No abstract available.
Animals ; Rats* ; Serotonin* ; Spinal Cord*

No abstract available.
Animals ; Cricetinae* ; Serotonin* ; Spinal Cord*

No abstract available.
Animals ; Brain Stem* ; Cricetinae* ; Raphe Nuclei* ; Serotonergic Neurons*

Although cystic teratoma is the most common benign tumor of the ovary, the association of sebaceous gland tumor with cystic teratoma is rare. We have recently experienced a case of sebaceous gland tumor, arising in the cystic teratoma of the ovary in a 78-year-old Korean woman. Histologically, the tumor was characterized by an organoid lobular architectures of the sebaceous glands which are exculsively composed of germinative and mature sebaceous cells. Although it is difficult to come to a valid conclusion due to the presence of atypical mitosis and necrosis, this tumor was regarded as benign from the viewpoint of preserved organoid structures, and absence of capsular invasion or metastasis.
Female ; Humans

No abstract available.
Actinomycosis*

BACKGROUND: Brief episodes of coronary blood flow interruption, ischemic preconditioning (IP), following a prolonged ischemia induces myocardial tolerance to ischemia and improves myocardial function during reperfusion by undefined mechanism. Recently, it has been suggested that the signal transduction pathway of the cardiomyocyte itself may involve in this protection. The aims of the present study were : (1) to examine the effect of adenosine in early phase of IP, (2) to define the relationship between the adenosine and protein kinase C(PKC) METHOD AND RESULTS: Heart isolated from New Zealand White rabbit (1.2 - 1.5kg body weight, n=78) were perfused with Tyrode solution by non-recirculating Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to receiving 45min global ischemia (I) and 120min reperfusion (R) with or without IP. IP was induced by a single dose of 5min I and 10min R. A part of the IP hearts, calphostin C (200nmol/L), a PKC inhibitor, was administered 5min before IP and sustained during IP regimen. Left ventricular function and coronary flow were monitored. Infarct size was determined by staining with 1% triphenyltetrazolium chloride solution and computerized planimetry. Adenosine concentration in the coronary flow was determined by HPLC. Myocardial cytosolic and membrane PKC activities were measured by (32)P-r-ATP incorporation into PKC specific peptide. Expression of PKC-e and PKC-o was determined by SDS-PAGE and Western blot. IP enhanced improvement of functional recovery (p<0.05, in the left ventricular developed and end-diastolic pressure ; p<0.01, in the coronary flow) during 120min R after 45min I. Preconditioned hearts showed reduction in the infarct size compared with the non-preconditioned hearts (p<0.05) ; however, IP-induced protection was lost by calphostin C. Adenosine release from the cardiomyocytes abruptly increased to 10-20 folds baseline just after IP manipulation and decreased rapidly on reperfusion. Cytosolic PKC activity significantly decreased in the preconidtioned hearts which received 45min I(p<0.05) and 45min I and 120min R(p<0.01), while the membrane fraction increased in the former(p<0.05) and the latter(p<0.01) groups. There was no significant difference in the PKC-o activity among all experimental groups in cytosolic and membrane fraction, however, the membrane PKC-e isoenzyme activity was increased in the preconditioned hearts which received 45min I. CONCLUSION: These results indicate that (1) a single dose of brief ischemia has an infarctlimiting effect and can improve post-ischemic contractile dysfunction after 45min subsequent sustained I ; and (2) increase of adenosine release in the earlier period of IP regimen and translocation of PKC from the cytosol to myocyte membrane may be important processes signal transduction for protection. These results suggest that cardioprotective mechanism responsible for IP in isolated rabbit heart may be initiated by adenosine and PKC.
Adenosine* ; Blotting, Western ; Body Weight ; Chromatography, High Pressure Liquid ; Cytosol ; Electrophoresis, Polyacrylamide Gel ; Heart ; Hemodynamics ; Ischemia ; Ischemic Preconditioning* ; Membranes ; Muscle Cells ; Myocytes, Cardiac ; New Zealand ; Protein Kinase C* ; Protein Kinases* ; Reperfusion ; Signal Transduction ; Ventricular Function, Left

Glassy cell carcinoma is an unusual neoplasm of the uterine cervix with highly aggressive clinical behavior. On cervico-vaginal smear examination, the tumor has well confused of atypical repair cell of the endocervix. Recently, we have experienced two cases of glassy cell carcinoma of the uterine cervix, diagnosed on cervico-vaginal smears and confirmed on following histologic sections. The cervico-vaginal smears revealed abundant clusters with well defined boarders. The cell clusters were composed of large tumor cells. The tumor cells had distinct granular cytoplasm and eosinophilic macronucleoli. Characteristic cytologic features of this tumor were discussed in view of differential diagnosis.
Adenocarcinoma ; Breast ; Cervix Uteri ; Cytoplasm ; Diagnosis, Differential ; Eosinophils ; Female ; Hydronephrosis*

BACKGROUND: It has been reported that one or more intermittent reperfusion(s) during ischemia may be beneficial to the myocardium by washing out catabolites that have accumlated during ischemia. We evaluated the effect of four cycles of ichemia (2 minutes) and reperfusion (3 miutes), i.e., preconditioning on sustained ischemia (20 minutes) and reperfusion (60 minutes) using isolated Langendorff-perfused rabbit hearts. METHODS: After a fifty-minutes recovery phase, LVP , dLVP/dt and ECG were simultaneously recorded and ultrastructure of the stunned(or risk) area of the left ventricle was examined with conventional methods. RESULTS: In the preconditioned hearts, functional parameters such as LVPP(peak pressure), LVPP recovery rate and LVEDP(end-diastolic pressure) reached to 99.6+/-4.38mmHg, 98.0+/-4.67% and 14.0+/-2.90mmHg (109.3+/-2.91mmHg, 109.4+/-1.29mmHg and 10.7+/-2.67mmHg for the controls), respectively, after 30 minutes from the onset of reperfusion and maintained as in the controls(p>0.01). In contrast, in the ischemia-reperfusion hearts, LVPP and LVPP recovery rate were significantly reduced(81.6+/-6.83mmHg and 85.7+/-5.30%;p<0.05) and LVEDP elevated(21.2+/-3.00mmHg) but dP/dtmax, heart rate and ECG patterns were not significantly different between the preconditioned and the ischemia-refusion hearts during reperfusion. Furthermore, irreversible myocardial injury was homogeneous(both subendo- and subepicardial) in the ischmia-reperfusion hearts but only focal(subendocardial) in preconditioned hearts. CONCLUSION: These results suggest that preconditioning induced by very short periods of ischemia and reperfusion may enhance recovery of the left ventricular function and delay ultrastructhral changes to a certain extent during reperfusion.
Electrocardiography ; Heart Rate ; Heart Ventricles ; Heart* ; Ischemia ; Myocardium ; Reperfusion ; Ventricular Function, Left

No abstract available.
Lupus Erythematosus, Systemic* ; Polyarteritis Nodosa*