Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To elucidate the roles of SEK1/MKK4, a upstream kinase for both c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 kinase, on NO-induced apoptosis, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-Kl) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-Kl) with sodium nitroprusside (SNP), a NO generating agent, significantly decreased the cell viability up to 20% of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. For a while, caspase-3 like activity in NO treated RAW/SEK1-Kl cells was significantly increased with parallell to apoptotic death rate. However, caspase1 like activity was not affected by NO in any transfectants. The NO induced apoptosis in RAW/SEK1-Kl cells was significantly prevented by the addition of caspase-3 like inhibitor (N-Ac- DEVD-CHO). In addition, the phosphotransferase activity of JNK1 in NO-treated RAW/SEK1-WT is significantly increased, but not in RAW/SEK1-Kl cells. These results suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis.
Apoptosis ; Caspase 3 ; Cell Death ; Cell Survival ; Clone Cells ; Macrophages ; Mortality ; Nitric Oxide* ; Nitroprusside ; Phosphotransferases ; Protein Kinases

No abstract available.

Purpose: The Prescott nomogram has been utilized to forecast hepatotoxicity from acute acetaminophen poisoning. In developing countries, emergency medical centers lack the resources to report acetaminophen concentrations; thus, the commencement and cessation of treatment are based on the reported dose. This study investigated risk factors that can predict acetaminophen detection after 15 hours for safe treatment termination. Methods: Data were collected from an urban emergency medical center from 2010 to 2020. The study included patients ≥14 years of age with acute acetaminophen poisoning within 15 hours. The correlation between risk factors and detection of acetaminophen 15 hours after ingestion was evaluated using logistic regression, and the area under the curve (AUC) was calculated. Results: In total, 181 patients were included in the primary analysis; the median dose was 150.9 mg/kg and 35 patients (19.3%) had acetaminophen detected 15 hours after ingestion. The dose per weight and the time to visit were significant predictors for acetaminophen detection after 15 hours (odds ratio, 1.020 and 1.030, respectively). The AUCs were 0.628 for a 135 mg/kg cut-off value and 0.658 for a cut-off 450 minutes, and that of the combined model was 0.714 (sensitivity: 45.7%, specificity: 91.8%). Conclusion Where acetaminophen concentrations are not reported during treatment following the UK guidelines, it is safe to start N-acetylcysteine immediately for patients who are ≥14 years old, visit within 15 hours after acute poisoning, and report having ingested ≥135 mg/kg. Additional N-acetylcysteine doses should be considered for patients visiting after 8 hours.

PURPOSE: Recent studies indicate that widely used chemotherapeutic agents induce apoptosis in susceptible cells. One of the effector arms in this cell death pathway is composed of cysteine proteases belonging to the caspase family. In cells, caspase-3 has been shown to play an important role as a downstream member of protease cascade, where various cell death pathways converge into the same effector pathway. JNK, a member of the mitogen-activated protein kinase pathway, is activated in response to many stressful stimuli including heat shock, UV irradiation, protein synthesis inhibitors, and inflammatory cytokines. In this study, we investigated whether JNK1 & caspase-3 play a role in the apoptosis induced by adriamycin (ADR). METHODS: U937 cells were cultured in RPMI 1640 and treated with different concentrations of ADR. Cellular DNA was extracted and analyzed by electrophoresis on a 1.5% agarose gel to detect DNA fragmentation. The activity of caspase-3 was measured by the proteolytic cleavage of the fluorogenic substrate DEVD-AMC. The activity of JNK1 was measured by in vitro immunocomplex kinase assay with 2 microgram of GST-c Jun as a substrate and quanititated using phosphoimager analyzer. RESULTS: ADR induced the apoptotic death of U937 myeloid cells in a dose-dependent manner, which was characterized by increasing ladder-pattern DNA fragmentation. Consistent with apoptotic death of U937 cells, ADR induced the catalytic activation of caspase-3 as well as JNK1 at 2.5 microgram/mL of concentrations. CONCLUSION: Adriamycin induces apoptosis of human myeloid leukemic U937 cells via activation of caspase-3 and cJun-N terminal kinase1 (JNK1)/Stress activated protein kinase (SAPK).
Apoptosis* ; Arm ; Caspase 3* ; Cell Death ; Cysteine Proteases ; Cytokines ; DNA ; DNA Fragmentation ; Doxorubicin* ; Electrophoresis ; Fluorescent Dyes ; Hot Temperature ; Humans* ; Myeloid Cells ; Phosphotransferases ; Protein Kinases ; Protein Synthesis Inhibitors ; Sepharose ; Shock ; U937 Cells*

Compared with organophosphate or carbamate insecticides, neonicotinoids have several pharmacological benefits such as a broad spectrum of insecticidal activity, low application rate, and highly selective toxicity to insects. Imidacloprid was the first neonicotonid introduced in the market, in 1991. It has become one of the best selling insecticides globally. Several cases of imidacloprid intoxication have been reported worldwide, but few have been reported in Korea. Recently, we experienced a severe imidacloprid intoxication with delayed respiratory insufficiency and several toxicities. We report the case with the literature review.
Imidazoles ; Insecticides ; Insects ; Korea ; Nitro Compounds ; Respiratory Insufficiency

PURPOSE: Convulsive status epilepticus(SE) is a serious, life-threatening neurological condition that requires immediate treatment to avoid significant morbidity and mortality. Despite improvements in the diagnosis and treatment of SE in the last two decades, SE in young infancy is still associated with high morbidity and mortality. Thus, understanding the varied etiology and clinical presentation and prognosis of SE is very important for improving the methods of evaluation and treatment of this major neurological condition. METHODS: Eighty-eight cases with 53 who have been admitted to the Department of Pediatrics, Fatima Hospital during the period of July, 1992 to June, 1997 were included. We described age distribution, etiologic classification according to age, seizure type, neurologic outcome, recurrence of SE and epileptic seizure. RESULTS: SE was frequent in young infant less than 3 years of age. Major etiology of SE was acute symptomatic(34.1%) and febrile(31.8%). In the seizure type, the majority(92.1%) was generalized convulsive, many cases(69.3%) of SE were first seizures. The neurologic sequelae were found in 15.9% and mortality rate in 5.7%. The neurologic sequelae and mortality were higher in acute symptomatic. In sixty-three follow-up cases, eleven cases were epileptic seizure, eight cases were recurred SE and two cases were recurred febrile SE. CONCLUSION: SE is a life-threatening neurological condition and occurrs mostly in young infants less than 3 years of age. It requires immediate detection of etiology in SE and aggressive treatment for reducing mortality and morbidity rates.
Age Distribution ; Child* ; Classification ; Diagnosis ; Epilepsy ; Follow-Up Studies ; Humans ; Infant ; Mortality ; Pediatrics ; Prognosis ; Recurrence ; Seizures ; Status Epilepticus*

Carbon dioxide is a colorless, odorless, nonirritating gas with many practical uses. In particular, because it can displace oxygen from the environment, it is used as a fire extinguisher. We describe an incident that occurred as a result of malfunction of a carbon dioxide-based fire extinguishing system in our hospital. Twelve casualties reached our emergency department. Symptoms of exposure included nausea, dizziness, loss of consciousness, vomiting, chest discomfort, and seizure. Results of initial arterial blood gas analysis showed acidosis in five patients. A new pneumonic infiltration at the left. upper lung field was observed in one patient, while sinus tachycardia in electrocardiography (ECG) was observed in another patient. Oxygen was initially supplied to all casualties, until symptoms of intoxication had disappeared. Three patients were admitted to the hospital, but were discharged without complication. Despite occurrence of massive casualties, with significant symptoms due to unintentional exposure to high concentrations of carbon dioxide, patients' symptoms were relieved by supportive care.
Acidosis ; Blood Gas Analysis ; Carbon ; Carbon Dioxide ; Dizziness ; Electrocardiography ; Emergencies ; Fire Extinguishing Systems ; Fires ; Humans ; Lung ; Mass Casualty Incidents ; Nausea ; Oxygen ; Seizures ; Tachycardia, Sinus ; Thorax ; Unconsciousness ; Vomiting

Parvovirus B19 is a minute, single stranded DNA virus which has been identified as the etiological agent of pure red cell aplasia, erythremia infectiosum (5th disease), hydrops fetalis, or arthralgia. We report a case of pure red cell aplasia caused by parvoviurs B19 in renal transplantation. The patient was 39-year-old male who had been diagnosed as chronic renal failure 22 months ago and taken hemodialysis twice a week. He had been taken renal transplantation in October 30th, 1997. But anemia was not improved in first postoperative period. Bone marrow revealed hypocellularity (about 30%) with maturation arrest of erythroid series at pronormoblasts. The pronormoblasts showed very large size, deep blue cytoplasm, cytoplasmic projection, cytoplasmic vacuole and distinct intranuclear eosinophilic inclusions. The parvovirus B19 PCR and anti-parvovirus B19 IgM were positive, but anti-parvovirus B19 IgG was negative. The patient was treated with intravenous immunoglobulin and then reticulocyte count was increased three weeks later. The follow-up bone marrow revealed normal erythroid precursors and was not found infected giant pronormoblasts seven weeks later.
Adult ; Anemia ; Arthralgia ; Bone Marrow ; Cytoplasm ; DNA, Single-Stranded ; Eosinophils ; Erythroblasts ; Follow-Up Studies ; Humans ; Hydrops Fetalis ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulins ; Kidney Failure, Chronic ; Kidney Transplantation* ; Male ; Parvovirus* ; Polycythemia Vera ; Polymerase Chain Reaction ; Postoperative Period ; Red-Cell Aplasia, Pure* ; Renal Dialysis ; Reticulocyte Count ; Vacuoles

PURPOSE: In Korea, few studies have examined the acute toxicity of anti-obesity drugs. The purpose of this study is to analyze the general characteristics and clinical aspect of acute anti-obesity drug intoxication. METHODS: We retrospectively investigated patients admitted to the emergency department after anti-obesity drug intoxication between March, 2004 and February, 2012. The medical records of these patients were reviewed for demographic data, toxicologic history, time elapsed to presentation, clinical symptoms and signs, treatment, and outcome. RESULTS: There were a total of 18 anti-obesity intoxication cases during the study period; of 16 which were included in our study. The purchasing route of the anti-obesity drug was mainly through a doctor's prescription (68.8%), however, some were obtained through the internet and the pharmacies. The mean time to The most commonly ingested anti-obesity drug was sibutramine (31.3%) and many of the cases (62.5%) were multi-drug ingestions. The most common clinical manifestations were gastrointestinal symptoms (94%), but, CNS symptoms (75%) and cardiovascular symptoms (75%) were almost equally present. 13 patients (81%) were discharged after clearance of toxic symptoms and signs with a mean observational period of 7.0 hours. 3 patients were admitted for observation and treatment; of which 1 patient died due to fatal complications. CONCLUSION: Most anti-obesity intoxications show mild toxicity and a nonfatal clinical course. However, the recent trend toward prescribing psychostimulant anti-obesity medication, which can be fatal after an acute overdose, calls physicians' attention to treating of anti-obesity intoxications.
Anti-Obesity Agents ; Cyclobutanes ; Emergencies ; Humans ; Internet ; Korea ; Medical Records ; Obesity ; Pharmacies ; Prescriptions ; Retrospective Studies

PURPOSE: Flumazenil is the specific benzodiazepine (BZP)antagonist indicated for the reversal of the sedative effect of BZP. We evaluated the safety and the effectiveness of using flumazenil to treat suspected BZP overdoses in an emergency department setting. METHODS: From March 1998 and December 2002, 52 unconscious patients with suspected BZP overdose were treated with flumazenil. They were divided into two groups. Group A (low-risk) patients had a clinical picture compatible with an uncomplicated BZP overdose. Group B (risk) was comprised of all other patients. These patients were also categorized into three groups based on their responses to flumazenil: complete, partial, or no response. RESULTS: In group A (N=15), 9 patients showed a complete response to flumazenil while two showed a partial response. In group B (N=37), complete response was seen in 23 patients and partial response in 8. Based on responses to flumazenil: there were 32 complete responder, 10 partial responder, and 10 non-responder. There were 6 cases of endotracheal intubation and 8 cases of artificial ventilation, but none of these occurred in the complete response group. The frequent adverse effects after the administration of flumazenil were agitation (13.5%), hallucination (3.9%), and vomiting (3.9%). Serious adverse effects were reported in two patients and included seizure and cardiac arrhythmia. CONCLUSION: Flumazenil may serve as a useful therapeutic tool in the management of selected cases of unconscious patients with a BZP overdose.
Arrhythmias, Cardiac ; Benzodiazepines* ; Dihydroergotamine ; Emergencies* ; Emergency Service, Hospital* ; Flumazenil* ; Hallucinations ; Humans ; Hypnotics and Sedatives ; Intubation, Intratracheal ; Seizures ; Ventilation ; Vomiting