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Biomedical subjects

T Iwasaka

Publications and source records attributed to T Iwasaka.

At least 19 recordsLinked to original sources
PubMed2001

Early identification of impaired myocardial reperfusion with serial assessment of ST segments after percutaneous transluminal coronary angioplasty during acute myocardial infarction.

To evaluate the relation between ST-segment analysis and microvascular reperfusion in patients with acute myocardial infarction (AMI), we studied 51 patients with first AMI who were successfully treated by percutaneous transluminal coronary angioplasty (PTCA). The lead showing the greatest ST-segment elevation on the 12-lead electrocardiogram (ECG) was serially investigated until 24 hours after PTCA. Successful reperfusion was determined by technetium-99m tetrofosmin single-photon emission computed tomography. Impaired reperfusion (group 1: < 4 change in the sum of the defect score from before to immediately after PTCA) was observed in 24 patients, and successful reperfusion (group 2) was observed in 27 patients. Although ST-segment elevation was reduced significantly at 30 minutes after PTCA in group 2 (2.2 +/- 1.4 to 1.7 +/- 1.3 mm, p = 0.01), there was no significant change in group 1 (1.9 +/- 1.9 to 2.4 +/- 1.7 mm). Ten of 14 patients (71%) with persistent ST-segment elevation (DeltaST > 0 mm change in ST segment from before to 30 minutes after PTCA > 0) were in group 1, whereas 23 of 37 patients (62%) with ST-segment resolution (DeltaST < or = 0) were in group 2. The sensitivity and specificity of persistent ST-segment elevation for predicting impaired microvascular reperfusion were 42% and 85%, respectively. Thus, persistent ST-segment elevation 30 minutes after primary PTCA was a highly specific electrocardiographic marker of impaired reperfusion in patients with AMI.

Aged↗
PubMed2001

Implantation of bone marrow mononuclear cells into ischemic myocardium enhances collateral perfusion and regional function via side supply of angioblasts, angiogenic ligands, and cytokines.

BACKGROUND: Bone marrow implantation (BMI) was shown to enhance angiogenesis in a rat ischemic heart model. This preclinical study using a swine model was designed to test the safety and therapeutic effectiveness of BMI. METHODS AND RESULTS: BM-derived mononuclear cells (BM-MNCs) were injected into a zone made ischemic by coronary artery ligation. Three weeks after BMI, regional blood flow and capillary densities were significantly higher (4.6- and 2.8-fold, respectively), and cardiac function was improved. Angiography revealed that there was a marked increase (5.7-fold) in number of visible collateral vessels. Implantation of porcine coronary microvascular endothelial cells (CMECs) did not cause any significant increase in capillary densities. Labeled BM-MNCs were incorporated into approximately 31% of neocapillaries and corresponded to approximately 8.7% of macrophages but did not actively survive as myoblasts or fibroblasts. There was no bone formation by osteoblasts or malignant ventricular arrhythmia. Time-dependent changes in plasma levels for cardiac enzymes (troponin I and creatine kinase-MB) did not differ between the BMI, CMEC, and medium-alone implantation groups. BM-MNCs contained 16% of endothelial-lineage cells and expressed basic fibroblast growth factor>>vascular endothelial growth factor>angiopoietin 1 mRNAs, and their cardiac levels were significantly upregulated by BMI. Cardiac interleukin-1beta and tumor necrosis factor-alpha mRNA expression were also induced by BMI but not by CMEC implantation. BM-MNCs were actively differentiated to endothelial cells in vitro and formed network structure with human umbilical vein endothelial cells. CONCLUSIONS: BMI may constitute a novel safety strategy for achieving optimal therapeutic angiogenesis by the natural ability of the BM cells to secrete potent angiogenic ligands and cytokines as well as to be incorporated into foci of neovascularization.

Angiopoietin-1↗
PubMed2001

Conservative therapy for adenocarcinoma and atypical endometrial hyperplasia of the endometrium in young women: central pathologic review and treatment outcome.

Thirty-nine patients with endometrioid adenocarcinoma (EA) and atypical hyperplasia (AH) of the endometrium who received conservative treatment to preserve fertility were collected from member institutions of the Japan Gynecologic Oncology Study Group. Twenty-nine and ten were originally diagnosed with EA without myometrial invasion and AH, respectively. We performed a central pathological review to make definite diagnoses, and the diagnosis of EA in 29 cases was changed to AH in ten, complex hyperplasia in three and atypical polypoid adenomyoma in three, and AH in ten was changed to EA in one and simple hyperplasia in one. Nine of 12 women (75%) with EA and 15 of 18 women (83%) with AH had an initial response to medroxyprogesterone acetate (MPA) treatment. Two of nine responders with EA later developed relapse, and one of them had metastasis to the left obturator lymph node. Two became pregnant, and one delivered one full-term infant. One of the responders with AH had a relapse in the endometrium. Five became pregnant, and four delivered four normal infants. The young women with endometrial carcinoma localized in the endometrium who wish to preserve fertility may be treated as successfully with MPA as those with AH.

Adenocarcinoma↗
PubMed2001

Effect of angiotensin II type 2 receptor on tyrosine kinase Pyk2 and c-Jun NH2-terminal kinase via SHP-1 tyrosine phosphatase activity: evidence from vascular-targeted transgenic mice of AT2 receptor.

Angiotensin II (Ang II) has two major receptor isoforms, AT1 and AT2. AT1 transphosphorylates Ca(2+)-sensitive tyrosine kinase Pyk2 to activate c-Jun NH2-terminal kinase (JNK). Although AT2 inactivates extracellular signal-regulated kinase (ERK) via tyrosine phosphatases (PTP), the action of AT2 on Pyk2 and JNK remains undefined. Using AT2-overexpressing vascular smooth muscle cells (AT2-VSMC) from AT2-transgenic mice, we studied these undefined actions of AT2. AT1-mediated JNK activity was increased 2.2-fold by AT2 inhibition, which was abolished by orthovanadate. AT2 did not affect AT1-mediated Pyk2 phosphorylation, but attenuated c-Jun mRNA accumulation by 32%. The activity of src-homology 2 domain-containing PTP (SHP-1) was significantly upregulated 1 min after AT2 stimulation. Stable overexpression of SHP-1 dominant negative mutant in AT2-VSMC completely abolished AT2-mediated inhibition of JNK activation and c-Jun expression. These findings suggest that AT2 inhibits JNK activity by affecting the downstream signal of Pyk2 in a SHP-1-dependent manner, leading to a decrease in c-Jun expression.

Angiotensin Receptor Antagonists↗
PubMed2001

Angiotensin AT(1) and AT(2) receptors differentially regulate angiopoietin-2 and vascular endothelial growth factor expression and angiogenesis by modulating heparin binding-epidermal growth factor (EGF)-mediated EGF receptor transactivation.

Angiotensin II (Ang II)-mediated signals are transmitted via heparin binding epidermal growth factor (EGF)-like growth factor (HB-EGF) release followed by transactivation of EGF receptor (EGFR). Although Ang II and HB-EGF induce angiogenesis, their link to the angiopoietin (Ang)-Tie2 system remains undefined. We tested the effects of Ang II on Ang1, Ang2, or Tie2 expression in cardiac microvascular endothelial cells expressing the Ang II receptors AT(1) and AT(2). Ang II significantly induced Ang2 mRNA accumulations without affecting Ang1 or Tie2 expression, which was inhibited by protein kinase C inhibitors and by intracellular Ca(2+) chelating agents. Ang II transactivated EGFR via AT(1), and inhibition of EGFR abolished the induction of Ang2. Ang II caused processing of pro-HB-EGF in a metalloproteinase-dependent manner to stimulate maturation and release of HB-EGF. Neutralizing anti-HB-EGF antibody blocked EGFR phosphorylation by Ang II. Ang II also upregulated vascular endothelial growth factor (VEGF) expression in an HB-EGF/EGFR-dependent manner. AT(2) inhibited AT(1)-mediated Ang2 expression and phosphorylation of EGFR. In an in vivo corneal assay, AT(1) induced angiogenesis in an HB-EGF-dependent manner and enhanced the angiogenic activity of VEGF. Although neither Ang2 nor Ang1 alone induced angiogenesis, soluble Tie2-Fc that binds to angiopoietins attenuated AT(1)-mediated angiogenesis. These findings suggested that (1) Ang II induces Ang2 and VEGF expression without affecting Ang1 or Tie2 and (2) AT(1) stimulates processing of pro-HB-EGF by metalloproteinases, and the released HB-EGF transactivates EGFR to induce angiogenesis via the combined effect of Ang2 and VEGF, whereas AT(2) attenuates them by blocking EGFR phosphorylation. Thus, Ang II is involved in the VEGF-Ang-Tie2 system via HB-EGF-mediated EGFR transactivation, and this link should be considerable in pathological conditions in which collateral blood flow is required.

Angiopoietin-1↗
PubMed2001

Inhibition of cardiac delayed rectifier K+ currents by an antisense oligodeoxynucleotide against IsK (minK) and over-expression of IsK mutant D77N in neonatal mouse hearts.

The IsK (minK or KCNE1) protein is known to co-assemble with the KvLQT1 (KCNQ1) protein to form a channel underlying the slowly activating delayed rectifier K+ current (IKs). Controversy remains as to whether the IsK protein assembles with ERG (the ether-a-go-go-related gene) products to form or modulate the channel-underlying the rapidly activating delayed rectifier K+ current (IKr). We investigated the effects of antisense oligodeoxynucleotides (AS-ODN) against IsK and its mutant D77N [which underlies a form of long QT syndrome (LQT5) in humans] on the delayed rectifier K+ current (IK) of neonatal mouse ventricular myocytes in primary culture. Patch-clamp experiments on these cells showed that IK consists of IKs and IKr. IK was not recorded from ventricular cells transfected with AS-ODN, while it was recorded from cells transfected with the corresponding sense oligodeoxynucleotides (S-ODN). IK was not recorded from cells transfected with the D77N mutant, and the action potential duration was much longer than in cells transfected with wild-type IsK. Furthermore, HERG could not induce currents in COS-1 cells co-expressed with the D77N mutant and HERG (the human form of ERG). These results indicate that the IsK protein associates with both KvLQT1 and ERG products to modulate IKr and IKs in cardiac myocytes.

Action Potentials↗
PubMed2001

Evidence for infection with Helicobacter pylori in patients with acute myocardial infarction.

BACKGROUND: Anti-Helicobacter pylori (HP) IgA and IgG antibody titers were measured in patients with ischemic heart diseases. METHODS: There were 60 healthy individuals that served as control subjects, and 21 patients with acute myocardial infarction (AMI), 34 with old myocardial infarctions (OMI), 35 with effort angina (AP) and 41 with vasospastic angina (VSA). RESULTS: In the control group, the IgA and IgG anti-HP antibody titers were positively correlated with age. When the IgA and IgG antibody titers were compared among patient groups, IgG did not significantly differ between each patient group and the control group, whereas IgA was significantly higher in the AMI group (5.10+/-1.25 EV) than in the OMI (p<0.01), AP, or the control (p<0.05). Moreover, the positivity rate for IgA anti-HP antibody was the highest in the AMI group (90%), with an odds ratio to the age-matched control group of 4.09, whereas the positivity rate for IgG did not significantly differ between the groups when either the 10 or 55 U/ml cut-off value was used. CONCLUSIONS: These results suggest that an increased IgA antibody titer, which is an index of the active phase of HP infection, should be an etiological marker for acute myocardial infarction.

Antibodies, Bacterial↗
PubMed2001

Retinoic acid and interferon-alpha effects on cell growth and differentiation in cervical carcinoma cell lines.

OBJECTIVE: To investigate and compare the efficacy of all-trans retinoic acid (RA) and/or interferon-alpha (IFN-alpha) on premalignant and malignant models of cervical cancer. METHODS: Cell growth rate was examined after treatment for 4, 7, and 10 days with RA and/or IFN-alpha of human papillomavirus type 18 (HPV 18)-immortalized endo- and ectocervical cells, nontransformed serum-adapted cells, transformed cells, three adenocarcinoma, and three squamous cell carcinoma cell lines. The effect on epithelial differentiation by RA and IFN-alpha was examined in organotypic culture. Induction of apoptosis was examined by modified terminal transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) and DNA fragmentation. RESULTS: Cell growth rate was inhibited by RA, 84-96% in HPV 18-immortalized endocervical cells, SiHa, and ME180, 0% in OMC-4, and 18-62% in other cell lines; and by IFN-alpha about 75% in SiHa and ME180 and 14-40% in the other cell lines. Combining RA and IFN-alpha increased the antiproliferative effect in premalignant cell lines and some cancer cell lines except OMC-4, SiHa, and HT-3. In rafts, RA treatment reversed human endocervical cell metaplasia and HPV 18-immortalized endo- and ectocervical cell dysplastic epithelial differentiation. Interferon-alpha, not RA, treatment of HPV 18-immortalized endo- and ectocervical cells induced apoptosis. CONCLUSION: Cell growth inhibition by treatment with RA, IFN-alpha, and their combination differentially depends on treatment type and time, cell origin, cell line, and oncogenic state. In a premalignant model of cervical carcinoma, RA reduces dysplastic differentiation and IFN-alpha induces apoptosis. These data confirm that these treatments may be effective for preventing or treating premalignant cervical lesions.

Adenocarcinoma↗
PubMed2001

Prevalence and mortality of the Brugada-type electrocardiogram in one city in Japan.

OBJECTIVES: We sought to study the prevalence and mortality of subjects exhibiting the Brugada-type electrocardiogram (ECG) in a community-based population in Japan. BACKGROUND: The Brugada syndrome has been associated with sudden death in subjects without structural heart disease. Hospital-based studies showed 11% to 38% annual fatal arrhythmic events in patients with the Brugada syndrome. METHODS: Prevalence and mortality of the Brugada-type ECG were studied in subjects who had ECGs during a health examination in Moriguchi, Osaka, Japan. Information about death and relocation from Moriguchi city was obtained prospectively. RESULTS: The Brugada-type ECG was found in 98 of 13,929 study subjects (0.70%, 95% confidence interval [CI]: 0.57% to 0.86%). The typical coved-type with an rsR' pattern in V(1) lead ("typical" Brugada-type) was found in 0.12% of subjects (95% CI: 0.07% to 0.20%). The prevalence for male subjects with the Brugada-type ECG (81%) was significantly higher than it was for those without (26%, p < 0.0001). In male subjects, the Brugada-type ECG was found in 2.14% (95% CI: 1.70% to 2.66%), and the "typical" Brugada-type was found in 0.38% (95% CI: 0.21% to 0.64%). After 2.6 +/- 0.3 years of follow-up, there was 1 death (1.0%, 95% CI: 0.03% to 5.6%) of a subject with the Brugada-type ECG, whereas there were 139 deaths (1.0%, 95% CI: 0.85% to 1.2%) of those without the Brugada-type ECG (p = 0.9943, log-rank test). CONCLUSIONS: A substantial number of the Brugada-type ECG were observed in subjects in a community-based population in Japan, especially in men. The total mortality of subjects with the Brugada-type ECG did not differ from the mortality of those without the Brugada-type ECG in a community-based population.

Aged↗
PubMed2001

TIMI frame count immediately after primary coronary angioplasty as a predictor of functional recovery in patients with TIMI 3 reperfused acute myocardial infarction.

OBJECTIVES: The purpose of this study was to evaluate whether higher coronary blood flow, estimated by the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC), is related to better functional and clinical outcome after successful percutaneous transluminal coronary angioplasty (PTCA) in patients with acute myocardial infarction (AMI). BACKGROUND: Experimental studies have found that functional recovery of the infarcted myocardium was associated with increased blood flow (reactive hyperemia) to the infarcted bed shortly after reperfusion. METHODS: We measured CTFC immediately after successful (TIMI 3) primary PTCA in 104 consecutive patients with their first AMI. Wall motion score index (WMSI) and the presence of pericardial effusion were assessed by two-dimensional echocardiography before and one month after PTCA. RESULTS: The patients were divided into two groups according to mean CTFC for corresponding coronary artery of the control group: TIMI 3 slow group (45 patients, 40 > CTFC > or = 23) and TIMI 3 fast group (59 patients, CTFC < 23). There were no significant differences in the baseline characteristics and WMSI before reperfusion between the two groups. Improvement of WMSI in the TIMI 3 fast group was significantly greater than that of the TIMI 3 slow group (1.33 +/- 0.52 vs. 0.60 +/- 0.34, p < 0.001). Pericardial effusion and intractable heart failure were observed more frequently in the TIMI 3 slow group than in the TIMI 3 fast group (27 vs. 10%; p < 0.05, 36 vs. 17%; p < 0.05). Corrected TIMI frame count, assessed as a continuous variable, had a significant correlation with the change in WMSI (r = 0.60, p < 0.001) after adjusting for age, gender, history of hypertension, history of diabetes, elapsed time to PTCA, collateral grade, presence of antegrade flow before PTCA and number of diseased vessels. CONCLUSIONS: Lower CTFC of the infarct-related artery immediately after PTCA was associated with greater functional recovery; and hence, CTFC can predict clinical and functional outcome in patients with successful PTCA.

Aged↗
PubMed2001

A new method to analyze basic rest-activity cycle.

A new method was proposed to analyze a basic rest-activity cycle (BRAC), termed BRAC-A. This method calculates a significant cycle length by chi-squared method and the starting points of a resting phase and an active one by analysis of the array consisting of the segmented time series in the same length. Using 20 3-day computer-simulated time series of standard deviation in fetal heart rate fluctuation with known periodicity of the BRAC, we demonstrated that the BRAC-A was a useful tool to reveal the characteristics of the BRAC.

Activity Cycles↗
PubMed2001

Changes in fractal structure of heart rate variability during a nap in one case.

The objective of the present study was to analyze fractal structures of adult heart rate (HR) variability during a nap. Fractal analysis was carried out in one case over consecutive 10-min time series of HR, which were simultaneously recorded with electroencephalogram. Scaling relationships showed cross-over patterns characterized by alphas and alphal (i.e. slopes above and below a cross-over point). The alphas and alphal were black and white noise at Stage 4 of NREM sleep, and black and 1/f noise in REM sleep. Cross-over points changed from the first to second sleep cycle. We demonstrate the multifractal structures of HR variability during a nap in the present case.

Adult↗
PubMed2001

A longitudinal study of diurnal variation in baseline fetal heart rate in one dichorionic-diamniotic twin pregnancy.

A longitudinal study to analyse the diurnal variations in baseline fetal heart rate (FHR) and sustained fetal tachycardia (SFT) in twin pregnancy was performed on one dichorionic twin. Twenty-four hour FHR recordings on twins were made at 32, 34 and 36 weeks of gestation simultaneously. Significant diurnal variations were found in both twins in all gestational weeks. The diurnal variations in baseline FHR of twins were highly correlated with no phase-lag. No coincidence was recognized in the appearance of SFT between twins. These results suggest the maternal influence equally affects FHR in each fetus of dichorionic twin since 32 weeks of gestation, while the appearance of SFT might be independent from maternal influence.

Adult↗
PubMed2001

Expression of chromogranin/secretogranin mRNA in spontaneous mammary tumors in aging Fischer-344 rats.

There is a type of human breast cancer showing a neuroendocrine differentiation. Little is known, however, about the cell origin of this cancer or the process by which it expresses neuroendocrine features. Rat mammary tumors, either spontaneous or induced, have not been subjects for the investigation of aspects regarding the neuroendocrine differentiation of mammary epithelial cells. The aim of the present study was to show the potential of rat mammary tumors for expressing chromogranin (Cg)/secretogranin (Sg) mRNA. We examined CgA, SgI and SgII mRNA expression by reverse transcription-polymerase chain reaction in rat mammary adenocarcinoma and fibroadenoma which had arisen spontaneously in aging Fischer-344 rats. CgA and SgII mRNA were expressed in both mammary tumors, but SgI mRNA was not detected in either. The results of the present study show that rat mammary tumors can express chromogranin genes.

Adenocarcinoma↗
PubMed2001

Clinical significance of ST-segment elevation in lead V1 in patients with acute inferior wall Q-wave myocardial infarction.

BACKGROUND: This study was designed to determine the clinical significance of ST-segment elevation in the precordial leads (leads V1 and V2) in acute Q-wave inferior wall myocardial infarction. METHODS AND RESULTS: One hundred fifty-eight consecutive patients with acute Q-wave inferior wall myocardial infarction were classified into 3 groups on the basis of the initial ST-change in V1 (group 1 = 29 patients with ST elevation, group 2 = 97 patients with ST depression, and group 3 = 32 patients with no ST-segment change). The right coronary artery was the infarct-related artery in all the patients in group 1. Although there was no significant difference between groups 1 and 2, the number of left ventricular asynergic segments was larger and the incidence of major in-hospital arrhythmias was higher in groups 1 and 2 compared with group 3. Patients in group 1 had a significantly higher incidence of proximal lesion (86%) and right ventricular infarction (69%) than the other 2 groups did. When ST elevation in leads V1 and V2 was considered, 14 of 15 patients (93%) with ST elevation only in V1 had right ventricular infarction, whereas 6 of 14 patients (43%) with ST elevation in both V1 and V2 had right ventricular infarction (P =.011). CONCLUSIONS: ST-segment elevation in V1 on admission in patients with acute Q-wave inferior wall myocardial infarction indicates a right coronary artery lesion associated with a larger infarct size and a higher incidence of major in-hospital arrhythmias.

Adult↗
PubMed2001

Type 2 iodothyronine deiodinase expression is upregulated by the protein kinase A-dependent pathway and is downregulated by the protein kinase C-dependent pathway in cultured human thyroid cells.

Type 1 and 2 iodothyronine deiodinases (D1 and D2) catalyze thyroxine (T4) activation. In human thyroid, unlike rodents', both D1 and D2 are expressed. We have investigated the effects of thyrotropin (TSH), dibutyryl cyclic adenosine monophosphate [(Bu)2cAMP] (an activator of protein kinase A [PKA]), 12-O-tetradecanoylphorbor 13-actate (TPA) (an activator of protein kinase C [PKC]), T4, and triiodothyronine (T3) on the D2 mRNA levels and activity in cultured human thyroid cells. D2 mRNA levels were increased by TSH and (Bu)2cAMP, and the increment was faster and greater than that of D1 mRNA levels. The increment of the maximum velocity (Vmax) value for D2 by (Bu)2cAMP stimulation was similar to that of D2 mRNA levels, suggesting that (Bu)2cAMP enhances D2 activity mainly at the pretranslational level. Cycloheximide, a protein synthesis inhibitor, partially inhibited the increase of D2 mRNA levels by (BU)2cAMP, suggesting that de novo protein synthesis-dependent pathways are involved. TPA suppressed the D2 mRNA levels in the presence of (Bu)2cAMP. However, T3 and T4 did not significantly change the D2 mRNA levels and activity. In conclusion, D2 expression in human thyroid cells is more rapidly and strongly upregulated by the PKA pathway than D1 expression, and is downregulated by the PKC pathway.

Bucladesine↗
PubMed2001

Transvaginal ultrasound-guided embryo transfer improves pregnancy and implantation rates after IVF.

BACKGROUND: Attempts are constantly being made to improve clinical pregnancy rates after IVF and embryo transfer. Since November 1998, we have gradually been adopting transvaginal ultrasound guidance during embryo transfer. We retrospectively examined the efficacy of this method on pregnancy and implantation rates. METHODS: The results of 846 cycles from our IVF-embryo transfer programme were analysed and comparisons were made between those carried out using ultrasound guidance and those by the clinical touch method. RESULTS: Higher pregnancy and implantation rates (28.9 and 15.2% respectively) were found in the group using the transvaginal ultrasound guidance during embryo transfer compared with those in the group using the clinical touch method (13.1 and 7.0% respectively). The differences were statistically significant (P < 0.01). There was no significant difference in ectopic pregnancy rates between the two groups. CONCLUSION: The use of transvaginal ultrasound-guided embryo transfer significantly improved both pregnancy and implantation rates. Although technically difficult, we suggest its use may maximize the chances of achieving a successful pregnancy outcome.

Adult↗