Huge mass bordering on left atrium raises coronary artery.
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Coronary Angiography↗
Biomedical subjects
H Okamura
Publications and source records attributed to H Okamura.
Integration of mammalian circadian clock signals: from molecule to behavior.
The core oscillatory mechanism consisting of gene transcription and translation is a unique feature and the astonishing discovery in circadian biology is that the rhythm of gene transcription reflects the behavioral rhythm almost perfectly. This means that the clock gene oscillation generated by the core loop in each suprachiasmatic nucleus neuron is coupled and amplified, and harmonized strongly so that oscillating activities are spread into the whole brain and to all those peripheral organs which contain peripheral clocks. Additionally, circadian changes are induced in behavior and hormone secretion. Investigations of biological clocks open the fascinating perspective to analyze the integrational mechanism of 'time', providing a bridge between single genes and the living organism as a whole.
Animals↗
Metallothionein-1 messenger RNA transcription in steroid-secreting cells of the rat ovary during the periovulatory period.
An increase in metallothionein 1 (MT-1) mRNA was detected in the ovaries of immature Wistar rats that were primed with s.c. injection of 10 IU eCG followed 48 h later by 10 IU hCG s.c. to initiate the ovulatory process. Ovarian RNA was extracted at 0, 2, 4, 8, 12, 24, 72, 144, and 288 h after the primed animals were injected with hCG. These extracts were used for reverse transcription polymerase chain reaction (RT-PCR) differential display and Northern analyses that yielded complementary gene fragments for MT-1. Expression of MT-1 mRNA increased significantly by 24 h after hCG treatment and reached a peak at 144 h after hCG. In contrast, a disintegrin and metalloproteinase with thrombospondin motifs and a tissue inhibitor of metalloproteinase 1, which were also detected by the RT-PCR differential display procedure, reached a peak at 12 h after hCG and returned to control levels in the ovaries by 72 h after hCG. In situ hybridization indicated that most of the MT-1 mRNA was expressed in the vicinity of the theca interna of preovulatory follicles and in the lutein granulosa of postovulatory follicles. Thus, MT-1 mRNA expression is primarily in the vicinity of steroid-secreting areas of the ovary. The substantial increase in MT-1 mRNA expression might be important in protecting the ovarian tissues from oxidative stress generated by ovarian inflammatory events during the ovulatory process and luteinization.
ADAM Proteins↗
Isovector quadrupole resonance observed in the 60Ni(13C,13N)60Co reaction at E/A=100 MeV.
The charge-exchange reaction 60Ni(13C,13N)60Co at E/A=100 MeV has been studied to locate isovector (deltaT=1) non-spin-flip (deltaS=0) giant resonances. Besides the giant dipole resonance at E(x)=8.7 MeV, another resonance has been observed at E(x)=20 MeV with a width of 9 MeV. Distorted-wave Born approximation analysis on the angular distribution clearly indicated the L=2 multipolarity, attributing the E(x)=20 MeV state to the giant isovector quadrupole resonance.
Journal Article↗
Toxicity evaluation of new antifouling compounds using suspension-cultured fish cells.
A simple, rapid toxicity test was developed using the suspension-cultured fish cell line CHSE-sp derived from chinook salmon Oncorhynchus tshawytscha embryos in order to assess the toxicity of new marine antifouling compounds. The compounds tested were copper pyrithione, Diuron, Irgarol 1051, KH101, Sea-Nine 211, and zinc pyrithione, all of which have been nominated in Japan as possible replacements for organotin compounds. The in vitro acute toxicity (24-h EC50) of the six compounds to these fish cells was evaluated using the dye Alamar Blue to determine cell viability, and then correlated with the results of in vivo chronic toxicities (28-day LC50) to juvenile rainbow trout Oncorhynchus mykiss. The suspension-cultured fish cells were found to be suitable for the screening of such chemicals before performing an in vivo test. The toxicities of the test compounds obtained from both tests, shown in decreasing order, were as follows: copper pyrithione > zinc pyrithione > KH101 > or = Sea-Nine 211 > Diuron > Irgarol 1051. The herbicides Diuron and Irgarol 1051 showed the least toxicity, while the pyrithiones had the greatest toxicity.
Animals↗
Photodegradation of the antifouling compounds Irgarol 1051 and Diuron released from a commercial antifouling paint.
The antifouling compound Irgarol 1051 and its degradation product M1 (also known as GS26575), along with another antifouling compound Diuron, have recently been found in Japanese coastal waters. This study was undertaken to find the origin of these chemicals and investigate their aquatic fate. Five glass plates, each coated with 1 g of antifouling paint containing Irgarol and Diuron, were submerged in 250 ml of five different test waters and the plates removed after several months. The aqueous solutions were divided into two groups: one exposed to natural sunlight, and the other kept in the dark as a control. Irgarol and Diuron were detected in all aqueous solutions, suggesting leaching from antifouling paints is the origin of these antifouling biocides found in Japanese coastal waters. Under sunlight conditions, Irgarol underwent a rapid degradation to produce M1, which remained even after Irgarol had disappeared from the system. These compounds were persistent in any aqueous solutions tested under dark conditions, indicating high stability to hydrolysis. Diuron and M1 were more persistent than Irgarol under sunlight irradiation. Since these compounds have high herbicidal activities, their ultimate impact on aquatic ecosystems is closely related to their aquatic fate.
Diuron↗
Suppression of Egr-1 expression in human oral squamous carcinoma cells by okadaic acid.
We examined the expression of early growth response-1 (Egr-1) gene in human oral squamous carcinoma cell lines SCCKN and SCC-25 cells and human osteoblastic cell lines Saos-2 and MG63 cells treated with okadaic acid, a potent inhibitor of protein phosphatases type 1 and type 2A. Western blot analysis revealed that Egr-1 was strongly expressed in SCCKN cells and that okadaic acid decreased the expression of Egr-1 protein in these cells. However, Egr-1 was expressed at lower levels in SCC-25, Saos-2, and MG63 cells and transiently increased with the okadaic acid treatment. Suppression of Egr-1 protein expression in okadaic acid-treated SCCKN cells stemmed from the suppression of the Egr-1 mRNA level, as determined by the RT-RCR method. Formaldehyde-fixed and alcohol-permeabilized cultured SCCKN cells were reacted with the anti-Egr-1 antibody using immunohistochemical methods. Intense fluorescence was observed in the nuclei of the control SCCKN cells interacted with anti-Egr-1 antibody. However, only a weak reaction was observed in the nuclei in SCCKN cells treated with okadaic acid. A gel mobility shift assay showed that treatment of SCCKN cells with okadaic acid suppressed Egr-1 binding to the DIG-labeled Egr-1 consensus oligonucleotide probe. The present results indicate that the alteration of phosphorylation states in SCCKN cells regulates Egr-1 binding to its consensus sequence and its expression at the transcriptional level.
Carcinogens↗
Interleukin-18 and interleukin-12 synergistically inhibit osteoclastic bone-resorbing activity.
The effect of interleukin (IL)-18 on osteoclastic bone-resorbing activity was investigated in vitro. Osteoclast-enriched cells, about 70% of which were tartrate-resistant acid phosphatase (TRAP)-positive, were cultured on dentine slices, and then the total volume of resorption pits on each dentine slice was measured as bone-resorbing activity. When the effects of IL-18 alone at 1, 10, 100, and 1000 ng/mL were examined, bone-resorbing activity was significantly reduced only at 1000 ng/mL, by about 50%. However, IL-18 plus IL-12 (10 ng/mL each) reduced bone-resorbing activity by about 70%, whereas IL-12 alone had no significant effect. When the concentration of interferon (IFN)-gamma in the medium was measured, IL-18 or IL-12 was found to increase it slightly, and the combination of these two cytokines synergistically increased it. The inhibitory effect of the combination of the two cytokines was completely abolished by the addition of an anti-IFN-gamma neutralizing antibody to the medium, but IFN-gamma by itself did not inhibit osteoclastic bone resorption. IL-18 alone or in combination with IL-12 did not affect the number of TRAP-positive cells in culture of osteoclast-enriched cells. Osteoclasts prepared from osteoclast-enriched cells expressed mRNAs of IL-18 receptor, MyD88, and cathepsin K. Furthermore, IL-18 receptor protein was detected on the cell surface of osteoclasts. The present results indicate that the combination of IL-18 and IL-12 synergistically inhibits osteoclastic bone-resorbing activity, suggesting that IFN-gamma participates in the mechanism underlying this inhibition.
Animals↗
Effects of post-inhalation treatment with interleukin-12 on airway hyper-reactivity, eosinophilia and interleukin-18 receptor expression in a mouse model of asthma.
BACKGROUND: Correcting Th1/Th2 imbalance with administration of IL-12 before and during antigen challenge holds therapeutic promise in asthma. However, the effects of IL-12 on the established asthmatic responses have not fully been examined. OBJECTIVE: We investigated whether IL-12 administered after antigen challenge could diminish airway hyper-reactivity (AHR) and eosinophilia in mice actively sensitized to ovalbumin. We also have investigated the ability of administered IL-12 to induce IL-18 receptor (IL-18R) expression that may lead possible synergic action of IL-12 with endogenous IL-18. METHODS: C57BL/6 mice immunized to ovalbumin (OVA) by intraperitoneal (i.p.) injection, were challenged three times with an aerosol of OVA every second day for 8 days. Recombinant IL-12 (500 ng) was intravenously administered on a single occasion 1 h after the final challenge of mice. Mice were analysed for effects of IL-12 on AHR, inflammatory cell infiltration and cytokine levels in lung tissue as well as serum immunoglobulin (Ig) E levels. Immunohistochemistry for IL-18R was performed using rat monoclonal antibody specific for murine IL-18Ralpha (IL-1 receptor related protein; IL-1Rrp). RESULTS: An intravenous IL-12 administration diminished AHR, pulmonary eosinophilia and T lymphocyte infiltration, serum IgE, IL-4 and IL-13 in lung tissue. Expression of IL-18R was induced in the mononuclear cells in the lung of mice exposed to OVA. IL-12 administration enhanced the IL-18R expression compared with the control. CONCLUSION: These data indicate that IL-12 can attenuate established antigen-induced AHR and inflammation. In this mechanism it would be interpreted as follows: IL-12 administration in OVA-challenged mice decreased IL-4 production and IgE production thereafter through direct effect on inhibiting the activation of established Th2 cells response and also combined effect with up-regulation of IL-18R expression by inflammatory cells in the lung.
Administration, Inhalation↗
Can coronary flow velocity reserve determined by transthoracic Doppler echocardiography predict the recovery of regional left ventricular function in patients with acute myocardial infarction?
OBJECTIVE: To determine whether the early assessment of coronary flow velocity reserve (CFVR) by transthoracic Doppler echocardiography (TTDE) can predict myocardial viability after revascularisation in patients with acute myocardial infarction. METHODS: 29 patients with anterior acute myocardial infarction who were successfully treated by coronary angioplasty were studied. TTDE was used to record coronary flow velocities in the distal left anterior descending artery at rest and during hyperaemia induced by intravenous infusion of adenosine triphosphate. CFVR was calculated immediately and 24 hours after revascularisation and at discharge. Regional wall motion was analysed to calculate the anterior wall motion score index (A-WMSI) by two dimensional echocardiography before revascularisation and at discharge. RESULTS: CFVR immediately and 24 hours after revascularisation correlated significantly with A-WMSI at discharge (r = -0.58, p < 0.001 and r = -0.80, p < 0.0001, respectively). CFVR 24 hours after revascularisation was a better predictor of recovery of regional left ventricular function than CFVR immediately after revascularisation. The optimal cut off ratio for predicting viable myocardium was 1.5 for CFVR 24 hours after revascularisation (sensitivity = 94%, specificity = 91%). CONCLUSIONS: CFVR by TTDE was useful for predicting the recovery of left ventricular function after revascularisation in patients with acute myocardial infarction
Analysis of Variance↗
Increased circulating interleukin-18 in patients with congestive heart failure.
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Adult↗
[Influence of preoperative factors on off-pump coronary aortic bypass grafting success].
Heart displacement during off-pump CABG (OPCAB) might induce the hemodynamic instability. We attempted to show which preoperative factors would contribute to an increase in that incident during OPCAB. Between February 2000, and October 2000, 51 patients underwent CABG in Okamura Memorial Hospital. Of these patients, 42 patients (82.4%) underwent OPCAB and 9 patients (17.6%) were operated upon under cardiac arrest with cardiopulmonary bypass (NOPCAB). To expose target coronary arteries for OPCAB, 3 deep pericardial traction stitches were placed near the left lower pulmonary vein (LPV), the left of the inferior vena cava (IVC) and the mid portion between LPV and IVC. To further assist in providing good presentation, patients were placed in Trendelenburg position (30 degree head-down tilt) and the right decubitus (30 degree the right side-down tilt). There were no OPCAB patients to be converted to on-pump CABG during anastomosis. Mean number of grafts in OPCAB group was 2.5 +/- 0.1 per patient, while that in NOPCAB group was 3.4 +/- 0.2 (p < 0.01). The bypass patient rate were 97.1% (100/103) in OPCAB group and 100% (31/31) in NOPCAB group (p = NS). In both groups, bilateral internal thoracic arteries were actively used for reperfusion to the left coronary artery. In the preoperative catheterization findings, pulmonary capillary wedge pressure (PCW) and left ventricular end-diastolic pressure (LVEDP) were significantly higher in NOPCAB group than those in OPCAB group (PCW: 14.0 vs 7.9 mmHg, LVEDP: 14.0 vs 8.7 mmHg: p < 0.05), and there was a tendency of low preoperative ejection fraction (EF) and cardiac index (CI) in NOPCAB group compared with those in OPCAB group, although there were no differences in left ventricular end-diastolic and end-systolic volume index (LVEDVI and LVESVI) between both groups. These findings suggested that PCW and LVEDP within the normal limit could be credited for the success with OPCAB, while an increase of the left ventricular volume would not contribute to the actual success.
Aged↗
Neutrophil proteinase 3-mediated induction of bioactive IL-18 secretion by human oral epithelial cells.
IL-18, a potent IFN-gamma-inducing cytokine, is expressed by various nonimmune cells as well as macrophages, suggesting that it has important physiological and immunological roles. The present study focused on the mechanism of active IL-18 induction from human oral epithelial cells. The epithelial cells and the cell lines constitutively express IL-18 mRNA and the 24-kDa precursor form of IL-18. Bioactive IL-18 exhibiting IFN-gamma-inducing activity was detected in the supernatant of the cells on costimulation with neutrophil proteinase 3 (PR3) and LPS for 24 h after IFN-gamma-priming for 3 days. An active 18-kDa form of IL-18 was detected in lysate and supernatant of the cells only after the above treatment and the induction was inhibited by cycloheximide and by serine proteinase inhibitors. After the treatment, lactate dehydrogenase activity was not detected in the cell culture supernatant, and PR3 was detected only in the membrane and not in cytoplasm fractions of the cells. Caspase-1 was not detected in the cells even after the treatment and the IL-18 induction was not inhibited by a caspase-1 inhibitor. These results suggest that the PR3-mediated induction of bioactive IL-18 secretion from oral epithelial cells in combination with LPS after IFN-gamma-priming occurred via a caspase-1-independent pathway, and provide new insight into the possible involvement of a neutrophil proteinase in the induction of bioactive IL-18 in oral inflammation such as periodontitis.
Adult↗
Psychiatric disorders and associated and predictive factors in patients with unresectable nonsmall cell lung carcinoma: a longitudinal study.
BACKGROUND: Few longitudinal studies have investigated psychiatric disorders in patients with unresectable nonsmall cell lung carcinoma (NSCLC). This study addressed three questions: 1) Which psychiatric disorders are prevalent among patients with unresectable NSCLC? 2) What is the clinical course of psychological distress? 3) Which factors are associated with this distress, and do any antecedent variables predict subsequent psychological distress? METHODS: A series of 129 consecutive patients with newly diagnosed, unresectable NSCLC participated. Psychiatric assessments were conducted by using the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, 3rd edition revised between the time of diagnosis and initial treatment for NSCLC (baseline) and 6 months after diagnosis (follow-up). Potential associated and predictive variables, including sociodemographic, biomedical, and psychosocial factors, were explored. RESULTS: The most common psychiatric disorder at baseline was nicotine dependence (67%), followed by adjustment disorders (14%), alcohol dependence (13%), and major depression (5%). At follow-up, adjustment disorders were diagnosed in 16% of patients, and major depression was diagnosed in 3% of patients. Thirty-five percent of patients who experienced depressive disorders (adjustment disorders and/or major depression) at baseline continued to experience the same disorders at follow-up. Multivariate analysis revealed that relatively younger age and pain were associated significantly with psychological distress at baseline. Only self-reported anxiety and depression at baseline could predict subsequent psychological distress. CONCLUSIONS: Substance dependence and depressive disorders are common psychiatric disorders in patients with unresectable NSCLC. Although this form of malignant disease often is progressive, depressive disorders do not seem to increase during its clinical course. Pain management is essential for alleviating patients' depressive disorders, and self-rating depression and anxiety seems to be an indicator of subsequent depressive disorders.
Adjustment Disorders↗
Plasmodium berghei infection in mice induces liver injury by an IL-12- and toll-like receptor/myeloid differentiation factor 88-dependent mechanism.
Malaria, caused by infection with Plasmodium spp., is a life cycle-specific disease that includes liver injury at the erythrocyte stage of the parasite. In this study, we have investigated the mechanisms underlying Plasmodium berghei-induced liver injury, which is characterized by the presence of apoptotic and necrotic hepatocytes and dense infiltration of lymphocytes. Although both IL-12 and IL-18 serum levels were elevated after infection, IL-12-deficient, but not IL-18-deficient, mice were resistant to liver injury induced by P. berghei. Neither elevation of serum IL-12 levels nor liver injury was observed in mice deficient in myeloid differentiation factor 88 (MyD88), an adaptor molecule shared by Toll-like receptors (TLRs). These results demonstrated a requirement of the TLR-MyD88 pathway for induction of IL-12 production during P. berghei infection. Hepatic lymphocytes from P. berghei-infected wild-type mice lysed hepatocytes from both uninfected and infected mice. The hepatocytotoxic action of these cells was blocked by a perforin inhibitor but not by a neutralizing anti-Fas ligand Ab and was up-regulated by IL-12. Surprisingly, these cells killed hepatocytes in an MHC-unrestricted manner. However, CD1d-deficient mice that lack CD1d-restricted NK T cells, were susceptible to liver injury induced by P. berghei. Collectively, our results indicate that the liver injury induced by P. berghei infection of mice induces activation of the TLR-MyD88 signaling pathway which results in IL-12 production and activation of the perforin-dependent cytotoxic activities of MHC-unrestricted hepatic lymphocytes.
Adaptor Proteins, Signal Transducing↗
Lack of contact transmission of recombinant Marek's disease virus type 1 expressing the fusion protein of Newcastle disease virus.
To clarify the level of excretion of a recombinant Marek's disease virus type 1 (rMDV1) that confers good protection in chickens against both Marek's and Newcastle diseases, even in the presence of maternal antibodies, contact transmission tests were conducted. Naïve chickens kept in the same cage or room with chickens inoculated with rMDV1 did not produce antibodies against MDV1 or the fusion protein of Newcastle disease virus. Moreover, the rMDV1 was not isolated from the dander of chickens inoculated with rMDV1. Even under the stressful conditions of forced molting and a high temperature environment, rMDV1 was not isolated from the dander of inoculated birds. The viral DNA, however, was detected from the dander of chickens inoculated with rMDV1 as well as a commercial vaccine. These findings indicate that dander from chickens inoculated with rMDV1 includes viral DNA, but does not contain infectious virus.
Animals↗
Angiotensin II induces circadian gene expression of clock genes in cultured vascular smooth muscle cells.
BACKGROUND: Daily rhythms of mammalian physiology and endocrinology are regulated by circadian pacemakers. The master circadian pacemaker resides in the suprachiasmatic nucleus, which is located in the hypothalamus of the brain, but circadian oscillators also exist in peripheral tissues. Because many studies have demonstrated apparent circadian variations in the frequency of cardiovascular disorders, it is of great interest to investigate a possible relation between circadian gene expression and cardiovascular function. We examined whether a circadian oscillation system exists in the aorta and/or in cultured vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: The mRNA levels of clock genes were assayed by northern blot analysis. The mouse aorta showed a clear circadian oscillation in the expression of mPer2, dbp, and Bmal1. Brief treatment of VSMCs with angiotensin II induced a robust increase in mPer2 gene expression, followed by a marked reduction in mPer2 mRNA levels and subsequent synchronous cycling of mPer2, dbp, and Bmal1 mRNAs. The induction of mPer2 in VSMCs by angiotensin II was completely abolished by treatment with CV11947, a specific angiotensin II type1 receptor antagonist. CONCLUSIONS: The present results demonstrate that the aorta and VSMCs possess a circadian oscillation system which is comparable to that of the suprachiasmatic nucleus and that the circadian gene expression in VSMCs is induced by angiotensin II through the angiotensin II type1 receptor. Our in vitro system will provide a useful tool to further analyze the physiological significance of the peripheral clock in cardiovascular function.
ARNTL Transcription Factors↗
Visualization of mPer1 transcription in vitro: NMDA induces a rapid phase shift of mPer1 gene in cultured SCN.
Many physiological and behavioral phenomena are controlled by an internal, self-sustaining oscillator with a periodicity of approximately 24 hr. In mammals, the principal oscillator resides in the suprachiasmatic nucleus (SCN). A light pulse during the subjective night causes a phase shift of the circadian rhythm via direct glutamatergic retinal afferents to the SCN [1]. Along with the accepted theoretical models of the clock, it is suggested that behavioral resetting of mammals is completed within 2 hr [2]; however, the molecular mechanism has not been elucidated. Here, we show the real-time image of the transcription of the circadian-clock gene mPer1 in the cultured SCN by using the transgenic mice that carry a luciferase reporter gene under the control of the mPer1 promoter [3]. The real-time image demonstrates that the mPer1 promoter activity oscillates robustly in a circadian manner and that this promoter activity is reset rapidly (within 2-3 hr) when a phase shift occurs.
2-Amino-5-phosphonovalerate↗