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Biomedical subjects

H Inoue

Publications and source records attributed to H Inoue.

At least 199 records · Page 11Linked to original sources
PubMed2001

Microtensile bond strength evaluation of three adhesive systems in cervical dentin cavities.

PURPOSE: To evaluate the influence of the orientation of dentinal tubules on the bonding performance, microtensile bond strengths (MTBS) to dentin in cervical dentin cavities were measured for three current bonding systems. MATERIALS AND METHODS: Wedge-shaped cervical cavities (5 x 5 x 3 mm) prepared in extracted human premolars were treated with one of the three adhesive systems, Gluma One Bond, UniFil Bond and Mega Bond in combination with a hybrid-type resin composite. After storage in water for 24 h, the teeth were sectioned longitudinally through the restoration for determination of MTBS, either at the coronal or at the apical wall of the lesion. In an additional group, either the coronal or the apical walls were coated with vaseline prior to adhesive bonding and insertion of the resin composite, and then MTBS was measured. RESULTS: MTBSs (mean +/- SD, MPa) to coronal and apical dentin were 35.1 +/- 19.1 and 16.4 +/- 7.9 for Gluma One Bond, 37.7 +/- 11.5 and 18.6 +/- 8.6 for UniFil Bond, and 27.0 +/- 15.2 and 30.3 +/- 17.0 for Mega Bond, respectively. MTBS to the coronal wall was higher than to the apical wall (p < 0.05) with Gluma One Bond and UniFil Bond, whereas no difference was found with Mega Bond. With all three systems, vaseline coating had no effect on the bond strength (p > 0.05), indicating that the wall-to-wall contraction stresses exerted in the noncoated group had no influence on the bond strength generated. CONCLUSION: In cervical dentin cavities, apart from the individual adhesive's bonding capacity, the dentinal tubular orientation may have an influence on the bond strength.

Adhesives↗
PubMed2000

Thapsigargin, a Ca(2+)-ATPase inhibitor, relaxes guinea pig tracheal smooth muscle by producing epithelium-dependent relaxing factors.

A non-phorbol ester-type tumor promoter, thapsigargin has been reported to deplete Ca(2+) stores in endothelial cells by inhibiting Ca(2+)-ATPase, which in turn increases intracellular Ca(2+) by mobilization of extracellular Ca(2+), leading to activation of constitutive nitric oxide synthase (cNOS) and resultant generation of nitric oxide (NO). In the present study, to evaluate the role of Ca(2+) in the release of epithelium-dependent relaxing factor (EpDRF), we determined the effect of thapsigargin (10(-6) M) on the contraction evoked by exogenous Ca(2+) or acetylcholine (10(-5) M) in epithelium-denuded or epithelium-intact smooth muscle from guinea pig trachea. The following results were obtained: (1) In epithelium-denuded smooth muscle, the contraction evoked by exogenous Ca(2+) in Ca(2+)-free solution or by acetylcholine (10(-5) M) in Ca(2+)-containing solution did not change within 20 min after thapsigargin application, but the contraction evoked by exogenous Ca(2+) increased markedly after 120 min, indicating that thapsigargin had no effect on smooth muscle itself within 20 min of application. The following experiments were performed within 20 min of thapsigargin application. (2) In epithelium-intact smooth muscle, thapsigargin significantly suppressed the contraction evoked by acetylcholine, suggesting that thapsigargin stimulate the epithelium to produce EpDRF. N(G)-nitro-L-arginine methylester (L-NAME) partly, but significantly, attenuated this inhibitory effect of thapsigargin. (3) In epithelium-denuded smooth muscle, atropine (10(-6) M) and L-NAME (10(-5) M) did not change the contraction evoked by exogenous Ca(2+) after application of thapsigargin, suggesting that thapsigargin did not stimulate acetylcholine and NO release from nerve terminals. These results suggest that thapsigargin (10(-6) M) may stimulate EpDRF, including NO and other factor(s) by Ca(2+)-dependent mechanisms.

Acetylcholine↗
PubMed2000

Low doses of oral dexamethasone for hormone-refractory prostate carcinoma.

BACKGROUND: Although glucocorticoids have been used to treat patients with hormone-refractory prostate carcinoma (HRPC), reports have varied regarding the types and doses of glucocorticoids used as well as their clinical benefits. In the current study, low doses of dexamethasone were investigated for their specific beneficial effects and the feasibility of long term treatment. METHODS: Thirty-seven patients diagnosed with HRPC were treated with oral dexamethasone (0.5-2 mg/day). The patients ranged in age from 53-89 years (median, 74 years). Thirty-two patients, including 6 with lymph node metastases, had bone involvement whereas only 5 patients were found to have elevated serum prostate specific antigen (PSA) levels. RESULTS: Twenty-three patients (62%) who received no other concomitant therapy demonstrated a decline in their serum PSA level of > or = 50%, which was confirmed by a second PSA value obtained > or = 4 weeks later. The median time to PSA progression was 9 months. Among 18 patients with bone pain, 11 (61%) had improvement and in 5 patients (28%) the pain became stable. Among 21 patients with interpretable bone scans, 4 (19%) showed improvement and 8 (38%) achieved stable disease. Both symptomatic and objective responses of bone metastases were correlated with declines in the serum PSA level of > or = 50%. Ten patients achieved an increase in their hemoglobin level of at least 2 g/dL. Patients whose PSA level declined by > or = 50% with therapy had significantly prolonged survival (median, 22 months). As pretreatment markers, a longer interval before the initial evidence of disease progression appeared was found to correlate significantly with posttherapy PSA declines of > or = 75%. All side effects of the glucocorticoids were reported to be mild. CONCLUSIONS: Low doses of dexamethasone were found to be beneficial in the treatment of HRPC, decreasing the severity of anemia and osseous disease as well as reducing serum PSA levels. A posttherapy serum PSA decline of > or = 50% appears to be a reliable marker of improved survival with this therapy.

Administration, Oral↗
PubMed2000

Prognostic impact of tissue inhibitor of matrix metalloproteinase-1 in esophageal carcinoma.

Tissue inhibitor of metalloproteinase-1 (TIMP-1) inhibits the activity of matrix metalloproteinase, which may play an important role in carcinoma invasion and metastasis. TIMP-1 is thus considered to inhibit carcinoma invasion and metastasis. However, TIMP-1 possesses another important function, cell growth promotion. The clinical significance of TIMP-1 expression has not been fully determined in esophageal carcinoma. We thus examined the expression of TIMP-1 mRNA in tumor (T) and corresponding normal (N) tissues of 85 esophageal carcinoma cases by RT-PCR. The T:N ratio of TIMP-1 mRNA expression in each case was evaluated semi-quantitatively with adjustment by an internal control gene. The mean T:N ratio was 2.0 (range 0.2-6.5). When comparing high-expression cases (T:N > 2.0, n = 37) with low-expression cases (T:N < or = 2.0, n = 48), the former showed a significantly higher frequency of lymph vessel invasion, vascular vessel invasion, lymph node metastasis and advanced-stage disease. The former cases showed a poorer prognosis than the latter. Multivariate analysis disclosed that TIMP-1 expression status was an independent determining factor for prognosis. Our findings suggest that TIMP-1 expression correlates with tumor extension of esophageal carcinoma and might, if validated, prove useful as a novel prognostic marker for esophageal carcinoma.

Aged↗
PubMed2000

A reverse transcriptase-polymerase chain reaction assay in the diagnosis of soft tissue sarcomas.

BACKGROUND: Many types of sarcomas are characterized by specific chromosomal translocations that result in the production of novel chimeric genes. Detection of these fusion genes could be a sensitive molecular diagnostic assay. However, to the authors' knowledge there have been few systemic comparisons between the current histopathologic diagnosis and the presence or absence of particular fusion genes in patients with adult soft tissue sarcomas (STSs). METHODS: Total RNA was extracted from 75 cases of STS and analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) assay for the detection of a variety of fusion transcripts. The results of the molecular assay were compared with standard histopathologic diagnoses. RESULTS: Of the 18 tumors diagnosed as synovial sarcoma, 17 (94%) expressed SYT-SSX chimeric transcripts. All nine myxoid liposarcomas were positive for FUS-CHOP fusion transcripts. Of the four cases of Ewing sarcoma, two had an EWS-FLI1 fusion transcript and one had an EWS-ERG fusion transcript. A clear cell sarcoma had a EWS-ATF1 fusion transcript. None of 19 cases of malignant fibrous histiocytoma nor 3 leiomyosarcomas contained a fusion transcript. Three cases with an initial diagnosis other than synovial sarcoma expressed a SYT-SSX fusion transcript. A review of the slides and additional examination showed that a diagnosis of synovial sarcoma was appropriate for these cases. There was a trend for biphasic synovial sarcoma to contain the SYT-SSX1 fusion. CONCLUSIONS: The authors believe RT-PCR assay for the detection of a specific fusion gene provides a useful tool for confirmation of the diagnosis of adult STS in diagnostically difficult cases and in retrospective studies.

DNA Primers↗
PubMed2000

Regulation of constitutive cyclooxygenase-2 expression in colon carcinoma cells.

Cyclooxygenase-2 (COX-2) is not normally expressed in the human large intestine, but its levels are increased in the majority of human colorectal carcinomas. Here we investigate the regulation of constitutive COX-2 expression and prostaglandin production in human colorectal carcinoma cells. Both COX-2 mRNA and protein were expressed in well differentiated HCA-7, Moser, LS-174, and HT-29 cells, albeit at different levels. COX-2 expression was not detected in several poorly differentiated colon cancer cell lines including DLD-1. Transcriptional regulation played a key role for the expression of COX-2 in human colon carcinoma cells, and both the nuclear factor for interleukin-6 regulatory element and the cAMP-response element were responsible for regulation of COX-2 transcription. COX-2 mRNA was more stable in HCA-7 cells than in the other cell lines tested. Both transcriptional and post-transcriptional regulation of COX-2 involved the MAP kinase pathway. Modulation of the Akt/protein kinase B or Rho B signaling pathways altered the levels of COX-2 expression. Furthermore, COX-2 protein is degraded through ubiquitin proteolysis, and its half-life was approximately 3.5-8 h. HCA-7 cells produced significant quantities of prostaglandin E(2) and other prostaglandins. Moser and LS-174 cells also generated prostaglandins, but levels were significantly lower than that observed in HCA-7 cells.

Colonic Neoplasms↗
PubMed2000

Effects of naltrexone on the accumulation of L-3, 4-dihydroxyphenylalanine and 5-hydroxy-L-tryptophan and on the firing rate induced by acute ethanol administration.

In order to characterize the effects of naltrexone, a mu-opioid receptor antagonist, on acute ethanol-induced functional modification of dopaminergic neurons in the nigrastriatal and mesolimbic dopamine systems, the accumulation of L-3, 4-dihydroxyphenylalanine (L-DOPA) in the cerebral cortex, dorsal striatum and nucleus accumbens and of 5-hydroxy-L-tryptophan (5-HTP) in the hippocampus was measured in normal rats using the mu-hydroxybenzylhydrazine dihydrochloride (NSD-1015) enzymatic inhibition method. In addition, the firing rates of dopaminergic neurons were recorded in the substantia nigra and ventral tegmental area. Naltrexone resulted in a decrease in the dopaminergic neuronal firing rates activated by ethanol and eventually in a reduction of the dopamine synthesis induced by ethanol in the dorsal striatum and nucleus accumbens, but not in the cerebral cortex. Mesolimbic dopamine neurons were slightly more sensitive to ethanol and naltrexone than were nigrostriatal dopamine neurons. The widespread inhibitory action of naltrexone also decreased the ethanol-induced stimulation of hippocampal serotonin synthesis.

5-Hydroxytryptophan↗
PubMed2000

Risk factors for thromboembolism in patients with paroxysmal atrial fibrillation.

There is some controversy concerning which clinical characteristics predict thromboembolism and whether treatment with class I antiarrhythmic drugs reduces thromboembolim in patients with paroxysmal atrial fibrillation (AF). This retrospective, multicenter study was undertaken to determine risk factor or factors for thromboembolism in patients with paroxysmal AF. Seven hundred forty patients with paroxysmal AF (mean age 56 years) without prior thromboembolic events were followed retrospectively. Cerebral thromboembolism, including transient ischemic attack and embolism of peripheral arteries, were selected as primary end points. Independent risk factors were determined with multivariate analysis, and event-free survival curves were estimated. During 3.4-year follow-up period, primary end points occurred in 55 patients (2.2% per year). Patients with thromboembolism had a higher prevalence of underlying heart disease (p <0.01), less frequent treatment with antiarrhythmic drugs (p <0.01), and received diuretics more often (p <0.01) compared with patients without thromboembolism. Age (>/=65 years, RR 3.33, p = 0.0001) and gender (male, RR = 2, p = 0.0291) emerged as predictors of thromboembolism by multivariate analysis with Cox's proportional hazard model. Treatment with antiarrhythmic drugs (RR = 0.57, p = 0.0578) and aspirin (RR = 0.52, p = 0.1094) showed trends toward reducing thromboembolic risks. It is suggested that elderly men (>/=65 years) with paroxysmal AF are at risk for thromboembolism, but the risk tended to be reduced by treatment with antiarrhythmic drugs and aspirin.

Atrial Fibrillation↗
PubMed2000

Expression of connective tissue growth factor in cartilaginous tumors.

BACKGROUND: Connective tissue growth factor (CTGF) predominantly is expressed in hypertrophic chondrocytes and its specific receptors are demonstrated on chondrocytic cells. Therefore, CTGF may be involved in the proliferation and/or differentiation of cartilage cells. In the current study, CTGF expression was examined both in chondrosarcoma and enchondroma to clarify the relation between the expression of CTGF and the grade of malignancy. METHODS: The expression of CTGF and proliferating cell nuclear antigen (PCNA) were analyzed immunohistochemically in 34 cartilaginous tumor specimens. Eighteen tumors were determined to be chondrosarcoma including 8 Grade 1 tumors, 6 Grade 2 tumors, and 4 Grade 3 tumors. The percentage of CTGF positive and PCNA positive cells was quantified using at least 500 cells. RESULTS: CTGF was expressed in 70.1% of enchondroma cells, 84.0% of Grade 1 chondrosarcoma cells, 53.7% of Grade 2 tumor cells, and 26.8% of Grade 3 tumor cells (rho = -0.501; P = 0.0053). In chondrosarcoma cases, CTGF expression was correlated closely with tumor grade (rho = -0.920; P = 0.0001). There was a strong correlation between PCNA expression and tumor grade (rho = 0.907; P < 0.0001) and a strong negative correlation between CTGF and PCNA expression (rho = -0.493; P = 0.0061). In chondrosarcoma cases, patients with high expression of CTGF (>/= 30%) showed higher overall survival compared with those with low expression (< 30%) (P = 0.004). CONCLUSIONS: The current study revealed a correlation between the histologic grade of chondrosarcoma and prognosis, and the concomitant association between CTGF immunostaining and tumor grade and prognosis. Therefore, immunohistochemical staining with CTGF is a useful procedure for assessing the tumor grade and clinical course in patients with chondrosarcoma.

Adolescent↗
PubMed2000

Direct effects of methamphetamine on hypertrophy and microtubules in cultured adult rat ventricular myocytes.

Morphological alterations occasionally found in the myocardium of methamphetamine (MAP) abusers include hypertrophy, atrophy, disarrangement of myofibrils and fibrosis. These cardiac alterations have been thought to be due to an indirect action of MAP via catecholamines released by MAP administration. However, the direct effect of MAP on cardiomyocytes is not clear. In previous studies, we showed that cell size of isolated adult rat ventricular cardiomyocytes (ARCs) exposed to MAP was larger than that of untreated cells in culture supplemented with 10% fetal calf serum (FCS). In this study, to determine further the direct effect of MAP on cardiomyocytes, cultured ARCs were exposed to 0.05, 0.1 and 0.5 mM MAP for 7 days in culture medium without FCS following 6-day normal culture in medium containing FCS. Myocyte size was measured and microtubular (MT) structures which were associated with functional disorder of hearts were immunohistochemically observed using confocal microscopy. The size in treated ARCs significantly increased time- and dose-dependently as compared with untreated cells, but it decreased 7 days after exposure to 0.5 mM MAP. The increases in cell size, however, were lower than that in serum-supplemented cultures. MT structures in intact ARCs appeared as a filamentous network throughout the cytoplasm and around the nucleus. MAP exposure for 3 days promoted MT assembly, but in 7-day treated cells, MT and actin structures were injured. These results suggested that MAP directly induced cellular hypertrophy and might lead to cardiac functional disorder.

Amphetamine-Related Disorders↗
PubMed2000

Screening and determination of benzodiazepines in whole blood using solid-phase extraction and gas chromatography/mass spectrometry.

Benzodiazepines are one of the most widely prescribed drugs for the treatment of a wide spectrum of clinical disorders. They are used as anticonvulsants, anxiolytics, hypnotics or muscle relaxants with different duration of action. In this paper, a simple and sensitive method for the determination of benzodiazepines in whole blood using solid-phase extraction and gas chromatography/mass spectrometry (GC/MS) is described. The drugs spiked in whole blood were extracted with an Oasis HLB solid-phase extraction cartridge (Waters), which contains a copolymer designed to have a hydrophilic-lipophilic balance. GC/MS analysis was performed using a Shimadzu QP-5000 equipped with a BPX5 capillary column (15 mx0.32 mm I.D., film thickness 0.25 microm, SGE). Nineteen benzodiazepines and two thienodiazepines were well separated from each other on their SIM chromatograms and also on the TIC with the exception of oxazolam to cloxazolam separation. The blank extract from whole blood gave no peaks that interfered with all benzodiazepines and thienodiazepines on the chromatogram. The calibration curves for selected benzodiazepines with fludiazepam as an internal standard showed excellent linearity over the concentration range 5-500 ng/ml blood with a correlation coefficients of >0.995. The detection limits ranged from 0.2 to 20 ng/ml blood. The method is simple and sensitive for the determination of benzodiazepines in whole blood and seems to be useful in the practice of forensic science.

Anti-Anxiety Agents↗
PubMed2000

Cyclooxygenase-2 participates in the late phase of airway hyperresponsiveness after ozone exposure in guinea pigs.

We examined the role of cyclooxygenase in airway hyperresponsiveness and inflammation after ozone exposure in guinea pigs using a non-selective (indomethacin) and a selective (JTE-522) cyclooxygenase-2 inhibitor. Spontaneously breathing guinea pigs were exposed to ozone (3 ppm) for 2 h after treatment with vehicle, indomethacin (10 mg/kg) or JTE-522 (10 mg/kg). Airway responsiveness to inhaled histamine (PC(200)) and bronchoalveolar lavage were assessed before, immediately and 5 h after ozone exposure. Ozone caused a significant airway hyperresponsiveness immediately after exposure, which persisted after 5 h. Neither JTE-522 nor indomethacin affected airway hyperresponsiveness immediately after ozone exposure, but significantly attenuated airway hyperresponsiveness 5 h after exposure, suggesting that cyclooxygenase-2 may participate in the late phase of airway hyperresponsiveness but not in the early phase. Ozone caused a significant increase in the concentration of prostaglandin E(2) and thromboxane B(2) in bronchoalveolar lavage fluid immediately after exposure, which decreased to the basal level 5 h after exposure. This increase in prostaglandin E(2) and thromboxane B(2) was significantly inhibited by JTE-522. An expression of cyclooxygenase-2 was detected not only after ozone exposure but also before, and there was no difference in the number of cyclooxygenase-2-positive cells at any time point. An exogenously applied thromboxane A(2) mimetic, U-46619 (10(-5) M), induced airway hyperresponsiveness 5 h after inhalation, but not immediately or 3 h after inhalation. These data suggest that cyclooxygenase-2 may be constitutively expressed before ozone exposure in guinea pig airway and may synthesize prostaglandin E(2) and thromboxane A(2) transiently under ozone stimulation and that thromboxane A(2) may, in turn, induce the late phase of airway hyperresponsiveness.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2000

Feedback control of cyclooxygenase-2 expression through PPARgamma.

Cyclooxygenase-2 (COX-2), a rate-limiting enzyme for prostaglandins (PG), plays a key role in inflammation, tumorigenesis, development, and circulatory homeostasis. The PGD(2) metabolite 15-deoxy-Delta(12, 14) PGJ(2) (15d-PGJ(2)) was identified as a potent natural ligand for the peroxisome proliferator-activated receptor-gamma (PPARgamma). PPARgamma expressed in macrophages has been postulated as a negative regulator of inflammation and a positive regulator of differentiation into foam cell associated with atherogenesis. Here, we show that 15d-PGJ(2) suppresses the lipopolysaccharide (LPS)-induced expression of COX-2 in the macrophage-like differentiated U937 cells but not in vascular endothelial cells. PPARgamma mRNA abundantly expressed in the U937 cells, not in the endothelial cells, is down-regulated by LPS. In contrast, LPS up-regulates mRNA for the glucocorticoid receptor which ligand anti-inflammatory steroid dexamethasone (DEX) strongly suppresses the LPS-induced expression of COX-2, although both 15d-PGJ(2) and DEX suppressed COX-2 promoter activity by interfering with the NF-kappaB signaling pathway. Transfection of a PPARgamma expression vector into the endothelial cells acquires this suppressive regulation of COX-2 gene by 15d-PGJ(2) but not by DEX. A selective COX-2 inhibitor, NS-398, inhibits production of PGD(2) in the U937 cells. Taking these findings together, we propose that expression of COX-2 is regulated by a negative feedback loop mediated through PPARgamma, which makes possible a dynamic production of PG, especially in macrophages, and may be attributed to various expression patterns and physiological functions of COX-2.

Animals↗
PubMed2000

Identification of a protein phosphorylated by cAMP-dependent protein kinase in drosophila brain.

In the present study, we examined the effects of reagents that elevate cAMP concentration on protein phosphorylation in Drosophila brain cells. Application of forskolin or dopamine to brain cells that were prelabeled with (32)Pi enhanced phosphorylation of a 25-kDa protein (p25a). To identify p25a, we isolated the protein, and partial amino acid sequences were analyzed. Database searches showed that p25a is a J-domain protein, dJDP that contains the J-domain found in the DnaJ (heat shock protein 40) family of molecular chaperones.

Animals↗
PubMed2000

Effect of dimethylthiourea, a hydroxyl radical scavenger, on cigarette smoke-induced bronchoconstriction in guinea pigs.

Cigarette smoke exposure causes bronchoconstriction in guinea pigs by stimulating cholinergic and excitatory nonadrenergic, noncholinergic (eNANC)-nerves in vagus system. The aim of this study is to elucidate the role of hydroxyl radical (OH(-)), contained in cigarette smoke, in bronchoconstriction. Anaesthetized animals were exposed to 80 puffs of smoke for 4 min. Pretreatment with dimethylthiourea, a OH(-) scavenger, significantly inhibited cigarette smoke-induced bronchoconstriction. To investigate its site of action, effects of dimethylthiourea were examined on vagally mediated bronchcoconstriction by electrical stimulation and on the bronchoconstriction by intravenous acetylcholine and neurokinin-A. Dimethylthiourea did not inhibit bronchoconstriction evoked by vagal stimulation, acetylcholine or neurokinin-A. These results suggest that dimethylthiourea inhibits cigarette smoke-induced bronchoconstriction by scavenging the smoke-derived OH(-), but not by inhibiting airway nerve function.

Acetylcholine↗