Color Doppler sonographic findings of fetal upper respiratory tract obstruction.
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Adult↗
Biomedical subjects
M Okamura
Publications and source records attributed to M Okamura.
Placental aminopeptidase A as a possible barrier of angiotensin II between mother and fetus.
Aminopeptidase A (AP-A EC 3.4.11.7), which is a membrane-bound zinc metalloprotease, is present in the placenta. AP-A selectively hydrolyzes N-terminal glutamyl and aspartyl residues and cleaves angiotensin II to form angiotensin III. To determine the role of placental aminopeptidase A under physiological and pathological conditions, we evaluated its immunolocalization and enzymatic activities in the placenta. AP-A was localized in the basal zone of the syncytiotrophoblast, in the membranes of the cytotrophoblast, and in fetal arterioles and venules within the stem villi. AP-A activity in the microsomal fraction of placental villi seemed to be remained essentially constant throughout gestation. The renin-angiotensin system is considered to be accelerated in pre-eclampsia. This AP-A activity was higher in pre-eclampsia (2.86+/-0.30 nmol beta NA/mg protein/h) than in uncomplicated pregnancy from 28 to 41 weeks of gestation (2.08+/-0.18 nmol beta NA/mg protein/h). Angiotensin II evoked AP-A activity in first trimester trophoblast, and Losartan and PD 123177 in combination significantly inhibited this induction of AP-A activity. The results of immunohistochemical evaluation and enzymatic activity suggested that placental aminopeptidase A may play a role as a component of the barrier of angiotensin II between mother and fetus.
Adult↗
Relationship of renal histological damage to glomerular hypertension in patients with immunoglobulin A nephropathy.
OBJECTIVE: Studies of experimental animals show glomerular hypertension to be important in the progression of glomerular disease. We evaluated this connection clinically by examining the relationship between glomerular hemodynamics and histological changes in patients with immunoglobulin (Ig)A nephropathy. METHODS: The subjects were 23 patients with IgA nephropathy. All patients underwent renal biopsies. Glomerular hemodynamics, in terms of glomerular capillary hydraulic pressure (PGC) and the whole-kidney ultrafiltration coefficient, were calculated from the renal clearance, plasma total protein concentration, and pressure-natriuresis relationship. The severity of glomerulosclerosis, tubulointerstitial damage and mesangial matrix expansion was evaluated semiquantitatively. RESULTS: PGC ranged from 33-69 mm Hg, and the mean arterial pressure (MAP) from 79-112 mm Hg. Their correlation was not significant (r= 0.29, P= 0.18). PGC was significantly correlated with the glomerulosclerosis score, and also with the score for tubulointerstitial damage (r= 0.65, P < 0.001 and rs = 0.59, P = 0.007, respectively), but not with the score for mesangial matrix expansion (r= 0.08, P= 0.72). MAP was significantly correlated only with the score for tubulointerstitial damage (rs = 0.63, P = 0.004). In multiple linear regression analysis of the histological changes and hemodynamics, the glomerulosclerosis score and the score for tubulointerstitial damage were correlated with PGC, but not with MAP. CONCLUSION: These clinical results support the speculation that glomerular hypertension is involved in the glomerulosclerosis and tubulointerstitial damage that occurs in IgA nephropathy.
Adult↗
Oxytocin stimulates the translocation of oxytocinase of human vascular endothelial cells via activation of oxytocin receptors.
Oxytocinase (OTase) degrades several small peptides such as oxytocin (OT), and thus plays important roles in fetal development and maintenance of human homeostasis during pregnancy. The physiological effects of OT are mediated via its receptor (OTR). Although the interactions between OT and OTR have studied extensively, the relationship to OTase remains to be clarified. It is known that human umbilical vascular endothelial cells express OTR messenger RNA; therefore, they were selected for examination of this question in the present study. RT-PCR experiments confirmed the existence of messenger RNA for OTase, and assessment of protein levels and activity clarified that OT increases the activity of OTase at the cell surface via binding to OTR. This stimulation appears to involve translocation of OTase from cytosolic to the cell surface in response to cellular signal transduction pathways linked to the OTR. Protein kinase C stimulation significantly increased the cell surface activity of OTase, whereas its inhibition resulted in reduction. In summary, our findings provide clear evidence that OT triggers directly OTase translocation in human umbilical vascular endothelial cells via a protein kinase C-dependent pathway coupled to OTR.
Biological Transport↗
[Adenocarcinoma of the ileal segment with transitional cell carcinoma of the bladder following ileocytoplasty: a case report].
A 67 year-old woman visited our hospital complaining of pollakisuria. She had undergone left nephrectomy and augmentation ileocystoplasty for tuberculous bladder atrophy 40 years previously. She underwent a total cystectomy and tubeless ureterocutaneostomy with a preoperative diagnosis of muscle-invading transitional cell carcinoma of the bladder. The pathological diagnosis was adenocarcinoma of the ileal segment and transitional cell carcinoma of the original bladder. This is the first case report of adenocarcinoma of the ileal segment and transitional cell carcinoma of the original bladder among 22 patients suffering from bladder cancer after ileocystoplasty.
Adenocarcinoma↗
[Evaluation of cerebral metabolism by multi-voxel proton magnetic resonance spectroscopy imaging in chronic unilateral internal carotid artery occlusion].
Proton magnetic resonance spectroscopy(1H-MRS) has less been used to analyze cerebral metabolism in ischemic lesions compared to single photon emission computed tomography or positron emission computed tomography. Recent advances in magnetic resonance imaging apparatus and the related software have made possible obtaining multi-voxel 1H-MRS in a single study. We examined multi-voxel 1H-MRS in patients with unilateral internal carotid artery(ICA) occlusion to study the relationship between cerebral metabolism and cerebral blood flow. Fifteen patients(male 11; female 4, 47-76; average 67.1 year-old) with chronic unilateral ICA occlusion and without any marked infarction were studied. 1H-MRS was obtained using a 1.5 T Siemens Magnetom Vision scanner. Multi-voxel spectra were recorded using a SE-2 D-CSI sequence(TR/TE = 1500/135 ms). The volume of interest was 90 x 90 x 20 mm3, placed axially above the lateral ventricle. The single voxel size was 10 x 10 x 20 mm3. N-acetyl aspartate/creatine ratios(NAA/Cr) were calculated on each voxel and were averaged in view of the cortex and the white matter. The regional cerebral blood flow(CBF) was measured by Xenon-CT method. Eight patients were also examined by acetazolamide challenge to evaluate the cerebrovascular reserve capacity. NAA/Cr ratios in normal subjects were 1.905 +/- 0.090(mean +/- standard deviation) in the cortex and 2.183 +/- 0.258 in the white matter in 40's(n = 6), 2.046 +/- 0.166 in the cortex and 2.039 +/- 0.288 in the white matter in 60's(n = 5). The study revealed 7 patients with normal NAA/Cr ratio and CBF, 5 with reduced NAA/Cr ratio and normal CBF, and 3 with reduced NAA/Cr ratio and CBF in the affected cortex. A low correlation coefficient of 0.46 was noted between NAA/Cr ratio and the cerebrovascular reserve capacity calculated by acetazolamide challenge in the affected cortex. In the range of less than +10%(lower limit) in percentile change of regional CBF after acetazolamide injection, NAA/Cr ratio was distributed between 1.600 and 2.044, which were normal or slightly under the lower limit(mean-2 x standard deviation). Multi-voxel 1H-MRS is useful for the evaluation of cerebral metabolism, because it enables to quantify different chemicals in many fields at one time and to compare its distribution with regional CBF. In patients with unilateral ICA occlusion, NAA/Cr ratio of the affected cortex varies depending on the collateral circulation and the contralateral ICA lesions. The Extracranial-Intracranial Bypass should be considered if the case with unilateral ICA occlusion reveals reduced CBF and normal or slightly decreased NAA/Cr ratio in the affected cortex.
Aged↗
Cytomegalovirus associated pancreatitis in a patient with systemic lupus erythematosus.
Pancreatitis can develop as a complication of systemic lupus erythematosus (SLE). Steroids are considered one of the possible causes of this complication, but the pathological mechanism is unclear. We describe an autopsy case of a 29-year-old woman with cytomegalovirus (CMV) associated pancreatitis that developed during steroid therapy for her SLE. Many parenchymal cells with cytomegalic inclusions were seen in the patient's pancreas, especially in lesions showing active inflammation, and transcripts of CMV major immediate-early and late genes, markers of active viral replication, were detected. These findings suggest that CMV played an etiological role in the pancreatic disorder.
Adult↗
Identification of an ATP-binding cassette transporter involved in bicarbonate uptake in the cyanobacterium Synechococcus sp. strain PCC 7942.
Exposure of cells of cyanobacteria (blue-green algae) grown under high-CO(2) conditions to inorganic C-limitation induces transcription of particular genes and expression of high-affinity CO(2) and HCO(3)(-) transport systems. Among the low-CO(2)-inducible transcription units of Synechococcus sp. strain PCC 7942 is the cmpABCD operon, encoding an ATP-binding cassette transporter similar to the nitrate/nitrite transporter of the same cyanobacterium. A nitrogen-regulated promoter was used to selectively induce expression of the cmpABCD genes by growth of transgenic cells on nitrate under high CO(2) conditions. Measurements of the initial rate of HCO(3)(-) uptake after onset of light, and of the steady-state rate of HCO(3)(-) uptake in the light, showed that the controlled induction of the cmp genes resulted in selective expression of high-affinity HCO(3)(-) transport activity. The forced expression of cmpABCD did not significantly increase the CO(2) uptake capabilities of the cells. These findings demonstrated that the cmpABCD genes encode a high-affinity HCO(3)(-) transporter. A deletion mutant of cmpAB (M42) retained low CO(2)-inducible activity of HCO(3)(-) transport, indicating the occurrence of HCO(3)(-) transporter(s) distinct from the one encoded by cmpABCD. HCO(3)(-) uptake by low-CO(2)-induced M42 cells showed lower affinity for external HCO(3)(-) than for wild-type cells under the same conditions, showing that the HCO(3)(-) transporter encoded by cmpABCD has the highest affinity for HCO(3)(-) among the HCO(3)(-) transporters present in the cyanobacterium. This appears to be the first unambiguous identification and description of a primary active HCO(3)(-) transporter.
ATP-Binding Cassette Transporters↗
Comparative studies of modulatory effect to the function of rat peritoneal neutrophils treated with new quinolones.
Some of the immunological effects of a variety of new quinolones on adhesion, phagocytosis, and production of reactive oxygen intermediators in neutrophils were studied. Ofloxacin, lomefloxacin, fleroxacin, and levofloxacin potentiated the phagocytosis of Escherichia coli in neutrophils. Moreover, lomefloxacin, and sparfloxacin significantly potentiated adhesion of neutrophils. In contrast, tosufloxacin was effective in significantly and persistently potentiating the production of superoxide anion, whereas the other agents markedly inhibited such production. Furthermore, tosufloxacin was effective in significantly potentiating the production of hydrogen peroxide, whereas sparfloxacin markedly inhibited such production. These results suggest that the new quinolones at a therapeutic concentration may affect functions such as phagocytosis, and production of superoxide anion in neutrophils.
4-Quinolones↗
Wortmannin, an inhibitor of phosphatidylinositol kinases, blocks the MgATP-dependent recovery of Kir6.2/SUR2A channels.
1. In order to investigate the mechanism underlying MgATP-dependent recovery of ATP-sensitive potassium (KATP) channels, we expressed Kir6.2/SUR2A (inwardly rectifying K+ channel subunit/sulfonylurea receptor) or C-terminal-truncated Kir6.2 (Kir6.2DeltaC26) in COS7 cells (Green monkey kidney cells), and carried out inside-out patch clamp experiments. 2. After patch excision in ATP-free internal solution, the activity of Kir6.2/SUR2A channels could be maximally recovered by the application of 5 mM MgATP. Subsequent application of 100 microM Ca2+ induced a rapid decay of Kir6.2/SUR2A activity to 11.6 +/- 1.1 % (mean +/- s.e.m.) of the control level (Ca2+-induced run-down; n = 64). 3. MgATP (5 mM) recovered 99.4 +/- 4.2 % (n = 13) of the Ca2+-induced run-down. Protein kinase inhibitors such as W-7, H-7, H-8 and genistein did not inhibit this reaction. However, wortmannin, an inhibitor of phosphatidylinositol 3- and 4-kinases, blocked the MgATP-dependent recovery in a concentration-dependent manner; the magnitudes of recovery were 35.7 +/- 7.2 % (10 microM) and 4.3 +/- 2.5 % (100 microM) of the Ca2+-induced run-down. 4. MgUDP (10 mM) reversed the Ca2+-induced run-down of Kir6.2/SUR2A channels by 60.4 +/- 7.6 % (n = 5). Wortmannin failed to modify this reaction. 5. Kir6.2DeltaC26 channels, which opened in the absence of SUR2A, were less sensitive to Ca2+; Kir6.2DeltaC26 channels were inactivated to 44.8 +/- 4.4 % (n = 14) by 100 microM Ca2+. MgATP recovered the Ca2+-induced run-down of Kir6.2DeltaC26 by 89.8 +/- 7. 7 % (n = 9), and 100 microM wortmannin inhibited this reaction (1.8 +/- 2 %, n = 7). 6. Application of 10 microM phosphatidylinositol-4, 5-bisphosphate (PI-4,5-P2) recovered the activity of Kir6.2/SUR2A channels after Ca2+-induced run-down (104.3 +/- 6.4 %, n = 10). Even after the MgATP-dependent recovery was blocked by 100 microM wortmannin, PI-4,5-P2 reactivated the channels (102.3 +/- 8.6 %, n = 5). Similar results were obtained with Kir6.2DeltaC26. 7. These results suggest that the entity of MgATP-dependent recovery may be membrane lipid phosphorylation rather than protein phosphorylation, and that synthesis of PI-4,5-P2 or phosphatidylinositol-3,4, 5-trisphosphate may upregulate Kir6.2 channels.
ATP-Binding Cassette Transporters↗
Spontaneous regression associated with apoptosis in a patient with acute-type adult T-cell leukemia.
We describe a 76-year-old man with acute-type adult T-cell leukemia, who demonstrated a spontaneous decrease in leukemic cell number, apparently coincident with apoptotic cell death. On admission the patient's white blood cell count was 38.9 x 10(9)/l with 77% abnormal lymphocytes. He also had hypoproteinemia (4.3 g/dl) from protein losing enteropathy. After admission the leukemic cell count decreased without chemotherapy, reaching 5.9 x 10(9)/l after 2 months. Studies of peripheral lymphocytes demonstrated appearance of the apoptotic cells and DNA ladder formation from the beginning of regression. Same truncated proviral DNA was recognized in primary ATL cells through the whole clinical course. The hypoproteinemia improved with intravenous nutrition, followed by increase of the leukemic cells. This case is the first report that demonstrates tumor-cell apoptosis induced clinical regression in adult T-cell leukemia. Further, we speculate that the hypoproteinemia may have been involved in the leukemic cell apoptosis.
Aged↗
Fetal sacrococcygeal teratoma visualized by ultra-fast T2 weighted magnetic resonance imaging.
We report here a fetal sacrococcygeal teratoma found at 26 weeks of gestation. An ultra-fast T2 weighted imaging method enables the clear visualization of morphological details of the fetus without motion artifacts. Complete surgical resection was performed immediately after cesarean birth, and no evidence of tumor recurrence was confirmed at 1 year of age.
Adult↗
Control elements of muscarinic receptor gene expression.
Studies describing the structures of the M1, M2 and M4 muscarinic acetylcholine receptors (mAChR) genes and the genetic elements that control their expression are reviewed. In particular, we focus on the role of the neuron-restrictive silencer element/restriction element-1 (NRSE/RE-1) in the regulation of the M4 mAChR gene. The NRSE/RE-1 was first identified as a genetic control element that prevents the expression of the SCG-10 and type II sodium channel (NaII) genes in non-neuronal cells in culture. The NRSE/RE-1 inhibits gene expression by binding the repressor/silencer protein NRSF/REST, which is present in many non-neuronal cell lines and tissues. Our studies show that although the expression of the M4 mAChR gene is inhibited by NRSF/REST, this inhibition is not always complete. Rather, the efficiency of silencing by NRSF/REST is different in different cells. A plausible explanation for this differential silencing is that the NRSF/RE-1 interacts with distinct sets of promoter binding proteins in different types of cells. We hypothesize that modulation of NRSF/REST silencing activity by these proteins contributes to the cell-specific pattern of expression of the M4 mAChR in neuronal and non-neuronal cells. Recent studies that suggest a more complex role for the NRSE/RE-1 in regulating gene expression are also discussed.
Animals↗
Prevalence of infection with TT virus (TTV), a novel DNA virus, in healthy Japanese subjects, newborn infants, cord blood and breast milk.
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Adolescent↗
Effect of cysteine protease of Porphyromonas gingivalis on adhesion molecules in gingival epithelial cells.
We examined the effect of cysteine protease of Porphyromonas gingivalis (P. gingivalis) on cell adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and very late antigen-4 (VLA-4) of human gingival epithelial cells. The cells were incubated for 48 hr with or without P. gingivalis protease. Their cell adhesion molecule expression levels were increased at 12 hr, but decreased at 18-48 hr. This result suggests that protease degrades cell adhesion molecules. After the stimulation with protease for 12 hr, P. gingivalis fimbrial binding to a monolayer of the cells was effectively inhibited by the addition of the cell adhesion molecules, suggesting the fimbrial binding to the cells occurred through cell surface adhesion molecules.
Bacterial Adhesion↗
[Human placental lactogen (hPL)].
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Female↗
[Case of primary aldosteronism associated with heart and kidney failure].
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Aldosterone↗
Hepatocyte growth factor in human amniotic fluid promotes the migration of fetal small intestinal epithelial cells.
OBJECTIVE: Previously we reported on the abundant existence of hepatocyte growth factor in amniotic fluid. This study was conducted to clarify the effects of hepatocyte growth factor in amniotic fluid on fetal intestinal epithelial cells. STUDY DESIGN: Amniotic fluid samples were obtained from 22 cases at various gestational ages. The effects of amniotic fluid and recombinant human hepatocyte growth factor on proliferation, migration, and morphogenesis of intestine 407 cells (a cell line derived from fetal intestinal epithelial cells) were investigated. RESULTS: The mobility of intestine 407 cells was stimulated by amniotic fluid in proportion to the concentration of hepatocyte growth factor in amniotic fluid with the same effect observed with recombinant human hepatocyte growth factor. This activity was neutralized by addition of antihuman hepatocyte growth factor antibody. Neither increased deoxyribonucleic acid synthesis nor morphogenesis in response to amniotic fluid was identified under the conditions used. CONCLUSION: Amniotic fluid stimulates intestinal epithelial cell migration by way of hepatocyte growth factor in amniotic fluid during development of the fetal intestine.
Amniotic Fluid↗