BACKGROUND: Fas is a member of the tumor necrosis factor (TNF)/nerve growth factor (NGF) receptor family. Triggering of the Fas receptor pathway by its ligand results in apoptosis. Soluble Fas consists of the extracellular region of Fas receptor and it binds to Fas ligand to inhibit the Fas and Fas ligand induced apoptosis. Recently some evidence indicates that the Fas/Fas ligand system represents an important pathway responsible for the induction of apoptosis in bone marrow CD34+ cells of patients with aplastic anemia. METHODS: We measured serum soluble Fas levels in 27 patients with aplastic anemia at diagnosis using ELISA to define the status of soluble Fas in this disorder. RESULTS: Levels of serum soluble Fas in patients with aplastic anemia were lower com-pared with that of normal healthy controls. No difference was noted in the serum soluble Fas levels according to severity of disease. No correlation was found between serum soluble Fas levels and hematologic parameters at diagnosis such as neutrophil count, lymphocyte count, platelet count and corrected reticulocyte count. CONCLUSION: These results indicate that serum soluble Fas levels are decreased in patients with aplastic anemia. Further studies recruiting more patients and measuring Fas receptor on peripheral blood lymphocyte subsets and bone marrow CD34+ cells concomitantly may be helpful to determine pathophysiology of bone marrow failure.
Anemia, Aplastic* ; Antigens, CD95 ; Apoptosis ; Bone Marrow ; Diagnosis ; Enzyme-Linked Immunosorbent Assay ; Fas Ligand Protein ; Humans ; Lymphocyte Count ; Lymphocyte Subsets ; Neutrophils ; Platelet Count ; Reticulocyte Count ; Tumor Necrosis Factor-alpha

We studied the effects of bile acids on the induction of apoptosis in HepG2 human hepatocellular carcinoma cells. Treatment with either ursodeoxycholic acid (UDCA) or lithocholic acid (LCA) resulted in a dose- and time-dependent decrease in cell viability assessed by MTT assay. Both UDCA and LCA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these bile acids induce cell death was through apoptosis. Cycloheximide, a protein synthesis inhibitor, blocked the apoptosis induced by these bile acids, implying that new protein synthesis may be required for the apoptosis. Intracellular Ca2+ release blockers (dantrolene and 3,4,5-trimethoxybenzoic acid-8-(diethylamino)octyl ester) inhibited decreased cell viability and DNA fragmentation induced by these bile acids. Treatment of HepG2 cells with calcium ionophore A23187 induced DNA fragmentation. These results suggest that UDCA and LCA induce apoptosis in the HepG2 cells and that the activation of intracellular Ca2+ signals may play an important role in the apoptosis induced by these bile acids.
Apoptosis* ; Bile Acids and Salts* ; Bile* ; Calcimycin ; Calcium ; Carcinoma, Hepatocellular* ; Cell Death ; Cell Survival ; Cycloheximide ; DNA Fragmentation ; Hep G2 Cells ; Humans* ; Lithocholic Acid ; Ursodeoxycholic Acid

PURPOSE: To evaluate imaging findings and lung density changes after 95% oxygen inhalation in rat. MATERIALS AND METHODS: A total of 18 rats were divided into three groups on the basis of inhalation time: group I(n=6) inhaled 95 % oxygen for 24 hours, and group II(n=6) for 48 hours, group III(n=6) for 60 hours. A control group(n=6) inhaled room air(21% oxygen). Chest radiograph and high resolution computed tomography were performed, and pathologic and imaging findings were compared. RESULTS: Chest radiograph showed abnormality only in group III. High resolution CT, however, revealed abnormal findings in all three groups : diffuse ground glass opacity in groups I, II and III, additional focal patchy consolidation at the peripheral portion in group II, and diffuse consolidation in group III. Lung density was sig-nificantly higher in group I than in controls(p <0.05), while density in group II was not significantly different from that in group I(p >0.05). In group III, density was significantly higher than in group II. The lung density changes seen in all groups showed a bilateral diffuse increased pattern. but, in group III, changes were more severe in the central, peripheral and posterior portion of the lower lung. Ground glass opacity and focal patchy consolidaton seen on HRCT were found on pathologic examination to be due to alveolar cell hyperplasia and septal thickening. Consolidation was caused by alveolar edema and hemorrage. Pathologic lesions were randomly distributed in both lungs. CONCLUSION: One HRCT images, rat exposed to hyperoxia showed ground glass opacity, patchy consolidation and diffuse consolidation. Depending on exposure time, the pathologic findings also indicated increased lung density and a bilateral, diffuse distribution pattern, as well as alveolar cell hyperplasia and septal thickening, alveolar edema and hemorrage. HRCT may be more helpful than simple X-rays for the early detection of pulmonary oxygen toxicity.
Animals ; Edema ; Glass ; Hyperoxia ; Hyperplasia ; Inhalation ; Lung* ; Oxygen* ; Radiography, Thoracic ; Rats*

Although growth associated protein-43 (GAP-43) is known to play a significant role in the regulation of axonal growth and the formation of new neuronal connections in the hippocampus, there is only a few studies on the effects of acute stress on GAP-43 mRNA expression in the hippocampus. Moreover, the effects of repeated citalopram treatment on chronic mild stress (CMS)-induced changes in GAP-43 mRNA expression in the hippocampus have not been explored before. To explore this question, male rats were exposed to acute immobilization stress or CMS. Also, citalopram was given prior to stress everyday during CMS procedures. Acute immobilization stress significantly increased GAP-43 mRNA expression in all subfields of the hippocampus, while CMS significantly decreased GAP-43 mRNA expression in the dentate granule cell layer (GCL). Repeated citalopram treatment decreased GAP-43 mRNA expression in the GCL compared with unstressed controls, but this decrease was not further potentiated by CMS exposure. Similar decreases in GAP-43 mRNA expression were observed in CA1, CA3 and CA4 areas of the hippocampus only after repeated citalopram treatment in CMS-exposed rats. This result indicates that GAP-43 mRNA expression in the hippocampus may differently respond to acute and chronic stress, and that repeated citalopram treatment does not change CMS-induced decreases in GAP-43 mRNA expression in the GCL.
Animals ; Axons ; Citalopram ; GAP-43 Protein ; Hippocampus ; Humans ; Immobilization ; Male ; Neurons ; Rats ; RNA, Messenger

BACKGROUND AND OBJECTIVES: The failure of ST-segment resolution (STR) after primary percutaneous coronary intervention (pPCI) is associated with adverse clinical outcomes. However, the clinical predictors on admission for incomplete STR are poorly known. SUBJECTS AND METHODS: Patients undergoing pPCI (n=101, 79 males and 22 females, mean age 60.0 years) were divided into complete STR group (> or =70%, n=58) and incomplete STR group (<70%, n=43). The groups were compared according to clinical factors including history, electrocardiographic (ECG) patterns, angiographic features and laboratory data. RESULTS: The incomplete STR group contained more frequent hypertensive patients (p=0.04) and patients displaying longer tendency in total chest pain duration (p=0.08). This group was associated with worse clinical factors such as low ejection fraction (p=0.06), higher Killip class (p=0.08) and more death (p=0.042). Grade 3 ischemia pattern of ECG and precordial ST elevation (i,e anterior myocardial infarction) at admission were more frequent in the incomplete STR group (p=0.001 and 0.002, respectively). Initial troponin I, creatinin kinase -MB and brain natriuretic peptide levels were higher in the incomplete STR group (p=0.001, 0.002, and 0.043, respectively). Coronary angiography showed that culprit lesions were more frequent in left anterior descending artery than other arteries in the incomplete STR group of patients (p=0.002). Thrombolysis In Myocardial Infarction (TIMI) flow grades 2 or less before PCI was more frequent in the incomplete STR group (p=0.029). However, TIMI flow grade after PCI was not appreciably different between the two groups. Logistic regression analysis demonstrated that TIMI flow grade 2 or less was most powerful predictor for incomplete STR {odds ratio (OR)=12.12, 95% confidence interval (CI) 1.23-119.35, p=0.032}. Other independent predictors were anterior infarction (OR=3.39, CI 1.46-10.57, p=0.007), ischemia grade 3 ECG at admission (OR=3.87, CI 1.31-11.41, p=0.014), and hypertensive patients (OR=3.03, CI 1.13-8.15, p=0.027). CONCLUSION: Incomplete STR after pPCI is associated with poor prognostic clinical factors. TIMI flow grade 2 or less before pPCI, ST elevation on precordial leads, ischemia grade 3 pattern of initial ECG, and hypertensive patients are independent predictors for incomplete STR in the early stage.
Arteries ; Chest Pain ; Coronary Angiography ; Coronary Circulation ; Electrocardiography ; Female ; Humans ; Infarction ; Ischemia ; Logistic Models ; Male ; Myocardial Infarction ; Natriuretic Peptide, Brain ; Percutaneous Coronary Intervention ; Phosphotransferases ; Troponin I

Endobronchial lipomas are rare lesions that usually obstruct a major bronchus and cause irreversible pulmonary damage distally. Herein, a case of an endobronchial lipoma combined with broncholithiasis, found 3 months after first noticing symptoms including dry cough, and voice change, successfully removed by surgical resection is reported
Bronchi ; Cough ; Lipoma* ; Voice

Pneumatosis cystoides intestinalis is a relatively rare condition, characterized by multiple gas-filled cysts of varying size in the wall of gastrointestinal tract. Although the etiology of pneumatosis intestinalis remains uncertain, the possibility that both the gas-forming bacteria and mechanical theories develop pneumocysts has recently been advocated. We experienced a case of pneumotosis cystoides intestinalis found by colonoscopy in a 31-year old woman with intermittent abdominal pain.
Abdominal Pain ; Adult ; Bacteria ; Colonoscopy ; Female ; Gastrointestinal Tract ; Humans ; Pneumatosis Cystoides Intestinalis*

PURPOSE: Severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug reaction with eosinophilia and systemic symptoms (DRESS) to antiepileptic drug (AED), are rare, but result in significant morbidity and mortality. We investigated the major culprit drugs, clinical characteristics, and clinical course and outcomes of AED-induced SCARs using a nationwide registry in Korea. METHODS: A total of 161 patients with AED-induced SCARs from 28 referral hospitals were analyzed. The causative AEDs, clinical characteristics, organ involvements, details of treatment, and outcomes were evaluated. We compared the clinical and laboratory parameters between SJS/TEN and DRESS according to the leading causative drugs. We further determined risk factors for prolonged hospitalization in AED-induced SCARs. RESULTS: Carbamazepine and lamotrigine were the most common culprit drugs causing SCARs. Valproic acid and levetiracetam also emerged as the major causative agents. The disease duration and hospital stay in carbamazepine-induced SJS/TEN were shorter than those in other AEDs (P< 0.05, respectively). In younger patients, lamotrigine caused higher incidences of DRESS than other drugs (P= 0.045). Carbamazepine, the most common culprit drug for SCARs, was associated with a favorable outcome related with prolonged hospitalization in SJS (odds ratio, 0.12; 95% confidence interval, 0.02-0.63, P= 0.12), and thrombocytopenia was found to be a risk factor for prolonged hospitalization in DRESS. CONCLUSION: This was the first large-scale epidemiological study of AED-induced SCARs in Korea. Valproic acid and levetiracetam were the significant emerging AEDs causing SCARs in addition to the well-known offending AEDs such as carbamazepine and lamotrigine. Carbamazepine was associated with reduced hospitalization, but thrombocytopenia was a risk factor for prolonged hospitalization. Our results suggest that the clinical characteristics and clinical courses of AED-induced SCARs might vary according to the individual AEDs.
Anticonvulsants ; Carbamazepine ; Cicatrix ; Drug Hypersensitivity Syndrome ; Epidemiologic Studies ; Hospitalization ; Humans ; Incidence ; Korea ; Length of Stay ; Mortality ; Referral and Consultation ; Risk Factors ; Stevens-Johnson Syndrome ; Thrombocytopenia ; Valproic Acid

PURPOSE: Nonsteroidal anti-inflammatory drugs (NSAIDs) are common cause of severe cutaneous adverse reactions (SCARs). The present study aimed to investigate the characteristics of SCARs induced by NSAIDs in the Korean SCAR registry. METHODS: A retrospective survey of NSAID-induced SCARs recorded between 2010 and 2015 at 27 university hospitals in Korea was conducted. Clinical phenotypes of SCARs were classified into Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), SJS-TEN overlap syndrome and drug reaction with eosinophilia and systemic symptoms (DRESS). Causative NSAIDs were classified into 7 groups according to their chemical properties: acetaminophen, and propionic, acetic, salicylic, fenamic and enolic acids. RESULTS: A total of 170 SCARs, consisting of 85 SJS, 32 TEN, 17 SJS-TEN overlap syndrome and 36 DRESS reactions, were induced by NSAIDs: propionic acids (n=68), acetaminophen (n=38), acetic acids (n=23), salicylic acids (n=16), coxibs (n=8), fenamic acids (n=7), enolic acids (n=5) and unclassified (n=5). Acetic acids (22%) and coxibs (14%) accounted for higher portions of DRESS than other SCARs. The phenotypes of SCARs induced by both propionic and salicylic acids were similar (SJS, TEN and DRESS, in order). Acetaminophen was primarily associated with SJS (27%) and was less involved in TEN (10%). DRESS occurred more readily among subjects experiencing coxib-induced SCARs than other NSAID-induced SCARs (62.5% vs. 19.7%, P = 0.013). The mean time to symptom onset was longer in DRESS than in SJS or TEN (19.1 ± 4.1 vs. 6.8 ±1.5 vs. 12.1 ± 3.8 days). SCARs caused by propionic salicylic acids showed longer latency, whereas acetaminophen- and acetic acid-induced SCARs appeared within shorter intervals. CONCLUSIONS: The present study indicates that the phenotypes of SCARs may differ according to the chemical classifications of NSAIDs. To establish the mechanisms and incidences of NSAID-induced SCARs, further prospective studies are needed.
Acetaminophen ; Acetates ; Acetic Acid ; Anti-Inflammatory Agents, Non-Steroidal ; Cicatrix ; Classification ; Cyclooxygenase 2 Inhibitors ; Diethylpropion ; Drug Hypersensitivity ; Drug Hypersensitivity Syndrome ; Hospitals, University ; Incidence ; Korea ; Phenotype ; Propionates ; Prospective Studies ; Retrospective Studies ; Salicylates ; Salicylic Acid ; Stevens-Johnson Syndrome