Tumor angiogenesis has been found to have prognostic significance in many tumor types for predicting an increased risk of metastasis. We assessed tumor vascularity in 28 cases of borderline malignancy and 71 cases of carcinoma of the ovary which had been resected and diagnosed, using the highly specific endothelial cell marker CD34. The numbers of microvessels were counted in 200 magnification in three highly vascularised areas. The numbers of microvessels in carcinomas were higher than that in the borderline malignancy of serous and mucinous tumors. The number of microvessels of mucinous carcinomas was significantly higher than that of serous carcinomas. There were neither significant differences in the number of microvessels according to histological tumor types (p=0.075) nor significant differences in the number of microvessels according to FIGO stages (p=0.072). But in serous carcinomas, the number of microvessels was higher in the FIGO III-IV stage than in the FIGO I-II stage (p=0.017). This study showed higher neovascularization in malignant tumor than borderline malignancy, and in the advanced stage (FIGO III-IV) than less advanced stage (FIGO I-II) of serous carcinomas.
Adenocarcinoma, Mucinous ; Endothelial Cells ; Female ; Microvessels ; Mucins ; Neoplasm Metastasis ; Ovary

BACKGROUND: Eosinophil cationic protein (ECP), one of the eosinophil granule proteins released during allergic reactions, may play a major role in the allergic inflammatory process. The measurement of ECP in serum may be a useful indicator of eosinophil activity in ongoing inflammatory processes. We investigated the clinical utility of ECP measurement in serum in patients with bronchial asthma, allergic rhinitis and atopic dermatitis, after standardizing sample processing. METHODS: We measured the serum ECP levels in patients with bronchial asthma (n=38), chronic obstructive pulmonary diseases (COPD) (n=13), respiratory symptoms (n=19), allergic rhinitis (n=26), non-allergic rhinitis (n=24), and atopic dermatitis (n=10) and in normal healthy controls (n=16) by the fluoroenzyme immunoassay using Pharmacia CAP System, and evaluated the correlation between ECP level and blood eosinophil number, or ECP and IgE levels. Blood eosinophil number was counted by the automated cell counter. RESULTS: Serum ECP levels were significantly higher in patients with bronchial asthma (15.6+/- 12.6 g/L), COPD (13.3+/-7.2 g/L), allergic rhinitis (23.8+/-13.2 g/L), and atopic dermatitis (20.6+/- 18.4 g/L) than in normal controls (7.5+/-4.2 g/L) (P <0.05). ECP levels were also significantly higher in patients with bronchial asthma and COPD than in patients with simple respiratory symptoms (6.9+/-4.7 g/L), whose ECP levels did not statistically differ from those in normal controls. ECP levels were also significantly higher in patients with allergic rhinitis than in patients with non-allergic rhinitis (9.5+/-5.1 g/L), whose ECP levels did not statistically differ from those in normal controls. Serum ECP level and eosinophil number in peripheral blood were correlated only in patients with bronchial asthma (r=0.53, P <0.01) and no correlation between ECP and IgE levels was found in all of the patients. CONCLUSIONS: ECP is the one of the secretory components released from the eosinophil granule and measurement of ECP in serum might be one of the noninvasive tool to assess the activity in relation to eosinophil involvement in various allergic diseases.
Asthma ; Cell Count ; Dermatitis, Atopic ; Eosinophil Cationic Protein* ; Eosinophil Granule Proteins ; Eosinophils ; Humans ; Hypersensitivity ; Immunoassay ; Immunoglobulin E ; Lung Diseases, Obstructive ; Pulmonary Disease, Chronic Obstructive ; Rhinitis

BACKGROUND: The product of oxygen-free radicals inf1ict oxidative injuries on healthy cells. Antioxidants such as superoxide dismutase(SOD), glutathione peroxidase, and reduced glutathione(GSH) are present in almost all cells and play important roles in metabolism, transport, and cellular protection. We measured blood GSH levels in healthy controls and patients with non insulin dependent diabetes mellitus(NIDDM) for evaluation of the clinical usefulness of GSH. METHODS: Erythrocyte GSH levels were measured in fifty healthy controls and thirty NIDDM patients with diabetic retinopathies by Beutler's method. We also tested within-run precision, between-run precision, linearity and recovery rate to evaluate this method measuring erythrocyte GSH levels. RESULTS: The GSH levels (mean +/-SD) of NIDDM patients (5.03+/-0.67mumo1/Hb) were significantly lower than those of healthy control group (6.46+/-0.85mumo1/Hb)(P<0.001). The results of within-run precision and between-run precision when stored at 4degrees Cwere excellent (coefficient of variation were 2.79% and 2.42%, respectively), however, when stored at the room temperature the GSH levels were sharply declined. The linearity and recovery rate were acceptable. CONCLUSIONS: The prescision, linearity, and recovery rate of GSH measurement were excellent. The GSH levels in NIDDM patient group were reduced, and this probably contributes to the defective defense mechanism against increased oxidative stress. Additional measurement of other antioxidants such as superoxide dismutase and glutathione Peroxidase may be required to clarify the pathologic significance of glutathione metabolism in various diseases.
Antioxidants ; Diabetes Mellitus, Type 2 ; Diabetic Retinopathy ; Erythrocytes* ; Glutathione Peroxidase ; Glutathione* ; Humans ; Insulin ; Metabolism ; Oxidative Stress ; Superoxide Dismutase ; Superoxides

Therapeutic irradiation can induce angiosarcoma. Radiation-induced angiosarcoma constitutes 20% of all angiosarcomas. Although its common site of origin is the skin and subcutaneous tissue, it rarely arises in small or large bowels with a presentation as multifocal abdominal angiosarcomatosis. We report a case of intra-abdominal angiosarcomatosis involving the jejunum, ileum, transverse colon, mesentery and right ovary in a 63-year-old female. It developed 10 years after therapeutic irradiation for squamous cell carcinoma of uterine cervix. She developed panperitonitis due to intestinal perforation. She died from sepsis 3 days after segmental resection of the small bowel and right oophorectomy. We reviewed the previously reported cases and describe the clinicopathologic features of this tumor.
Carcinoma, Squamous Cell ; Cervix Uteri ; Colon, Transverse ; Female ; Hemangiosarcoma ; Humans ; Ileum ; Intestinal Perforation ; Jejunum ; Mesentery ; Middle Aged ; Ovariectomy ; Ovary ; Sepsis ; Skin ; Subcutaneous Tissue

No abstract available.
Humans ; Nursing*

PURPOSE: To evaluate the feasibility of in-vivo 1H magnetic resonance spectroscopy (1H-MRS) for differentiation between hepatic and renal cysts, with emphasis on the analysis of cystic content. MATERIALS AND METHODS: The 1H-MR spectra of 43 cystic lesions (15 hepatic and 28 renal) obtained using in -vivo 1H-MRS at 1.5 T and with a localized proton STEAM sequence were evaluated. We calculated the ratio of the peak area of lipid/water (Rlipid/water), protein/water (Rprotein/water) and lipid/protein (Rlipid/protein), paying particular attention to identifying differences in peak area ratios between the two types of cyst. RESULTS: The 1H-MR spectra from 26.7% (4/15) of hepatic and 67.9% (19/28) of renal cysts showed the lipid peak as most prominent. Mean+/-standard deviations of the Rlipid/water of hepatic and renal cysts were 0.38+/-0.30x10-6 and 8.42+/-23.24x10-6, respectively; for Rprotein/water the corresponding figures were 0.83+/-0.74x10-6 and 1.50+/-2.94x10-6, and for Rlipid/protein, 0.57+/-0.64 and 2.44+/-3.26. All differences were statistically significant (p<0.05), and positive correlation between lipid and protein in hepatic and renal cysts was demonstrated. CONCLUSION: The different in-vivo 1H-MRS findings, for hepatic and renal cysts can be used in comparative study of cystic tumors of the liver and kidney.
Kidney ; Liver ; Magnetic Resonance Spectroscopy ; Protons ; Steam

BACKGROUND: Although normal vascular endothelium prevents adhesion and aggregation of platelets by the release of nitric oxide (NO) and prostacyclin, circulating blood cells, such as polymorphonuclear leukocytes (PMNs) and mononuclear leukocytes (ML) may be considered to be also important in modulating platelet aggregation. Recently, nitric oxide synthase (NOS) activity was found in PMNs and ML, so these cells can also release NO to inhibit platelet aggregation. We studied platelet-ML interactions using an experimental model in which isolated ML were placed in the aggregometer in contact with human platelets, stimulated by collagen. METHODS: Platelet count in platelet-rich plasma (PRP) was adjusted to approximately 300x109/L. ML were separated using Ficoll-Hypaque (specific gravity 1.077) and finally resuspended at 1, 3 and 5x109/L, in Tyrode albumin buffer (TAB), respectively. Platelet aggregation was measured with Chrono-Log Aggregometer (USA) after adding variable numbers of the ML, stimulating with 2.5, 5 and 10 microgram/mL of collagen. Mechanisms of ML to inhibit the platelet aggregation were evaluated after incubating the ML with 10 micrometer indomethacin and 300 micrometer NG-monomethyl-L-arginine (L-NMMA). RESULTS: Non-stimulated ML (3x109/L) inhibited (43.2 +/- 19.6 versus TAB control 69.2 +/- 10.7% transmission) the platelet aggregation induced by 2.5 microgram/mL of collagen. The inhibition was not attenuated by increasing the concentration of collagen from 5.0 microgram/ mL (50.1 +/- 18.0% versus TAB control 75.5 +/- 13.1%, P<0.001) to 10 microgram/mL (62.9 +/- 17.3% versus TAB contol 82.3 +/- 12.6%, P<0.01). In addition, it was dependent on the number of ML and incubation time. While preincubation of the ML with indomethcin did not affect the antiaggregating capacity of the ML (63.4 +/- 11.1 versus TAB control 73.3 +/- 7.3%), preincubation of the ML with L-NMMA slightly inhibit the antiaggregating capacity of the ML (86.6 +/- 6.8 versus TAB control 73.3 +/- 7.3%). CONCLUSION: These findings suggest that blood ML inhibited the collagen-induced platelet aggregation, of which mechanism appears to be only partly dependent on NO and to be independent on prostaglandins. Release of other substances affecting platelet aggregation from ML requires to be clarified. Using our experimental model, it has been demonstrated that cell-cell contact may facilitate the exchange of a wide array of mediators between platelets and ML which may influence the cellular responses. This experimental model thus allows to study interactions between platelets and ML.
Blood Cells ; Blood Platelets* ; Collagen ; Endothelium, Vascular ; Epoprostenol ; Gravitation ; Humans ; Indomethacin ; Leukocytes, Mononuclear* ; Models, Theoretical ; Neutrophils ; Nitric Oxide ; Nitric Oxide Synthase ; omega-N-Methylarginine ; Platelet Aggregation* ; Platelet Count ; Platelet-Rich Plasma ; Prostaglandins

Verapamil overdose results in cardiac arrhythmia including the complete A-V block, and hypotension due to decreased peripheral resistance and decreased myocardial contractility. However, sustained-release verapamil overdose frequently has atypical presentations, such as delayed and prolonged course of toxic signs and symptoms. Although several cases of sustained-release verapamil overdose have been reported worldwidely, the specific treatment modalities and prognostic indicators for verapamil overdose have not been well-defined. Recently, we experienced a case of sustained-release verapamil overdose in 30-year-old female. 10 hours after verapamil ingestion she presented in severe bradycardia and hypotensive shock state. Initial EKG showed the complete AV block and her systolic blood pressure was below 60 mmHg. Temporary cardiac pacemaker was performed and she was treated with activated charcoal, glucagon, amrinone, and several sympathomimetics, and 48 hours after admission, she was fully recovered.
Adult ; Amrinone ; Arrhythmias, Cardiac ; Atrioventricular Block ; Blood Pressure ; Bradycardia ; Charcoal ; Eating ; Electrocardiography ; Female ; Glucagon ; Humans ; Hypotension ; Shock ; Sympathomimetics ; Vascular Resistance ; Verapamil*

BACKGROUND AND OBJECTIVES: According to our previous study Ginkgo biloba extract (EGb 761) induces inhibition of cell proliferation and apoptosis in SCC 1483 oral cavity cancer cells. On the other hand, in lipopolysaccharide-stimulated RAW 264.7 cells, activation of mitogen activated protein kinase (MAPK) is the key event in the inhibition of inflammation by EGb 761. Therefore, we have investigated whether MAPK pathway is involved in the apoptotic process by EGb 761 in oral cavity cancer cell lines or not. SUBJECTS AND METHOD: In SCC 1483 oral cavity cancer cell lines, Western blot analysis, Fluorescence-activated cell sorter (FACS) analysis, and transient transfection using MAPK-dominant negative constructs were used. RESULTS: When SCC 1483 oral cavity cancer cell lines were treated with the concentration of 250 microgram/ml EGb 761, activation of extracellular signal-regulated kinase (ERK) and apoptosis were noted. This apoptosis was inhibited by the treatment with ERK inhibitor (PD 98059). In the transiently transfected cells by MAPK/ERK kinase 1 (MEK1)-dominant negative construct, phosphorylations of ERK and p90 ribosomal S 6 protein kinase (RSK1) were inhibited which led to the inhibition of apoptosis by EGb 761. The inhibition of apoptosis was also noted in the transfected cells by RSK1 dominant negative construct and cAMP response element binding protein (CREB)-dominant negative construct. CONCLUSION: In conclusion, the apoptosis of SCC 1483 oral cavity cancer cell lines by EGb 761 is linked to the activation of ERK and it can happen via ERK MAPK/RSK1/CREB signal transduction pathway.
Apoptosis* ; Blotting, Western ; Cell Line* ; Cell Proliferation ; Cyclic AMP Response Element-Binding Protein ; Ginkgo biloba* ; Hand ; Inflammation ; Mouth Neoplasms ; Mouth* ; Phosphorylation ; Phosphotransferases ; Protein Kinases ; Signal Transduction ; Transfection

BACKGROUND: It has been well known that the bone and kidney are the principle organs of parathyroid hormine (PTH) actions. Although patients with primary hyperparathyroidism show a high incidence of LVH and trophic effects of PTH on adult rat ventricular cardiomyocytes were investigated in vitro, effect of PTH on the cardiac tissue in vivo is unknown. METHODS: We examined the effects of PTH on the cardiomyocyte and interstitial tissue using adult rat heart. Twenty-two female Sprague-Dawley rats were ovariectomized bilaterally at three months old and weighing in 250 - 300 gm in order to exclude the trophic effect of estrogen. We administrated human parathyroid hormone (20 ug subcutaneously 5 times per week) to 12 rats for 4 weeks after raising for 8 weeks (PTH group):the remaining 10 rats received only normal saline (control). We measured left ventricular thickness [IVS+LVPW)/2] and number of cardiomyocytes and interstitial fibrosis on LM (H & E and Masson's trochrome stain) and EM. RESULTS: 1) LV wall thickeness tended to increase in PTH group as compared with control (2.16+/-0.31 vs 1.12+/-0.21 mm, p=0.099). 2) The number of cardiomyocyte in PTH group was significantly less than that of control (61.2+/-13.1 vs 70.5+/-14.9, p=0.003, Magnification x 400). 3) There was no significant change of interstitial fibrosis between PTH group and control. CONCLUSION: These results shggest that PTH may produce left ventricular hypertrophic effects in aged ovariectomized rat that resulted form hypertrophy of cardiomyocyte without increase of interstitial connetive tissue.
Adult ; Animals ; Estrogens ; Female ; Fibrosis ; Heart ; Humans ; Hyperparathyroidism, Primary ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Incidence ; Kidney ; Myocytes, Cardiac ; Ovariectomy ; Parathyroid Hormone* ; Rats* ; Rats, Sprague-Dawley