results suggest that some red ginsneng components contained in RGC fraction normalize the depressed peripheral glucose unitlization and insulin response and eventually lead to an improvement of abnormal glucose tolerance developed in rats poisoned with small doses of Vacor.

• Journal of The Korean Society of Clinical Toxicology
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• v.9 no.2
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• pp.88-94
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• 2011

Purpose: Delayed neuropsychological sequelae (DNS) commonly occurs after recovery from acute carbon monoxide poisoning. The aim of this article is to identify the factors associated with DNS development. Methods: We retrospectively evaluated patients, admitted to the medical center emergency department from June 2005 to March 2011, who were suffering from acute carbon monoxide (CO) poisoning. We categorized the patients into two groups - those with DNS, and those without DNS. Multiple regression analysis was performed to identify the factors related to manifestation of DNS. Results: Of the total one hundred fifty seven patients (157) recruited for the study, twenty two (22) developed DNS. Longer CO exposure times and lower GCS scores were positively associated with development of DNS symptoms. Conclusion: Our study identified two potential factors which are predictive of DNS development in CO intoxication, however, more studies are needed. Adequate follow-up after hospital discharge to monitor for and accurately identify manifestation of DNS, is also important.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.46-49
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• 2015

Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

• Journal of Auto-vehicle Safety Association
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• v.13 no.2
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• pp.15-23
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• 2021

Even though the number of CO poisoning casualties caused by unintended idling for the vehicles equipped with keyless ignition systems is more than 70, the problem still remains unsolved and became social issue in the US, and Senates introduced the bill which urges NHSTA to make regulation for this accordingly. To meet market safety needs and the regulations, we decided to provide automatic shut-off system very soon. In this paper, we would like to describe how to validate vehicle shut-off timing including defining required tests and case selections considering vehicle condition, garage/room size and temperatures with several assumptions. We believe that safe implementation of the shut-off function is possible via this methodology and the results. As NHTSA must be interested in shut-off timing, the methodology can be enhanced and conclusions could be reflected highly in the future regulation in case we continue this study with NHTSA or any other 3-rd party institutes.

• YAKHAK HOEJI
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• v.36 no.3
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• pp.269-277
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• 1992

The effects of ginseng saponins on the distribution of nerve cells in cerebral cortex of carbon monoxide (CO)-intoxicated mice were studied in the young ($5{\sim}8$ weeks) and aged ($43{\sim}52$ weeks) mice. Mice were exposed to 5000 ppm of CO for 40 minutes (72% HbCO). After that, nerve cells in motor(area 4), somatosensory(area 3) and visual(area 17) area of cerebral cortex was observed. In young mice, the number of nerve cells in each area was significantly decreased on 1st, 7th and 14th day after CO intoxication. In aged mice, that was also decreased after CO intoxication. Especially the number of the nerve cells in motor and somatosensory area was significantly decreased on 1st and 7th day, while that in visual area was decreased only on 1st day. The number of nerve cells in young mice pretreated with ginseng saponins were significantly decreased less on 7th and 14th day than that of untreated mice. The number of nerve cells in each area of normal aged mice was larger than that of normal young mice. The results suggest that CO exposure causes local degeneration or disturbance of nerve cells and delayed neurologic sequelae, while ginseng saponins might play a role of protective action on the nerve cells which were damaged by CO.

• YAKHAK HOEJI
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• v.36 no.3
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• pp.278-284
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• 1992

This study was performed to investigate the effects of ginseng saponins on the cerebral energy metabolite's contents influenced by carbon monoxide(CO) intoxication. Each experimental group was divided young ($5{\sim}8$ weeks) and aged ($43{\sim}52$ weeks) rats, and they were exposed at 5,000 ppm CO (72%HbCO) for 30 min. One of the other groups was pretreated with ginseng saponins for 5 days before CO intoxication. The contents of cerebral energy metabolites in cerebral cortex, stratum and hypothalamus were measured. In cerebral cortex of both young and aged rats, the levels of ATP and creatine phosphate were significantly decreased, while those of lactate were significantly increased. There was no difference between the levels of cerebral energy metabolites of young and aged rats. Pretreatment of ginseng saponins before CO intoxication lowered decrease of the levels of cerebral energy metabolites and ATP levels were significantly recovered. On the other hands, contents of lactate in stratum and hypothalamus of young rats were significantly increased and the levels of ATP and creatine phosphate in stratum and hypothalamus were completely recovered at 2 weeks after CO intoxication. The results suggest that ginseng saponins have an ameliorating action against disturbance of the cerebral energy metabolites by CO intoxication.

• Journal of The Korean Society of Clinical Toxicology
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• v.7 no.2
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• pp.143-149
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• 2009

Purpose: Suicide attempts are known to be influenced by mass media reports. The purpose of this study was to evaluate the effects of mass media reporting celebrity suicides on an increase of intentional carbon monoxide (CO) poisoning and suicide attempts. Methods: We retrospectively reviewed the medical records of the consecutive patients who presented with suicide attempts to the Emergency Department of Ajou University Hospital during a 24 month period. We obtained the demographic data, any past history of suicide attempt and the methods of suicide attempts from the medical records of the suicide attempters. Time series analysis was conducted for evaluating the influence of mass media reporting of celebrity suicide on the suicide rates. Results: We finally enrolled 770 patients during the study period. The total number of suicide attempts by CO poisoning was 18 and the average number of suicide attempts by CO was $0.33{\pm}0.73$ per week. All of the suicide attempts by CO poisoning occurred after a celebrity committed suicide using CO from burning charcoal. Conclusion: This study showed that celebrity suicide by CO poisoning resulted in the Werther effect, which made the rate of intended CO poisoning increase, and the study provided further evidence for the need to actively restrain mass media reporting of suicide to decrease the Werther effect.

• YAKHAK HOEJI
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• v.24 no.2
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• pp.79-86
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• 1980

CO-intoxication is a serious problem in public health since the coal briquette has been used as one of fuels from 1950's. It has been discussed that the treatment with acetic acid vapor may be effective for CO-intoxication. This study was undertaken to investigate the action of acetic acid therapy, comparing with the spontaneous air treatment The acetic acid vapor was introduced to the blood combined with CO (in vivo and in vitro). The dissociation of COHb, the production of COHb, the levels of Hb and adrenaline and nor-adrenaline were measured. The effect of acetic acid vapor on dissociation of COHb was about 7-9% more effective than the spontaneous air treatment. The acetic acid vapor treatment for the dissociation of COHb was similar effect to the spontaneous air treatment. In an experiment of the combining CO gas with blood, the acetic acid vapor treatment was less effective in the production of COHb than that of spontaneous air treatment. Treatment with the acetic acid vapor to rabbit intoxicated with CO gas induced a little amount of Hb in blood comparing with the spontaneous air treatment. But, it is not a significant increment statistically. By the acetic acid vapor treatment after CO gas intoxication the adrenaline was increased and noradrenaline was decreased. With these results, it is assumed that the effect of acetic acid therapy on CO-gas intoxication would be caused by inductions of Hb and adrenaline and to be reduction of nor-adrenaline.

• The Korean Journal of Physiology
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• v.2 no.2
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• pp.93-99
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• 1968

The Present study attempted to analyze the fate of CO diffused into the circulating blood through the alveoli. Dogs were induced to CO poisoning by rebreathing CO gas mixture contained in Krog's spirometer, by closed circuit method, for 60 minutes. The spirometer was filled initially with 282 ml of CO and 20 liters of air and oxygen, so the composition of gases were arranged as 1.4% in CO and 50% in $O_2$ at the begining of the rebreathing. Oxygen was added corresponding to the utilization of $O_2$ by the animal in proceeding of the experiment. At 60th minutes of CO rebreathing, the concentration of CO in arterial blood and in mixed venous blood were analysed and compared with each other after the CO contents were corrected with the hematocrit measured in the arterial and mixed venous blood. The distribution of CO gas to other tissues was estimated by the analysis of CO diffused into the cystic bile and into the peritoneal gas pocket which was formed by injection of 300 ml air into the peritoneal cavity prior to the CO gas rebreathing. The blood volume was measured by dilution method using $^{51}Chromium$ tagged red cells. CO amount vanished in the animal body was calculated by subtraction of total CO content in blood stream and the CO remained in closed circuit breathing system from the CO amount given to the breathing system at the begining of the experiment. Results obtained are summarized as follows: 1. The content of CO corrected by the hematocrit value was slightly less in mixed venous blood than in arterial blood. The amount of CO diffused into the cystic bile and into the peritoneal cavity was averaged to 0.1% and 0.4% of the CO amount in 100 ml of blood, respectively. 2. For 60 minutes of CO rebreathing, CO-hemoglobin saturation reached about 77% at the 60th minutes, CO amount vanished in the experimental animal averaged 36.1 ml/dog/hr., or 21% of the total CO volume in the blood stream. The average vanishing rate of CO during 60 minutes of CO rebreathing per kg of body weight was 2.71 ml/hr. Production of CO measured in ten dogs under hypoxic condition averaged 0.023 ml/kg/hr. The major part of the CO vanished in the dogs seemed to be oxidized to $CO_2$ by various tissues of the animal. The conclusion might be delivered as such oxidation of CO to $CO_2$ by animal tissues can play a role in part of the process of recovery and protection of animal from CO-poisoning.

• Journal of Preventive Medicine and Public Health
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• v.27 no.1 s.45
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• pp.84-106
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• 1994

Hyperbaric oxygen (HBO) therapy for carbon monoxide (CO) poisoning eventually inducing the hypoxia-reoxygenation condition, may produce oxygen free radicals, which forms 8-hydroxydeoxyguanosine (8-OH-dG) by attacking C-8 position of deoxyguanosine (dG) in DNA. Effects of oxygen partial pressure or duration of HBO therapy with or without CO poisoning on the tissue 8-OH-dG formation were investigated. Male Sprague-Dawley rats were grouped and exposed to air (control group), 4000 ppm of CO for 10 to 30 minutes (CO only group), air for 30 minutes after 30 minute exposure to 4000 ppm of CO(CO-air exposure group), HBO after 30 minute exposure to 4000 ppm of CO(CO-HBO group), or HBO therapy fo. $10{\sim}120$ minutes(HBO only group). The 8-OH-4G concentrations in the brain and the lung tissues were measured with high performance liquid chromatography and electrochemical detector (ECD). Average concentrations of the 8-OH-dG of each group were statistically compared. In the brain tissues, 8-OH-dG concentrations of the CO only group, the CO-air exposure group, and the CO-HBO group did not significantly differ from those of the control group. Similar insignificance was also found between the CO-HBO group and the HBO only groups. No appreciable dose-response relationship was observed between the 8-OH-dG concentration and the oxygen partial pressure or the duration of HBO. However, the 8-OH-dG concentrations of the 30 minute CO only group were higher than those of the CO-air exposure group (p-value<0.05). In the lung tissues, there were no significant differences between the 8-OH-dG concentrations of the control group and those of the CO only group, the CO-air exposure group, and the CO-HBO group. However, mean 8-OH-dG concentration of the CO-air exposure group was significantly higher than that of the CO only group under the same CO exposure condition(p-value<0.05). With the duration of CO exposure, the 8-OH-dG concentrations of the lung tissues decreased significantly (p-value<0.05). The concentrations of 8-OH-dG in the lung tissues proportionally increased with the duration of HBO, but no such relation was observed with the oxygen partial pressure. These results suggest that the brain may be more resistant to oxygen free radicals as compared with the lungs, and that oxygen toxicity following HBO may be affected by factors other than oxygen free radicals.