No abstract available.
Neck*

No abstract available.
Angioplasty*

BACKGROUND: Bronchial asthma is an inflammatory disease of the airways that is associated with airway remodeling. The vascular endothelial growth factor (VEGF) is a potent, multifunctional cytokine that contributes to angiogenesis and inflammation. Matrix metalloproteinase-9 (MMP-9) is a major proteolytic enzyme that induces bronchial remodeling in asthma. However, there is no data available on the possible role of the VEGF or on the potential relationship between the VEGF and MMP-9 in acute asthma. Therefore, the VEGF was studied to determine whether or not it participates in airway inflammation during acute asthma. An additional aim of this study was to determine whether or not the VEGF levels correlated with the MMP-9 levels in the sputum of acute asthma patients. METHODS: Both the VEGF and MMP-9 levels were measured by an enzyme immunoassay and zymographic analysis in the sputum of patients with either stable asthma or with acute asthma. The VEGF and MMP-9 levels were also evaluated during a spontaneous asthma attack. RESULTS: The VEGF levels were significantly higher in the sputum of acute asthmatic patients than in either the stable patients the control subjects. The VEGF levels in the sputum during asthma exacerbation were significantly higher than those on the remission days, and those levels decreased after decreased after asthma therapy. In acute asthmatic patients, the VEGF levels in the sputum correlated with the number of neutrophils and eosinophils. In addition, a significant correlation was established between the VEGF and MMP-9 levels in the sputum. CONCLUSION: These results suggest that VEGF overproduction is associated with airway inflammation during acute asthma and is related to the MMP-9 function.
Airway Remodeling ; Asthma* ; Eosinophils ; Extracellular Matrix ; Humans ; Immunoenzyme Techniques ; Inflammation ; Matrix Metalloproteinase 9* ; Neutrophils ; Sputum ; Vascular Endothelial Growth Factor A*

A brief period of cerebral ischemia produces neuronal damage in the vulnerable regions of the brain, such as the CA1 area of the hippocampus. However, mild ischemic episodes may limit damage from subsequent ischemic insults, the phenomenon known as ischemic tolerance or preconditioning. We used hippocampal slices as an experimental model to investigate the possible utilization of ischemic tolerance, and to determine the effects of various drugs acting on glutamate and adenosine receptors following a conditioned ischemic insult. Preconditioning ischemic insult was induced in hippocampal slices of 450nm thickness for 60-70 seconds. Glutamate and adenosine receptors were pretreated 1 hour later with D,L-2-amino-5-phosphonovaleric acid(AP-5, 50nM), propentofylline(PPF, 200nM), 6-cyano-7-nitroquinoxaline-2,3-dione(CNQX, 10nM), 8-cyclopentyl-3,7-dihydro-1,3-dipropyl-1H-purine-2,6-dione(DPCPX, 1, 10nM) and 2-chloro-N6-cyclopentyl-adenosine (CCPA, 1, 10, 50nM). The slices were reoxygenated for 3 hours, after then a second ischemic insult was induced by substituting 95% O2, 5% CO2 and glucose for 95% N2, 5% CO2 and sucrose for 10 minutes. Population spikes(PS) were estimated from extracellular electrophysiological recordings of the hippocampal CA3-CA1 synaptic conduction 1 hour following the second ischemic insult. The PS(mV) was 2.69+/-0.06 in the normal hippocampal slice, while it was reduced to 1.21+/-0.05 in the hippocampal slice induced with 10 minutes of ischemia. The effects of the A1 selective agonist CPPA revealed a reduction of PS to 0.98+/-0.06 with low concentration(1nM), similar PS as the control group with a concentration of 10nM, and an increase in ischemic tolerance of 1.78+/-0.05 at a higher concentration(50nM). The selective A1 antagonist DPCPX(1nM) showed minimal reduction in PS of 1.10+/-0.04, while the NMDA antagonist AP-5(5nM) had a more profound weakening effect(1.05+/-0.04). The adenosine uptake inhibitor profentophylline(200nM) augmented the PS to 1.56+/-0.06; this effect was not influenced by 1nM DPCPX(1.60+/-0.07), but was abolished by a higher concentration of 10nM(1.36+/-0.05). These results confirmed ischemic tolerance in the hippocampal experimental model. We conclude that adenosine plays an important role in ischemic tolerance as activation of adenosine receptors or adenosine uptake inhibition enhances ischemic tolerance.
Adenosine ; Brain ; Brain Ischemia ; Glucose ; Glutamic Acid ; Hippocampus ; Ischemia* ; Models, Theoretical ; N-Methylaspartate ; Neurons ; Receptors, Purinergic P1 ; Sucrose

PURPOSE: We intended to describe the clinical features including characteristic etiologies, therapeutic approaches and outcomes for Landau-Kleffner syndrome(LKS). METHODS: A retrospective chart reviews were done to reveal the clinical and electrophysiological features in 5 patients who were diagnosed as LKS and undergone extensive diagnostic work-up and various therapeutic interventions. RESULTS: Among five LKS patients, 2 patients were males and 3 were females. All patients showed well controlled seizure outcomes but cognitive function including auditory and/or expressive aphasia were not improved in spite of using various anticonvulsants. Only two patients responded to steroid therapy but one patient showed repeated deterioration after discontinuation of the durg. Among 3 patients who were on ketogenic diet(KD), one patient showed a dramatic improvement in liguistic and cognitive functions in spite of underlying mitochondrial complex I deficiency. Multiple subpial transections (MST) were done in the other two patients because of incomplete recovery from ketogenic diet, and only one patient showed fairly successful improvement. CONCLUSION: Cognitive regression induced by LKS could be successfully improved by various therapeutic modalities including steroid, KD and palliative MST in most patients.
Anticonvulsants ; Aphasia, Broca ; Female ; Humans ; Ketogenic Diet ; Landau-Kleffner Syndrome* ; Male ; Retrospective Studies ; Seizures

PURPOSE: This study sought to evaluate the clinical outcomes of various therapeutic modalities, including newly-developed anti-epileptic drugs (AEDs), prednisolone, ketogenic diet (KD) epilepsy surgery, and vagus nerve stimulation (VNS), in treating intractable childhood epilepsy. METHODS: Data of refractory epilepsy patients (n=297) treated from July 1995 through April 2003 at the epilepsy center of Sanggye Paik Hospital were retrospectively analyzed. RESULTS: Newly-developed AEDs were primarily prescribed to 290 patients, although only 20 patients (6.9%) maintained a seizure- free state. Of 138 patients for whom prednisolone was prescribed, 58 patients (42.0%) showed complete seizure controls while 41 patients experienced relapse. KD was attempted and evaluated at 12 months in 162 patients, at which time 74 (45.7%) remained on the diet and 68 (42.0%) showed seizure reduction of greater than 50%, including 37 (22.8%) who were completely seizure free. Epilepsy surgery was undergone in 38 patients, and Engel class I was identified in 25 (65.8%) patients. VNS was administered to five patients, only two of whom obtained a seizure reduction of more than 50%. RESULTS: Taken together, these findings suggest that considerable controls over intractable childhood epilepsy can be gained through KD and epilepsy surgery, whereas prednisolone treatment leads to somewhat more frequent relapses, and newly-developed AEDs are comparatively limited in their controls of refractory epilepsy.
Diet ; Epilepsy* ; Humans ; Ketogenic Diet ; Prednisolone ; Recurrence ; Retrospective Studies ; Seizures ; Vagus Nerve Stimulation

BACKGROUND: There are many risk factors for osteoporosis in patients with chronic obstructive pulmonary disease(COPD). These include smoking, a low body mass index, insufficient exercise, and the use of glucocortcoids. However, there is lack of data on the incidence of osteoporosis according to the different glucocorticoid administration methods in patients with COPD. This study compared the incidence of osteoporosis according to the different administration methods of glucocorticoid. METHODS: A matched case-controlled study (gender, age, cumulative steroid dose and pack-years of smoking) was conducted. Forty-five patients with documented COPD for at least a 3 year duration and a cumulative glucocorticoid dose above 1,000 mg were enrolled in study. The patients were classified into the following three groups. First, fifteen patients received continuous inhaled glucocorticoid with intermittent oral steroids but had no admission history due to an acute exacerbation(Group I). Secondly, fifteen patients received a multiple course of oral steroids with additional inhaled glucocorticoid but had no admission history due to their acute exacerbation(Group II). Lastly, fifteen patients received intermittent oral or inhaled glucocorticoids and had an admission history due to the acute exacerbation with intravenous steroid treatment for at least 2 weeks per year(Group III). The enrolled patients had apulmonary function test and bone densitometry performed at the lumbar spine and femoral neck. RESULTS: The patients from Group III had significantly high incidence of osteoporosis in the lumbar and femoral neck compared to Group I and Group II (p<0.01). CONCLUSION: The incidence of osteoporosis in patients with COPD appears to be strongly affected by the method of steroid administration. This result suggests that intravenous steroid administration is strongly associated with the risk of osteoporosis.
Body Mass Index ; Case-Control Studies ; Densitometry ; Femur Neck ; Glucocorticoids ; Humans ; Incidence* ; Osteoporosis* ; Pulmonary Disease, Chronic Obstructive* ; Risk Factors ; Smoke ; Smoking ; Spine ; Steroids

No abstract available.
Cyclophosphamide* ; Doxorubicin* ; Drug Therapy* ; Sarcoma* ; Vinblastine*

OBJECTIVE: Lung cancer arises after a series of morphological changes, which take several years to progress from normal epithelium to invasive cancer. Multiple molecular changes and growth factors factor production have been documented in lung cancers, both small cell and non-small cell types. Insulin-like growth factors(IGFs) are important mitogenic and anabolic peptides, both in vivo and in vitro, and are thought to be significant autocrine-paracrine factors involved in normal and malignant cell proliferation. In this study, we have investigated (delete) the degree of expression of IGF-1 on the immunohistochemical staining in human non-small cell lung cancer(NSCLC) cells and small cell lung cancer (SCLC) cells were investigated. METHODS: Immunohistochemical staining for IGF-1 was performed in 15 cases of small cell carcinoma, 15 cases of squamous cell carcinoma, 15 cases of adenocarcinoma, and 12 cases of bronchoalveolar carcinoma. RESULTS: The NSCLC cells showed significantly increased expression The expression of IGF-1 on the immunohistochemical staining significantly increased in NSCLC cells than in SCLC cells. CONCLUSION: These results suggest that IGF-1 are expressed the expression of IGF-1 in human lung cancer cells(.), and the (The) immunohistochemical staining of IGF-1 in lung cancer cell lines may help in differentiation of may assist in the differentiation of NSCLC and SCLC.
Adenocarcinoma ; Carcinoma, Small Cell ; Carcinoma, Squamous Cell ; Cell Line ; Cell Proliferation ; Epithelium ; Humans* ; Insulin-Like Growth Factor I ; Intercellular Signaling Peptides and Proteins ; Lung Neoplasms* ; Lung* ; Peptides ; Small Cell Lung Carcinoma