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H Okabe

Publications and source records attributed to H Okabe.

At least 127 records · Page 7Linked to original sources
PubMed1997

Carbohydrate antigen 19-9 expression by folliculo-tubular structures of normal and neoplastic pituitary.

We demonstrated immunohistochemically that follicular lining cells of anterior pituitary display carbohydrate antigen 19-9 (CA19-9) at their luminal surfaces. CA 19-9 was also demonstrated in the tubular structures of the intermediate lobe. Until now this antigen of exocrine ducts, such as pancreatic and salivary ducts, has not been demonstrated in endocrine tissue. Some CA19-9 positive follicular cells also showed endocrine markers such as chromogranin, synaptophysin and pituitary hormones. In pituitary adenomas, frequently-seen follicular structures showed immunohistochemical features similar to non-neoplastic follicles. Expression of CA19-9 in the adenohypophysis may be related to its origin from an anlage, the stomodeum shared with the parotid gland. The lining cells and mucin of Rathke's cleft cysts also revealed CA19-9. Accordingly, these cysts could have arisen from follicular cells with an exocrine ductal phenotype. The transitional cell tumor of Kepes also showed CA19-9 at the luminal surfaces of cells and in the mucin of large cysts. Given that smaller mucin-laden cysts appeared fairly frequently in adenomas, the transitional cell tumor may be a kind of pituitary adenoma with follicles in which many cells produce excessive mucin.

Adenoma↗
PubMed1997

Role of granulocyte elastase in indomethacin-induced gastric mucosal lesion formation in rats.

To investigate whether granulocyte elastase may be involved in indomethacin-induced gastric mucosal injury, we examined the effects of the granulocyte elastase inhibitors ONO-5046 and L-658,758 on gastric mucosal lesion formation in rats given indomethacin. Both gastric mucosal lesion formation and gastric mucosal vascular damage were markedly attenuated in animals with leukocytopenia and in those given granulocyte elastase inhibitors. The administration of indomethacin significantly increased gastric myeloperoxidase activity, a measure of leukocyte accumulation, 3 hours after the administration of indomethacin compared with activity in animals receiving saline solution. The administration of ONO-5046 or L-658,758 significantly prevented this increase. Histologic examinations revealed submucosal edema and marked infiltration by leukocytes, as well as widespread necrosis with loss of surface epithelium. ONO-5046 and L-658,758 markedly prevented these histologic changes. Although cimetidine significantly prevented mucosal lesion formation, it did not inhibit either granulocyte elastase release from activated neutrophils in vitro or gastric accumulation of leukocytes in vivo. These results suggest that granulocyte elastase as well as gastric acid may play an important role in the pathologic process by which indomethacin induces gastric mucosal lesions.

Animals↗
PubMed1997

Novel role of prostacyclin in stress-induced gastric mucosal lesion formation in rats.

We investigated the novel role of prostacyclin (PGI2) in gastric mucosal lesion formation induced by stress in rats. Gastric 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) levels were significantly increased 30 minutes after water-immersion restraint stress (WIR). Subcutaneous indomethacin (IM) (5 mg/kg) inhibited this increase but significantly exacerbated gastric mucosal lesion formation in rats subjected to WIR. Although gastric myeloperoxidase (MPO) activity was not increased by WIR, it significantly increased with time after WIR in animals pretreated with IM. NS-398, a selective inhibitor of cyclooxygenase-2, did not inhibit the WIR-induced increase in gastric 6-keto-PGF1alpha. Neither the gastric lesion index nor gastric MPO activity were affected in animals pretreated with NS-398 and subjected to WIR. WIR-induced mucosal lesion formation was significantly inhibited in animals given iloprost, a stable analog of PGI2, and in those with nitrogen mustard-induced leukocytopenia. Iloprost prevented the gastric leukocyte accumulation and exacerbation of gastric mucosal lesions induced by IM in animals subjected to WIR. These IM-induced events also were prevented in animals subjected to WIR with nitrogen mustard-induced leukocytopenia. These observations implicate leukocytes in the process leading to gastric mucosal lesions induced by WIR. The increase in WIR-induced gastric PGI2 synthesis, mainly mediated by cyclooxygenase-1, appears important in preventing lesion formation, not only by maintaining gastric mucosal blood flow but also by inhibiting leukocyte activation.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Lay-open pulmonary arterioplasty for postoperative hilar pulmonary artery stenosis.

OBJECTIVE: Lay-open pulmonary arterioplasty, a novel surgical technique to enlarge postoperative stenosis at the hilar pulmonary artery, was evaluated. METHODS: Lay-open arterioplasty, in which the enlarged hilar stenotic pulmonary artery is partially made up of previous surgical scar tissue instead of being covered by a patch, was performed on 10 patients whose ages ranged from 2.2 to 15.7 years. Surgical results were assessed by angiography. RESULTS: All patients tolerated the procedure without bleeding or embolic complications associated with pulmonary arterioplasty. Nine patients underwent concomitant procedures including total repair (n = 5), central interposing shunt (n = 3), and right ventricular outflow tract reconstruction (n = 1). No deaths or life-threatening events occurred during the total follow-up period of 18 patient-years. The stenotic segment was significantly enlarged from the preoperative diameter of 0.9 +/- 1.1 mm (mean +/- standard deviation) to the postoperative diameter of 8.0 +/- 1.3 mm, values which correspond to 7.0% +/- 8.8% and 68.4% +/- 11.5% of the normative values, respectively. A follow-up angiogram (n = 5) revealed an increase in the pulmonary artery diameter balanced with somatic growth (initial value, 65.2% +/- 9.0% of normal; second value, 69.1% +/- 7.7% of normal). No aneurysms or clinically significant restenoses were seen on the angiograms. CONCLUSIONS: Our initial midterm results with this method were promising. The pulmonary arteries subjected to this procedure grew in proportion to somatic growth.

Angioplasty↗
PubMed1997

Role of neutrophils in spinal cord injury in the rat.

Activated neutrophils are thought to be involved in tissue injury through the release of various inflammatory mediators. To understand the role of neutrophils in spinal cord injury, the effects of nitrogen mustard-induced leukocyte depletion and the administration of an anti-P-selectin monoclonal antibody on motor disturbances observed following spinal cord compression were examined in rats. Spinal cord injury was induced by applying a 20-g weight for 20 min at the level of the 12th thoracic vertebra, resulting in motor disturbances of the hindlimbs 24 h postcompression. Motor disturbances, evaluated using Tarlov's index, an inclined-plane test and climbing ability, were markedly attenuated in rats with nitrogen mustard-induced leukocytopenia. Administration of the anti-P-selectin monoclonal antibody, by which adhesion of activated neutrophils to endothelial cells may be inhibited, also attenuated motor disturbances. Histological examination revealed that intramedullary hemorrhages observed 24 h after compression at the 12th thoracic vertebra of the spinal cord were significantly attenuated in leukocytopenic animals and those which received the anti-P-selectin monoclonal antibody. The accumulation of neutrophils at the site of compression, as evaluated by measuring the tissue myeloperoxidase activity, significantly increased with time following the compression, peaking at 3 h postcompression. Spinal cord myeloperoxidase activity did not increase in sham-operated animals. Leukocyte depletion and administration of the anti-P-selectin monoclonal antibody both reduced the accumulation of neutrophils in the damaged spinal cord segment 3 h postcompression. These observations strongly suggest that activated neutrophils play an important role in compression-induced thoracic spinal cord injury and that a P-selectin-mediated interaction between activated neutrophils and endothelial cells may be a critical step in endothelial cell injury leading to spinal cord injury.

Animals↗
PubMed1997

Immunohistochemical demonstration of cytokeratin in human embryonic neurons arising from placodes.

Sensory neurons of the olfactory, trigeminal, facial, vestibulo-cochlear, glossopharyngeal and vagal nerves, and neurons migrating along the olfactory nerve to the brain have special anlagen, made up of placodes located in the epithelial layer. To investigate the characteristic phenotype of placode-derived neurons, immunohistochemical analysis of intermediate filaments was conducted on formalin-fixed human embryonic tissues. Neurons arising from placodes including luteinizing-hormone releasing hormone (LHRH) neurons migrating from the olfactory placode to the brain had immunoreactivity to antibodies specific to cytokeratin, AE1 and CAM5.2 during the embryonic stage. However, this immunoreactivity disappeared during the late embryonic to the post-embryonic stage and was not observed in the roots of these nerves in the post-natal stage. Immunoreactivity was detected in both the somata and processes, and the distribution differed from that described in rodent brain neurons. With this exception, no other human peripheral neurons, including spinal dorsal root ganglia, had immunoreactivity with anti-cytokeratin antibodies throughout the entire developmental stage. Although the cephalic neural crest also directly generates neurons to most of the cranial sensory ganglia, we could not find any evidence that it contributed to the genesis of cytokeratin-positive embryonic neurons. We concluded that cytokeratin is an intermediate filament common to human embryonic neurons of cephalic placodal origin and that this immunohistochemical marker may be useful in analyzing the developmental sequence of several congenital diseases involving the cranial nerves, such as Moebius syndrome and Goldenhar syndrome.

Adult↗
PubMed1997

Malignant lymphoma of the mandible: report of a case.

Extranodal malignant lymphoma is relatively rare. When it occurs in the oral region, it is sometimes misdiagnosed as inflammatory disease. This report details a case of malignant lymphoma that involved the fight mandibular region.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Rebamipide attenuates indomethacin-induced gastric mucosal lesion formation by inhibiting activation of leukocytes in rats.

Granulocyte elastase released from activated leukocytes plays an important role in leukocyte infiltration. Since activated leukocytes have been shown to be involved in the pathogenesis of gastric mucosal lesion formation induced by nonsteroidal antiinflammatory drugs, inhibition of granulocyte elastase release from activated leukocytes may be useful in the prevention of these lesions. Rebamipide, a novel antiulcer agent, inhibited granulocyte elastase release from activated neutrophils in vitro. Rebamipide and ONO-5046, a granulocyte elastase inhibitor, markedly inhibited gastric mucosal lesion formation in rats. Gastric myeloperoxidase activity was significantly increased 3 hr after indomethacin administration. This increase was significantly inhibited by rebamipide and ONO-5046. Cimetidine did not inhibit granulocyte elastase release from activated neutrophils. Although cimetidine markedly prevented the indomethacin-induced gastric mucosal lesion formation, it did not reduce the gastric myeloperoxidase activity. Therefore, unlike cimetidine, rebamipide may prevent indomethacin-induced gastric mucosal lesion formation by inhibiting neutrophil activation.

Alanine↗
PubMed1997

Molecular characterization of complement components (C3, C4, and factor B) in human saliva.

A molecular analysis of complement components (C3, C4, and factor B) in human saliva was performed by SDS-PAGE and immunoblotting. Complement C3 was detected as a molecule composed of a 115-kDa alpha-chain linked to a 70-kDa beta chain by disulfide bonds, and C3 levels ranged from 0.52 to 15.0 micrograms/ml (n = 15). C4 was detected as a triple-chain molecule (98-kDa alpha chain, 73-kDa beta chain, and 33-kDa gamma chain) linked by disulfide bonds, and C4 levels ranged from 0.086 to 4.8 micrograms/ml. Factor B was detected as a 100-kDa single chain, and factor B levels ranged from 0.042 to 0.62/microgram/ml. The sizes and subunit structures of the complement components in human saliva were compatible with those reported in human serum. The results of a hemolytic assay indicated that the complement molecules in human saliva were functionally active. These complement components may participate in the local immune and inflammatory responses in the oral cavity.

Complement C3↗
PubMed1997

Demonstration of thyroid stimulating activity within H chain fragments of TSAb-IgG by protease digestion and reduction.

OBJECTIVE: Whether or not the distribution of biologically active fragments in TSAb-IgG molecules parallels antigen-binding activity in other anti-thyroidal antibodies was examined. DESIGN: Both the thyroid stimulating (TS) activity (cAMP production in thyroid cells) and TSH binding inhibition (TBI) activity (determined by TSH receptor assay) were examined by measuring the reduction in TSAb-IgG followed by gel-filtration on Sephadex G-100. Two forms of IgG [IgG(kappa) and IgG(lambda)] were separated from TSAb-IgG by column chromatography using Protein L-Sepharose (specifically binds to kappa chain). The IgG(kappa) was reduced with dithiothreitol (DTT) and the unbound fraction (UF) (the free heavy (H) chain) and the bound fraction (BF) (the free kappa chain and the non-reduced IgG(kappa)) were separated using Protein L-Sepharose. The Fab fragment was separated by Protein A-Sepharose after papain hydrolysis of TSAb-IgG, then separated into two Fab(kappa) and Fab(lambda) forms by Protein L-Sepharose. The Fd fragment (or fragment containing Fd) was prepared from Fab(kappa) by DTT reduction followed by Protein L column. RESULTS: The free H chain fraction showed TS and TBI activity, but neither anti-thyroglobulin (Tg) nor anti-thyroid peroxidase (TPO) antibody activities. The free light (L) chain was not biologically active. Similar TS and TBI activities were found not only in IgG(kappa) and IgG(lambda) but also in the Fab(kappa) and Fab(lambda) fractions. Fd fragment that was not contaminated with free kappa chain had TS and weak TBI activities. CONCLUSIONS: The thyroid stimulating activity in 5 TSAb-IgG samples was found in IgG(kappa), IgG(lambda), Fab(kappa), Fab(lambda), H chain and Fd separated by papain digestion and reduction. These results showed that TSAb was polyclonal and that the Fd fragment was important as the biologically active site.

Chromatography↗
PubMed1997

Gabexate mesilate, a synthetic protease inhibitor, prevents compression-induced spinal cord injury by inhibiting activation of leukocytes in rats.

OBJECTIVE: Gabexate mesilate is a synthetic protease inhibitor capable of inhibiting both coagulation and cytokine production by monocytes. To investigate whether gabexate mesilate is useful for the prevention of posttraumatic spinal cord injury, we examined its effect on compression trauma-induced spinal cord injury in rats. DESIGN: Prospective, randomized, blinded, controlled study. SETTING: Research laboratory at a university medical center. SUBJECTS: Male Wistar rats weighing 300 to 350 g. INTERVENTIONS: Spinal cord injury was induced by applying a 20-g weight extradurally to the spinal cord at the level of the 12th thoracic vertebra for 20 mins. Spinal cord injury was evaluated by assessing the motor function of the rats 24 hrs posttrauma. The accumulation of leukocytes and histologic changes in the injured spinal cord tissue also were examined. Rats received gabexate mesilate (10 or 20 mg/kg i.p.) 30 mins before or after the compressive trauma. The effects of heparin or an inactive derivative of activated factor X (a selective inhibitor of thrombin generation) on compressive trauma-induced spinal cord injury also were examined. Leukocytopenia was induced by the administration of nitrogen mustard. MEASUREMENTS AND MAIN RESULTS: The motor disturbances observed following traumatic spinal cord compression, evaluated by Tarlov's score, and the accumulation of leukocytes in the injured tissue, evaluated by measuring tissue myeloperoxidase activity, were markedly reduced by leukocyte depletion induced by nitrogen mustard and by pre- or posttreatment of animals with gabexate mesilate. Neither heparin nor the inactive derivative of activated factor X prevented the motor disturbances and the accumulation of leukocytes. Histologic examination demonstrated that intramedullary hemorrhages observed 24 hrs after trauma at the 12th thoracic vertebra were significantly attenuated by nitrogen mustard-induced leukocytopenia and the administration of gabexate mesilate. CONCLUSIONS: The compression trauma-induced spinal cord injury demonstrated by this model was mainly mediated by leukocytes. Gabexate mesilate prevented spinal cord injury not by inhibiting coagulation, but by inhibiting the activation of leukocytes.

Amino Acid Chloromethyl Ketones↗
PubMed1997

Three-dimensional helical computed tomography with intravenous cholangiography for sclerosing cholangitis manifested as postcholecystectomy symptom.

A 46-year-old woman who had upper abdominal pain 10 years after cholecystectomy, and who had incidental sclerosing cholangitis (SC), was investigated by three-dimensional helical computed tomographic (3-DHCT) cholangiography with contrast medium, because endoscopic retrograde cholangiography (ERC) was unsuccessful and a second ERC was not permitted by the patient. The cholangiogram demonstrated annular strictures of the bilateral hepatic duct at the confluence of the common hepatic duct, and dilatation of the left intrahepatic biliary duct. Although we could not clarify the cause of the biliary tract deformity at the time of the 3-DHCT, the tentative diagnosis of postcholecystectomy deformity of the biliary tree led to successful treatment by right liver lobectomy and hepaticojejunostomy. Histologic findings were compatible with SC. From this experience and the literature, we suggest that 3-DHCT cholangiography with contrast medium can contribute to the preoperative diagnosis of morphological changes in the biliary tree in patients with postcholecystectomy symptoms.

Cholangiography↗
PubMed1997

Tumour necrosis factor-alpha up-regulates decay-accelerating factor gene expression in human intestinal epithelial cells.

The increased expression of decay-accelerating factor (DAF) has been detected in intestinal epithelial cells at the inflamed mucosa. In this study, we examined the effects of tumour necrosis factor (TNF)-alpha on DAF expression in three intestinal epithelial cell lines. DAF mRNA expression was evaluated by Northern blot analysis, and DAF protein expression was analysed by biotin labelling and immunoprecipitation. TNF-alpha induced a marked increase in DAF mRNA and protein expression in HT-29, T84 and Caco-2 cells. In HT-29 cells, the effects of TNF-a on DAF mRNA accumulation were observed in a dose-dependent manner; DAF mRNA accumulation reached a maximum at 3-6 hr, and then gradually decreased. These effects of TNF-alpha required de novo protein synthesis. Messenger RNA stability studies suggested that TNF-alpha partially regulated DAF gene expression by a posttranscriptional mechanism. Moreover, the combination of TNF-alpha and interleukin (IL)-4 induced an additive increase in DAF mRNA accumulation in HT-29 and T84 cells. In human intestinal epithelial cells, TNF-alpha acts as a potent inducer of DAF mRNA expression, indicating an important role for TNF-alpha in the regulation of DAF expression at the inflamed mucosa.

Blotting, Northern↗
PubMed1997

Latent infection with Epstein-Barr virus in odontogenic disorders: comparison among ameloblastoma, dentigerous cyst and odontogenic keratocyst.

In order to investigate the relationship between Epstein-Barr virus (EBV) latent infection and histogenesis of odontogenic disorders, in situ hybridization for EBV-encoded small RNA (EBER) was applied to the paraffin sections of ameloblastoma, dentigerous cyst, and odontogenic keratocyst. Eight cases (15%) of 53 ameloblastomas showed scattered signals for EBER in the parenchymal cells, whereas no reaction of EBER transcript was observed in the non-neoplastic cystic lesions. In the ameloblastoma, the follicular and plexiform types revealed the signals in the nuclei, but cystic, acanthomatous, granular, and basal cell types exhibited no reaction with EBER. The distribution of the signals without monoclonarity indicated that ameloblastoma cells may exclude EBV genomes or inactivate EBER-encoded genes. The results suggested that EBV participates as one of the transforming factors in the occurrence of ameloblastoma.

Adolescent↗
PubMed1997

Activated protein C prevents LPS-induced pulmonary vascular injury by inhibiting cytokine production.

We investigated the effect of activated protein C (APC) on pulmonary vascular injury and the increase in tumor necrosis factor (TNF) levels in lipopolysaccharide (LPS)-treated rats to determine whether APC reduces LPS-induced endothelial damage by inhibiting cytokine production. Intravenously administered LPS (5 mg/kg) induced pulmonary vascular injury, as indicated by an increase in the lung wet-to-dry weight ratio. LPS-induced pulmonary vascular injury was prevented by APC but not by active site-blocked factor Xa [dansyl glutamyl-glycyl-arginyl chloromethyl detone-treated activated factor X (DEGR-Xa)], a selective inhibitor of thrombin generation, or inactivated APC [diisopropyl fluorophosphate-treated APC (DIP-APC)]. APC, but not DEGR-Xa or DIP-APC, significantly inhibited the LPS-induced increase in the plasma level of TNF. APC significantly inhibited the production of TNF by LPS-stimulated monocytes in a dose-dependent fashion in vitro, but DIP-APC did not. APC did not inhibit the functions of activated neutrophils in vitro. These findings suggest that APC prevented LPS-induced pulmonary vascular injury by inhibiting TNF production by monocytes and not via its anticoagulant activity. The serine protease activity of APC appears to be essential for inhibition of TNF production.

Amino Acid Chloromethyl Ketones↗
PubMed1997

rhs-TM prevents ET-induced increase in pulmonary vascular permeability through protein C activation.

We have previously demonstrated that recombinant human soluble (rhs) thrombomodulin (TM) inhibits the endotoxin (ET)-induced increase in pulmonary vascular permeability by inhibiting leukocyte activation. In the present study, we examined whether rhs-TM could inhibit the ET-induced increase in pulmonary vascular permeability in rats by activating protein C. rhs-TM did not inhibit ET-induced increases in pulmonary vascular permeability when its protein C activation ability was selectively inhibited by a monoclonal antibody (MAb) against rhs-TM (MAb R5G12). Histological examination revealed that neutrophil infiltration in lung tissues after ET administration was significantly reduced by rhs-TM, but infiltration was not reduced by MAb R5G12-pretreated rhs-TM. ET-induced intravascular coagulation was prevented by rhs-TM and by MAb R5G12-pretreated rhs-TM. However, ET-induced coagulation was not prevented by rhs-TM that had been treated with MAb F2H5, which cannot bind thrombin or activate protein C. These observations strongly suggest that rhs-TM prevents ET-induced pulmonary vascular injury by inhibiting pulmonary accumulation of leukocytes through thrombin binding and the subsequent protein C activation and may prevent ET-induced intravascular coagulation through thrombin binding.

Animals↗
PubMed1997

Effect of nafamostat mesilate on pulmonary vascular injury induced by lipopolysaccharide in rats.

Nafamostat mesilate (NM) is a synthetic protease inhibitor that is capable of inhibiting the various coagulation factors such as factor VIIa and thrombin. To determine whether NM may also be useful in treating adult respiratory distress syndrome (ARDS) related in sepsis, we investigated the effect of NM on lipopolysaccharide (LPS)-induced pulmonary vascular injury in rats. The intraperitoneal administration of NM prevented the pulmonary vascular injury and coagulation abnormalities induced by LPS. DEGR-factor VIIa, a selective inhibitor of factor VIIa, prevented the coagulation abnormalities, but not the pulmonary vascular injury, induced by LPS. NM did not reduce LPS-induced increase in pulmonary accumulation of leukocytes. NM did not inhibit the increase in the plasma concentration of tumor necrosis factor-alpha (TNF-alpha) observed after administration of LPS. NM did not inhibit the function of activated neutrophils in vitro. Plasma values of total serum hemolytic complement (CH50) were markedly decreased after the administration of LPS. NM inhibited the LPS-induced decrease in plasma CH50 values. Findings suggest that NM may reduce the pulmonary vascular injury as well as the coagulation abnormalities induced by LPS. The former effect may be independent of the anticoagulant effect but dependent on the inhibitory effect of the activation of the complement system in rats administered LPS.

Animals↗