Prostaglandins which are produced from amnionic cells are known to play a major role in uterine contraction and cervical dilatation in human. Recently it is reported that aspirin increases the expression of PGHS-1 and PGHS-2 in trophoblast cells from placenta. We examined here the changes of immunoreactive prostaglandin H synthase (PGHS) level by aspirin in cultured cells from amniotic fluid and human amnionic WISH cells. PMA (10-7 M), an activator of protein kinase C increased the induction of PGHS-2 in both cells with or without fetal calf serum. PGHS-2 protein was also increased significantly by 10-4 M aspirin at 6 hours in both cells in the presence of serum but it was not increased in the absence of serum. The expression of PGHS-1 protein was enhanced by asprin but not by PMA in the absence of serum. Other anti-inflammatory drugs such as acetaminophen, indomethacin, dexame- thasone, and mefenamic acid increased the PGHS-2 protein level in WISH cells. PMA-induced PGHS-2 expression in WISH cells was not decreased by aspirin, on the contrary, the level was increased additively. Our results show that the increased expression of PGHS in amnion cells or other amniotic fluid cells by aspirin and other several anti-inflammatory drugs is through an unidentified effect rather than feedback effect by depletion of prostaglandin.
Acetaminophen ; Amnion* ; Amniotic Fluid ; Aspirin* ; Cell Line* ; Cells, Cultured* ; Cyclooxygenase 2 ; Female ; Humans ; Indomethacin ; Labor Stage, First ; Mefenamic Acid ; Placenta ; Pregnancy ; Prostaglandin-Endoperoxide Synthases* ; Prostaglandins ; Protein Kinase C ; Trophoblasts ; Uterine Contraction

No abstract available.
Endoderm* ; Endodermal Sinus Tumor*

No abstract available.
Hepatocytes*

BACKGROUND: This study was designed to investigate the effect of exercise training on defense mechanism of chronic degenerative disease, aging, and memory impairments of senescence-accelerated mouse (SAM)P8 under the hypothesis that "Senile dementia may be prevented by regular exercises". METHODS: To evaluate the effects of exercise training on the defense mechanism of aging and memory impairment, SAMP8 were divided into two groups, the control group and exercise training groups. the exercise training group were performed with low (O2max 25~33%), middle (O2max 50%) and high (O2max 66~75%) intensity exercise. All SAMP8 mice were fed experimental diet ad libitum until 4, 8 months, and dead period. RESULTS: Median lifespan in middle exercise group resulted in a significantly increased (23.5% and 18.7%, respectively), whereas these lifespan in high exercise group resulted in an unexpectedly decreased (13.5% and 12.1%, respectively) compared with control group. Body fat levels in 4 and 8 months of age were significantly decreased 43% to 51% in middle exercise group, whereas were remarkably deceased to 57% in high exercise group compared with control group. It is believed that extended median and maximum lifespan may be effected by calory restriction through the exercise training. Acetylcholine (ACh) levels were significantly increased 6.7% and 8.5% in middle and high exercise groups, and also choline acetyltransferase (ChAT) activities were significantly increased 10.3% and 11.9% in middle and high exercise groups. CONCLUSION: These results suggest that proper and regular exercises such as middle group (O2max 50%) may play an effective role in attenuating an oxygen radicals and may play an important role in improving a learning and memory impairments of senile dementia.
Acetylcholine ; Adipose Tissue ; Aging* ; Alzheimer Disease ; Animals ; Choline O-Acetyltransferase ; Dementia ; Diet ; Exercise ; Learning ; Memory* ; Mice ; Reactive Oxygen Species

Serous cystadenomas of the pancreas account for approximately a third of pancreatic cystic neoplasms. Their coexistence with a second tumor is extremely rare. We now report a case of a serous microcystic adenoma combined with an intraductal papillary mucinous tumor of the pancreas in a 69-year-old man. Abdominal computed tomography scans demonstrated an incidental cystic mass in the body with cystic dilatation of the duct in the head of the pancreas. Central pancreatectomy with pancreatico-jejunostomy, and cyst excision of the pancreatic head were performed. Histologic examination demonstrated a serous microcystic cystadenoma in the body coexisting with an intraductal papillary mucinous adenoma in the head of the pancreas. This case study highlights the importance of careful intra-operative and pathologic examination for synchronous pancreatic tumors.
Adenoma ; Aged ; Cystadenoma ; Cystadenoma, Serous ; Dilatation ; Head ; Humans ; Mucins ; Pancreas ; Pancreatectomy ; Pancreatic Cyst

No abstract available.
Animals ; Liver Regeneration* ; Liver Transplantation* ; Liver* ; Rats*

No abstract available.
Humans ; Infant, Low Birth Weight* ; Infant, Newborn

BACKGROUND: Increasing coronary perfusion pressure with phenylephrine is important treatment strategies for right ventricular dysfunction caused by pulmonary hypertension. We compared the effects of phenylephrine on systemic and pulmonary hemondynamics in patients with and without pulmonary hypertension. METHODS: Twenty patients undergoing a valvular replacement were divided into two groups according to pulmonary artery pressure (PAP): control group (mean PAP < 25 mmHg, n = 9) or pulmonary hypertension group (mean PAP > 25 mmHg, n = 11). When systolic blood pressure decreased below 100 mmHg after the induction of anesthesia, phenylephrine was infused to raise systolic blood pressure up to 30% and 50% over baseline. Hemodynamic variables were measured at each time. RESULTS: Phenylephrine failed to raise systolic blood pressure up to 50% above baseline in more than half of the patients with pulmonary hypertension in contrast to successful increases in all patients without pulmonary hypertension. However, the ratio of PAP to systolic blood pressure was significantly reduced in patients whose systolic blood pressure was successfully increased up to 50% over baseline in the pulmonary hypertension group whereas the PAP concomitantly increased as systolic blood pressure was increased in the control group. CONCLUSIONS: Phenylephrine couldn't increase systolic blood pressure in some patients with pulmonary hypertension unlike in control group and it seemed to occur more often in patients with greater the ratio of PAP to systolic blood pressure. The baseline systemic vascular resistance index was high and cardiacoutput was low in the pulmonary hypertension group and these conditions seemed to restrict the effect of phenylephrine.
Anesthesia ; Blood Pressure ; Hemodynamics* ; Humans ; Hypertension, Pulmonary* ; Perfusion ; Phenylephrine* ; Pulmonary Artery ; Vascular Resistance ; Ventricular Dysfunction, Right

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

GTPrS-dependent phospholipase D activity in human neutrophils was investigated using exogenous phospholipid as a substrate. Both cytosolic and membrane- associated phospholipase D activities were identified. The previously described 50 kDa cytosolic activating factor was resolved chromatographically from the cytosolic phospholipase D. Using exogenous phospholipid as substrate along with chromatographically resolved 50 kDa factor and recombinant ADP-ribosylation factor 1, plasma membrane was required for activity, indicating that the activity which was previously seen using endogenous phospholipid substrate was due to a phospholipase D located in the plasma membrane. In addition, ADP-ribosylation factor and the 50 kDa factor activated synergistically. Using neutrophil plasma membranes, a third regulator of neutrophil membrane phospholipase D was identified from bovine brain cytosol. This factor was resolved from ADP-ribosylation factor and Rho A by successive column chromatographies. The brain factor showed a synergistic effect with the 50 kDa neutrophil activator but an additive effect with recombinant ADP- ribosylation factor. Whether or not ADP-ribosylation factor or the brain factor were present, high activities were seen only when the 50 kDa factor was present, indicating that the 50 kDa cytosolic factor is a major activating factor for the neutrophil plasma membrane phospholipase D.
ADP-Ribosylation Factor 1 ; ADP-Ribosylation Factors* ; Brain* ; Cell Membrane ; Chromatography ; Cytosol* ; Fibrinogen ; Humans ; Membranes ; Neutrophils* ; Phospholipase D* ; Phospholipases*