No abstract available.
Osteoblastoma* ; Paranasal Sinuses*

BACKGROUND: Patients with chest pain are common among outpatients. Several researches shows that chest pain patients can suffer from psychiatric illnesses such as hypochondriasis, depression, anxiety, somatization, panic disorder and so on. This study aims to examine the pschogenic symptoms in patients with noncardiac chest pain METHODS: In this study, the 98 people who have undergone treadmill test for chest pain during the three months from June 1st to September 30 of 1998 were selected, and the 98 patients were asked to respond to the prepared questionnaire and SCL-MPD(symptom check list-minor psychiatric disorders) before they underwent treadmill test. And then, they were classified into two groups. One group consisted of patients with noncardiac chest,pain, and the other group of patients with cardiac chest pain. These two groups were compared in 10 measures, and the compared results were analyzed by t-test. RESULTS: Among the 25 patients with cardiac chest pain, 15 patients were males and 10 patients (38%) were females, and among the 44 patients with noncardiac chest pain, 31 patients (70%) were males, 13 patients (30%) were females. The average age was 47 years old. The average age in patients with noncardiac chest pain was 48, and the 46 for those patients with cardiac chest pain . In the statistical analysis between the patients with cardiac chest pain and those with noncardiac chest pain, significant difference(p<0.005) was shown in the measures such as somatization, depression, phobic anxiety, obsessive-compulsive, neurasthenic, hypochondriacal, anxiety, anger-hostility, interpersonal sensitivity. CONCLUSIONS: As in the analysis the patients with noncardiac chest pain showed significant difference in the symptom check list-minor psychiatric disorder compared to those with cardiac chest pain. We conclude that primary care physician should take more interest in evaluating psychiatric symptoms in patients with noncardiac chest pain.
Anxiety ; Chest Pain* ; Depression ; Exercise Test ; Female ; Humans ; Hypochondriasis ; Male ; Middle Aged ; Outpatients ; Panic Disorder ; Physicians, Primary Care ; Thorax* ; Surveys and Questionnaires

The authors studied the lung injury induced by endotoxemia and the effects of proteolytic agent on the lung changed by endotoxemia. Sprague-Dawley rats were intraperitoneally administrated with a single dose of endotoxin (4 mg/kg, E. coli 025 : B6 lipopolysaccharide) or with endotoxin and gabexate mesilate (200 mg/kg), a proteolytic agent, concomitantly. Rats of each group were scarificed at 9, 18, and 27 hours after injection. Light and electron microscopic examination were done. The results obtained were summarized as follows: Light microscopic exmination revealed congested capillaries and neutrophilic infiltration in both groups. Electron microscopic findings were interstitial and alveolar neutrophilic infiltration, endothelial swelling with increased pinocytotic vesicles and cytoplasmic process formation, and interstitial edema. Decrease of osmiophilic bodies in the type II pneumocytes had appeared at 9 hours after endotoxin injection. These changes were increased in severity at 18 hours and 27 hours after endotoxin injection. In the group of concomitant treatment of gabexate mesilated and endotoxin, there was no edema at 9 hours after injection. After 18 hours welling of endothelial cell and interstitial edema had appeared. However, the severity of the edema was markedly decreased. Type II pneumocytes showed well preserved osmiophilic bodies. According to these results, it is considered that administration of gabexate mesilate can significantly redeced the lung injury induced by endotoxemia.
Rats ; Animals

No abstract available.
Prostate*

No abstract available.
Otitis Media* ; Otitis*

This study was carried out to investigate the direct neurotoxicity of alcohol on CNS and the effects of piracetam or vitamins on ultrastructural changes of the rat cerebellar and hippocampal neurons during long-term alcohol treatment. To evaluate the results, quantitative analysis were done for light and electronic microscopic findings. On the light microscopy, red degeneration of pyramidal cells and Purkinje cells was found more apparently in the alcohol only treated group than in the control group. On the electron microscopy, increased lipofuscin pigments wee found in cerebellum and hippocampus. In quantitative analysis, vitamins significantly reduced red degeneration in both hippocampus and cerebellum. However, piracetam significantly reduced red degeneration in cerebellum but not in hippocampus. Lipofuscin pigments in Purkinje cells and pyramidal cells were significantly reduced in the alcohol with piracetam treated group than the alcohol only treated group. However, vitamin had no significant reducing effect of lipofuscin pigments in Purkinje cells and pyramidal cells. According to the results, it is concluded that vitamins deficiency might cause red degeneration of pyramidal cell after long-term alcohol treatment, but increment of lipofuscin pigments in pyramidal and Purkinje cell may be caused by alcohol itself or its metabolite rather than vitamins deficiency. Piracetam seems to improve cognitive function impairment caused by alcohol consumption.
Alcohol Drinking ; Animals ; Cerebellum ; Hippocampus ; Lipofuscin ; Microscopy ; Microscopy, Electron ; Neurons* ; Piracetam* ; Purkinje Cells ; Pyramidal Cells ; Rats* ; Vitamins*

A case of pulmonary alveolar proteinosis is reported. Most of the alveolar spaces were filled with amorphous deep eosinohilic material which revealed strong positive reaction to periodic acid-Schiff staining. Electron microscopic observation of this material showed numerous lamellar bodies in the alveolar spaces and cytoplasms of alveolar macrophages. A part of them were concentric multilamellated type A lamellar bodies and the other were finger printlike type B bodies. Combined type A and type B lamellar bodies were rarely present. From the above features it is suggested that both type A and B lamellar bodies could be transformed one another and those lamellar bodies may be originated from pulmonary surfactant.

PURPOSE: Vascular endothelial growth factor (VEGF) stimulates angiogenesis and vascular permeability. Tissue damage is related to angiogenesis, and induced by a delay in neutrophil apoptosis. This study was performed to investigate the effect of VEGF on the spontaneous neutrophil apoptosis via the activation of VEGFR-1 and phosphorylation of the p38-MAPK pathway. METHODS: Neutrophils were prepared from 10 healthy young donors, cultured for 20 h, and the apoptosis measured by the morphological changes and flow cytometry. The VEGF receptor expression and phosphorylation of mitogen activated protein kinase (MAPK) were measured using a Western blotting method. RESULTS: VEGF dose-dependently delayed the spontaneous neutrophil apoptosis, but this effect was blocked by pre-treatment of the cells with a VEGF receptor antagonist. VEGF increased the phosphorylated forms of the extracellular stress related kinase (Erk) and p38-MAPK. However, the VEGF-induced delay in apoptosis was not affected by the Erk inhibitor, PD98059 but was affected by the p38- MAPK inhibitor, SB203580. The VEGF receptor-1, but not the VEGF receptor-2, was detected in neutrophils, but its level was reduced in cultured neutrophils. CONCLUSION: VEGF delays neutrophil apoptosis through p38- MAPK activation.
Apoptosis* ; Blotting, Western ; Capillary Permeability ; Flow Cytometry ; Humans ; Neutrophils* ; Phosphorylation ; Phosphotransferases ; Protein Kinases ; Receptors, Vascular Endothelial Growth Factor ; Tissue Donors ; Vascular Endothelial Growth Factor A* ; Vascular Endothelial Growth Factor Receptor-1

PURPOSE: To investigate the spontaneous cerebral microbleeding occurring at gradient-echo MRI, and its relationship with associated stroke lesions and risk factors. MATERIALS AND METHODS: Between September 2001 and December, 2002, 32 patients (21 men and 11 women; mean age 63 years) in whom cerebral microbleeding occurred at gradient-echo MRI were retrospectively investigated. Using a 1.5 T MR imager, spin-echo T1-weighted, fast spin-echo T2-weighted, diffusion-weighted, and gradient-echo images were obtained. The number and location of microbleeds seen on gradient echo images, patient data, and associated stroke lesions such as intracerebral hemorrhage and lacunar and territorial infarction were assessed. RESULTS: Among the 32 patients, 563 microbleeds and between 1 and 66 (mean, 17.6) were noted at gradientecho imaging. Microbleeding occurred in the cortical/subcortical area (n=216), the basal ganglia (n=173), thalamus (n=92), cerebellum (n=41), brainstem (n=36) and corpus callosum (n=1), and in 20 patients was bilateral. Patients had a history of hypertension (n=26), hypertriglycemia (n=12), heart disease (n=4), and diabetes mellitus (n=3). Stroke lesions were seen in 27 patients, intracerebral hemorrhage in ten, lacunar infarction in 24, and territorial infarction in four. CONCLUSION: The incidence and number of microbleeds was greater in older patients and in those with hypertension, hypertriglycemia, and stroke lesions such as intracerebral hemorrhage or lacunar infarction. The detection of microbleeding at gradient-echo imaging is helpful, since it predicts the possibility of cerebral hemorrhage in these patients.
Basal Ganglia ; Brain Stem ; Cerebellum ; Cerebral Hemorrhage ; Corpus Callosum ; Diabetes Mellitus ; Female ; Heart Diseases ; Humans ; Hypertension ; Incidence ; Infarction ; Magnetic Resonance Imaging* ; Male ; Retrospective Studies ; Risk Factors ; Stroke* ; Stroke, Lacunar ; Thalamus

BACKGROUND: IGF-I is an important mitogen in many types of malignancies. Tumors also express many IGF binding proteins, which modulate IGF action. The purpose of this study was to evaluaste the effect of IGF-I and IGFBP on cell proliferation in mouse lung cancer cells (3LL). METHODS: The cellular proliferation of 3LL with the treatment of growth factors was evaluated using MTT assay. Western ligand blot was performed in order to determine whether 3LL cells secrete IGFBPs and we evaluated the effect of IGFBP on cellular proliferation. RESULTS: The treatment of 3LL cells with IGF-I increased cellular proliferation in a serum free media. Western ligand blot of conditioned medium of 3LL with 125I-IGF-I demonstrated one single major band with an estimated molecular mass of 24 kDa. This band was identified as IGFBP-4 with immunoblot analysis using antisera. The addition of anti-IGFBP-4 antibody to abrogate the effect of IGFBP-4 resulted in increased cellular prolife ration suggesting that IGFBP-4 inhibits cell growth. CONCLUSION: IGF-I increases cellular proliferation, however the secreted IGFBP- 4 has an ingibitory function on cell growth in 3LL. These findings suggest that IGF-I and IGFBP are involved in the cell proliferation.
Animals ; Carrier Proteins* ; Cell Proliferation ; Culture Media, Conditioned ; Culture Media, Serum-Free ; Immune Sera ; Insulin-Like Growth Factor Binding Protein 4 ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I ; Intercellular Signaling Peptides and Proteins ; Lung Neoplasms* ; Lung* ; Mice*