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Biomedical subjects

A Itoh

Publications and source records attributed to A Itoh.

At least 91 records · Page 5Linked to original sources
PubMed1999

Role of cytokines and adhesion molecules in ischemia and reperfusion in patients with acute myocardial infarction.

Although acute myocardial infarction (AMI) may involve both plaque rupture and ischemia-reperfusion injury, the pathogenesis of these phenomena is unclear. To elucidate the pathogenesis of AMI, serial measurements of platelet activating factor (PAF), interleukin-6 and cell adhesion molecules were made in patients with AMI. The PAF levels were measured upon hospital admission and at 24 and 72h in 8 patients with AMI. Serum levels of interleukin-6, soluble E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule- 1 (sVCAM- 1) were measured upon admission and at 24 h and 4 weeks in 30 patients with AMI and 15 patients with stable effort angina. PAF levels were higher in patients with AMI than in normal volunteers; the increased levels lasting at least 72h. In contrast, interleukin-6 increased at 24h. sE-selectin was elevated at admission and sVCAM-1 increased later. sE-selectin levels upon admission in patients with additional ST-segment elevation after reperfusion were significantly higher than those in patients without ST-elevation. In patients with AMI, the time-course of changes in blood levels of cytokines varied according to the individual substances. Although it is unclear what is the precise role of each of the cytokines in the pathophysiology of AMI, sE-selectin may be possibly related to the reperfusion injury in the infarcted myocardium.

Acute Disease↗
PubMed1999

Influence of calcium antagonists on long-term survival of patients treated with coronary angioplasty.

A meta-analysis reported that nifedipine increased mortality dose-dependently in patients with coronary artery disease. However, there have been few studies (specifically in Asians) on the long-term prognosis of patients treated with calcium antagonists after successful coronary angioplasty (PTCA). The subjects consisted of 583 consecutive patients (461 males, aged 59 +/- 10), who underwent successful elective PTCA between 1985 and 1990. First, they were divided into two groups; the calcium antagonist (+) group (n = 560) and the calcium antagonist (-) group (n = 23), and were evaluated in terms of total survival and cardiac events. Second, the calcium antagonist (+) group was further divided into 4 groups according to calcium antagonist type, i.e., short-acting nifedipine group (n = 156), long-acting nifedipine group (n = 203), diltiazem group (n = 184) and the other group (n = 17), and these groups were evaluated in the same way. The primary end-point was set as death from any cause. Secondary end-points were any cardiac events, including non-fatal acute myocardial infarction, coronary artery bypass surgery and repeat PTCA. The mean follow-up period was 4.5 +/- 1.8 years. A multivariate analysis was performed with the Cox proportional-hazard model. The Kaplan-Meier analysis showed that the calcium antagonist (-) group had significantly worse prognoses than the calcium antagonist (+) group (p < 0.05), and that there was no significant difference among the prognoses of the four calcium antagonists groups. The multivariate analysis revealed that the use of a calcium antagonist was one of the independent factors positively contributing to the prognosis. The use of any type of calcium antagonist did not increase mortality in patients who underwent successful elective PTCA, rather, it contributed to a favorable outcome.

Aged↗
PubMed1999

Three cases of spinal decompression sickness treated by U.S. Navy Treatment Table 7.

For patients of type 2 decompression sickness, recompression therapy using U.S. Navy Treatment Table 6 (TT6) and its extensions is the most common means of treatment. However, some cases are resistant to the recompression therapy, and the outcome of TT6 is not always satisfactory. Although a new table, the U.S. Navy Treatment Table 7 (TT7) was described in 1985 in the U.S. Navy Diving Manual, to date few cases who were treated using TT7 have been reported. Here, we report three cases of spinal decompression sickness who received treatment according to TT7. Two were sports scuba divers, and the other a commercial diver. TT7 was applied later than 4 d after onset in all three cases; two patients were remarkably improved during the recompression therapy, while the other improved to a certain extent after additional repetitive TT6. Mild impairment of lung function, probably due to pulmonary oxygen toxicity, was observed on lung function testing in one case. In all cases, after additional TT6 and/or rehabilitation, patients were able to return to active daily living.

Adult↗
PubMed1999

[Prognosis for patients with angina pectoris accompanied by chronic renal failure].

Chronic renal failure (CRF) is one of the risk factors of a worse outcome for patients with coronary artery disease. However, few studies have assessed the outcome in such patients. This study investigated the clinical characteristics, treatment modalities, and prognosis for patients with angina pectoris accompanied by CRF and evaluated the validity of current treatment strategy for these patients. A total of 593 patients (248 with stable angina and 345 with unstable angina) admitted to our institution were studied. Renal failure was defined as serum creatinine of > or = 2.0 mg/dl. Patients were divided into 2 groups, with renal failure (46 patients) and without renal failure (547 patients), and the former group was further divided into 2 groups with hemodialysis (26 patients) and without hemodialysis (20 patients). The mean follow-up period was 2.5 +/- 1.2 years and the follow-up rate was 99%. The prevalences of congestive heart failure (26% vs 3%, p < 0.001), hypertension (72% vs 45%, p < 0.005), and multivessel coronary artery disease (65% vs 33%, p < 0.001) were higher in patients with CRF. The left ventricular end-diastolic volume was greater in patients with CRF than in patients without CRF (114 +/- 36 vs 85 +/- 24 ml/m2, p < 0.001). The calcification score of both coronary arteries and abdominal aorta evaluated by electron-beam computed tomography was higher in patients with CRF (2,187 +/- 2,727 vs 631 +/- 841, p = 0.03; 4,091 +/- 3,068 vs 2,191 +/- 2,249, p = 0.02, respectively). In-hospital cardiac mortality was higher in patients with CRF than in patients without CRF (8.7% vs 0.7%, p < 0.001). The cumulative survival was 88% at 1 year and 65% at 3 years in patients with CRF and 99% and 97% in patients without CRF, respectively (p < 0.001). The incidence of re-hospitalization due to congestive heart failure was higher in patients with CRF (19% vs 1.3%, p < 0.0001). The cumulative survival in CRF was 93% at 1 year, 57% at 3 years in the medical treatment group and 87% and 75% in the invasive therapy group, respectively (p = 0.1). Patients with angina pectoris and CRF had a poor prognosis under the current treatment strategy. Newly developed therapeutic strategies, such as rotational atherectomy, minimally invasive direct coronary artery bypass surgery and combinations, will be necessary to improve the long-term prognosis for these patients.

Aged↗
PubMed1998

Four novel mutations of the connexin 32 gene in four Japanese families with Charcot-Marie-Tooth disease type 1.

DNA-based mutation analysis on the connexin 32 gene was performed in 49 families with Charcot-Marie-Tooth disease (CMT) type 1 but without duplication involving the chromosomal region, 17p12-p11.2. Mutations were identified in five of the 49 families, and four of the five mutations were hitherto undescribed: Va137Met, Glu57His, Arg142Glu, Val177Ala. X-linked CMT sometimes lacks evidence for X-linked transmission and cannot be differentiated from CMT type 2, especially in females with mildly decreased nerve conduction velocity. Therefore, molecular analysis is useful for molecular pathology of their disease.

Adolescent↗
PubMed1998

Cloning and expressions of three mammalian homologues of Drosophila slit suggest possible roles for Slit in the formation and maintenance of the nervous system.

In Drosophila embryogenesis, the slit gene has been shown to play a critical role in CNS midline formation. However, no slit homologues have been reported in vertebrates. Here, we have identified mammalian homologues of the slit gene (human Slit-1, Slit-2, Slit-3, and rat Slit-1). Each Slit gene encodes a putative secreted protein, which contains conserved protein-protein interaction domains including leucine-rich repeats (LRR) and epidermal growth factor (EGF)-like motifs, like that of the Drosophila protein. Northern blot analysis revealed that the human Slit-1, -2, and -3 mRNAs are exclusively expressed in the brain, spinal cord, and thyroid, respectively. In situ hybridization studies indicated that the rat Slit-1 mRNA is specifically expressed in the neurons of fetal and adult forebrains. Our data suggest that Slit genes form an evolutionary conserved group in vertebrates and invertebrates, and that the mammalian Slit proteins may participate in the formation and maintenance of the nervous and endocrine systems by protein-protein interactions.

Amino Acid Sequence↗
PubMed1998

Previous angina reduces in-hospital death in patients with acute myocardial infarction.

There is little information on how previous angina influences in-hospital deaths secondary to acute myocardial infarction (MI). This study evaluated the causes of in-hospital deaths in MI patients with and without previous angina. A total of 2,264 consecutive patients were admitted to our hospital due to acute MI. These patients were divided into 2 groups according to the presence or absence of prior MI. Both groups were further divided according to the presence or absence of previous angina. The causes of in-hospital deaths were classified into 4 categories: (1) cardiogenic shock or congestive heart failure, (2) cardiac rupture, (3) arrhythmia, and (4) other causes. In patients with a first MI, the in-hospital mortality rate was lower in patients with previous angina than those without (6.9% vs 11.4%, p <0.01). There was no significant difference between these patients with and without previous angina in in-hospital deaths due to cardiogenic shock or congestive heart failure, arrhythmia, or other causes. Death due to cardiac rupture was less frequent in patients with previous angina (1.4% vs 5.0%, p <0.01). In patients with prior MI, the in-hospital mortality rate was lower in patients with than without previous angina (17.7% vs 25.3%, p <0.05). In contrast to patients with their first MI, there was a trend toward a lower incidence of in-hospital death due to cardiogenic shock or congestive heart failure in patients with previous angina (12.8% vs 19.0%, p = 0.05). There were no significant differences in in-hospital deaths due to cardiac rupture, arrhythmia, and other causes between the 2 subgroups. In multivariate analysis, previous angina was an independent predictor of in-hospital death. Thus, in-hospital deaths after acute MI in patients with previous angina were less because of less cardiac rupture in patients with a first MI and less cardiogenic shock or congestive heart failure in patients with prior MI.

Aged↗
PubMed1998

Correlation of residual stenosis immediately after coronary angioplasty with long-term prognosis.

This study evaluated the correlation of residual stenosis after percutaneous transluminal coronary angioplasty with the long-term prognosis. Among consecutive 1,230 patients who underwent coronary angioplasty in the National Cardiovascular Center in Osaka, Japan, 894 patients had de novo lesions. Of these, the 70 patients with acute myocardial infarctions and 105 with unstable angina who had emergency coronary angioplasties were excluded from the study. Among the remaining 719 patients, successful dilatation of the main target vessel was achieved in 592 patients, who then comprised the study group. They were divided into three groups according to their residual stenosis (RS) immediately after coronary angioplasty: group A, RS < 15% (n=208); group B, 15% < or = RS < or = 35% (n=286), and group C, 35% < RS < 50% (n=98). The duration of follow-up was 1,668, 1,660, and 1,680 days in group A, B, and C, respectively. The groups A, B, and C were not significantly different in terms of age, history of myocardial infarction, left ventricular ejection fraction, number of diseased vessels and target vessels, and risk factors such as hypertension, hyperlipidemia, and diabetes mellitus. Primary end point of follow-up was defined as death from any cause and the second end point was occurrence of cardiac events. Kaplan-Meier survival analysis showed significant differences among the three groups. Moreover, survival curves seem to be dependent on the degree of post-procedural residual stenosis. Multivariate analysis using a Cox proportional hazard regression model showed that age, ejection fraction, and residual stenosis were independent determinants of event-free, cardiac, and total survival. Residual stenosis immediately after coronary angioplasty is an independent contributor to long-term clinical prognosis in patients treated with successful balloon coronary angioplasty.

Analysis of Variance↗
PubMed1998

Selective cytotoxicity of farnesylamine to pancreatic carcinoma cells and Ki-ras-transformed fibroblasts.

Farnesyl protein transferase (FPTase) catalyses the post-translational modification of proteins by a farnesyl pyrophosphate. One of the substrates of this enzyme is p21ras, the product of the ras oncogene. We examined whether farnesylamine, one of the FPTase inhibitors (FTI), is selectively cytotoxic in pancreatic carcinoma cells and Ki-ras-transformed fibroblasts. Furthermore, we investigated whether the cytotoxicity of farnesylamine is caused by the induction of apoptosis in these cells. Using the FPTase assay, we found that farnesylamine inhibited FPTase in vitro. Immunoprecipitation showed that farnesylamine inhibited farnesylation of p21ras in vivo. In addition, 24 and 5 microM farnesylamine were required to achieve 50% cytotoxicity in pancreatic carcinoma cells containing activated Ki-ras and Ki-ras-transformed NIH/3T3 cells, respectively. The parental NIH/3T3 cells were resistant to the cytotoxic effect of farnesylamine at concentrations less than 100 microM. After incubation with farnesylamine, DNA fragmentation was observed in both pancreatic carcinoma cells and Ki-ras-transformed fibroblasts at cytotoxic doses of this compound but not in NIH/3T3 cells. These results indicate that the mechanism of cell death induced by farnesylamine is apoptosis, and this apoptosis occurred specifically in pancreatic carcinoma cells containing mutated Ki-ras and the Ki-ras-transformed cells. Because raf is downstream of ras (p21ras) in the ras-raf-mitogen-activated protein kinase signaling pathway, we used c-raf-1-transformed fibroblasts, which proved to be resistant to apoptosis induced by farnesylamine. This supports the theory that inhibition of ras signaling may be related to the induction of apoptosis. These data further suggest that farnesylamine could be useful as a chemotherapeutic agent in cancers that very frequently contain a Ki-ras oncogene mutation, e.g., pancreatic cancer.

3T3 Cells↗
PubMed1998

Aggressive jejunal gamma deltaT-cell lymphoma derived from intraepithelial lymphocytes: an autopsy case report.

A 69-year-old man with massive ascites was referred to our hospital. Paracentesis revealed exudative ascites with many abnormal lymphocytes, which expressed T-natural killer (T-NK) cell surface markers and gamma deltaT-cell receptor (TCR). Although the ascites resolved for a short time with chemotherapy, gastrointestinal bleeding occurred and acute retention of ascites was observed. The patient died of panperitonitis. At autopsy, part of the jejunum revealed ulceration and marked mucosal thickening, and was perforated at the site of the severe ulceration. Histological examination showed massive infiltration of abnormal lymphocytes that were positive for CD45RO. Therefore, the cells responsible for the jejunal lymphoma and ascites were thought to be derived from gamma deltaIEL.

Aged↗
PubMed1998

Clinical feasibility of 0.018-inch intravascular ultrasound imaging device.

OBJECTIVES: Intravascular ultrasound imaging (IVUS) is limited by the size of the imaging catheter. To facilitate imaging before and during interventions, a 30-MHz ultrasonic imaging device was developed that is the same dimension as a 0.018-inch guide wire. The purpose of this study was to evaluate the clinical feasibility of this device. METHODS AND RESULTS: The imaging core was tested in 8 patients with the use of a monorail guiding sheath that was advanced through a 7F catheter. In addition, after coronary interventions, the standard guide wire was removed, the imaging core was placed inside a compatible balloon, and imaging was performed. In 4 patients, imaging was also performed with a standard 3.2F IVUS catheter. The lumen-plaque interface and the media-plaque interface were clearly visualized in all patients. There was no detectable loss in image quality between the new imaging device and the larger IVUS catheter, and measurements of lumen cross-sectional area were not statistically different. CONCLUSIONS: Improvements in manufacturing technology have permitted the development of a mechanically rotating ultrasound imaging core 0.018 inches in diameter. It is compatible with current balloon catheters without degradation of image quality.

Cardiac Catheterization↗
PubMed1998

AMPA receptor-mediated excitotoxicity in human NT2-N neurons results from loss of intracellular Ca2+ homeostasis following marked elevation of intracellular Na+.

Human NT2-N neurons express Ca2+-permeable alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid glutamate receptors (AMPA-GluRs) and become vulnerable to excitotoxicity when AMPA-GluR desensitization is blocked with cyclothiazide. Although the initial increase in intracellular Ca2+ levels ([Ca2+]i) was 1.9-fold greater in the presence than in the absence of cyclothiazide, Ca2+ entry via AMPA-GluRs in an early phase of the exposure was not necessary to elicit excitotoxicity in these neurons. Rather, subsequent necrosis was caused by a >40-fold rise in [Na+]i, which induced a delayed [Ca2+]i rise. Transfer of the neurons to a 5 mM Na+ medium after AMPA-GluR activation accelerated the delayed [Ca2+]i rise and intensified excitotoxicity. Low-Na+ medium-enhanced excitotoxicity was partially blocked by amiloride or dizocilpine (MK-801), and completely blocked by removal of extracellular Ca2+, suggesting that Ca2+ entry by reverse operation of Na+/Ca2+ exchangers and via NMDA glutamate receptors was responsible for the neuronal death after excessive Na+ loading. Our results serve to emphasize the central role of neuronal Na+ loading in AMPA-GluR-mediated excitotoxicity in human neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1998

Colour Doppler-guided spectral analysis of gall-bladder wall flow.

For the purpose of the present study to diagnose gall-bladder cancers, which cannot be detected or are only partly visible by conventional ultrasonography (US), we attempted differential diagnoses of 69 patients with gall-bladder diseases (12 with gall-bladder cancer, five with acute cholecystitis, 11 with chronic cholecystitis, 27 with cholesterol polyp and 14 with adenomyomatosis) using the evaluation of gall-bladder wall blood flow (GWBF). GWBF was evaluated by colour Doppler-guided spectral analysis (CDSA). Thirty-three healthy volunteers were selected as controls at random. Two parameters of GWBF, namely flow velocity and resistive index (RI), were compared between patients with gall-bladder diseases and healthy volunteers. GWBF could be ultrasonically evaluated in 92 (90%) of 102 subjects. All 12 patients with gall-bladder cancer had a significantly rapid blood flow value compared with other patients and healthy volunteers. There was no significant difference in RI among patients and healthy volunteers. When cut-off level of the flow velocity was set at 30 cm/s, gall-bladder cancer could be diagnosed by flow velocity with 100% sensitivity (12/12) and 96% specificity (50/52). Using the same cut-off level of the flow velocity, 17 patients were analysed prospectively. In four asymptomatic gall-bladder cancers and two acute cholecystitis cases with some symptoms, the flow velocity was over 30 cm/s. In two of four patients with gall-bladder cancer, only a part of the tumour was visualized on conventional abdominal US. In conclusion, CDSA was more useful for diagnosing gall-bladder lesions than the conventional abdominal US due to estimation of arterial flow velocity in the gall-bladder wall.

Blood Flow Velocity↗
PubMed1998

Secretion of GM-CSF by inflammatory cells in the lung of patients with sarcoidosis.

Several cytokines are involved in the pathophysiology of sarcoidosis. Granulocyte-macrophage colony-stimulating factor (GM-CSF) may be one of these cytokines because its mRNA is expressed by inflammatory cells obtained from the sarcoid lung. We thus asked two questions. Is GM-CSF secreted by bronchoalveolar lavage (BAL) cells? What type of cells express GM-CSF? GM-CSF secreted by the cultured BAL cells from 19 untreated sarcoid patients was measured by an enzyme-linked immunosorbent assay. The individual cells expressing GM-CSF mRNA were identified by in situ hybridization in seven patients. Spontaneous release of GM-CSF by BAL cells was demonstrated in one patient. When stimulated, BAL cells secreted GM-CSF in all subjects studied. In situ hybridization with digoxigenin-labelled GM-CSF cRNA probe revealed that the positive cells were round in shape and larger than lymphocytes, but smaller than large alveolar macrophages that are often irregular in shape. These results strongly indicated that small alveolar macrophages secrete GM-CSF in the sarcoid lesion. This phenomenon may contribute to the enhanced immunological activities observed in sarcoidosis.

Bronchoalveolar Lavage Fluid↗
PubMed1998

New electrophysiologic features and catheter ablation of atrioventricular and atriofascicular accessory pathways: evidence of decremental conduction and the anatomic structure of the Mahaim pathway.

INTRODUCTION: Several modalities of catheter ablation have been proposed to eliminate Mahaim pathway conduction. However, limited research has been reported on the electrophysiologic nature of this pathway in its entity. METHODS AND RESULTS: In seven patients, electrophysiologic study was performed, and radiofrequency energy was applied to investigate the electrophysiologic clues for successful ablation. In all seven patients, the Mahaim pathway was diagnosed as a right-sided atriofascicular or atrioventricular pathway with decremental properties. In two patients, two different kinds of electrograms were recorded through the ablation catheter positioned at the Mahaim pathway location: one was suggestive of conduction over the decremental portion, demonstrating a dulled potential; and the other of nondecremental conduction, demonstrating a spiked potential. All but one of the Mahaim pathways were eliminated successfully at the atrial origin where the spiked Mahaim potential was recorded. Radiofrequency energy application was performed at the slow potential site resulting in failure to eliminate the conduction over the Mahaim pathway. Conduction block at the site between the slow and fast potential recording sites was provoked by intravenous administration of adenosine, concomitant with a decrease in the amplitude of the Mahaim potential. In one patient, the clinical arrhythmia was a sustained monomorphic ventricular tachycardia originating from the ventricular end of the Mahaim fiber. CONCLUSION: The identification of Mahaim spiked potentials may be the optimal method to permit their successful ablation. Detailed electrophysiologic assessment is indispensable for successful ablation of tachycardias associated with Mahaim fibers because tachycardias unassociated with Mahaim fibers can occur despite complete elimination of the Mahaim fiber.

Adolescent↗
PubMed1998

Time-dependent effects of Klebsiella pneumoniae endotoxin on hepatic drug-metabolizing enzyme activity in rats.

The time-dependent effects of Klebsiella pneumoniae endotoxin on hepatic cytochrome P450-dependent drug-metabolizing capacity (cytochrome P450 and b5 content, activity of aminopyrine N-demethylase, p-nitroanisole O-demethylase, aniline hydroxylase and benzphetamine N-demethylase) and on the pharmacokinetics of antipyrine have been determined in rats. Measurement of enzyme activity and antipyrine (after intravenous injection of 20 mg kg(-1)) were performed 2, 24 and 96 h after a single intraperitoneal injection of endotoxin (1 mg kg(-1)) and after repeated doses (once daily for 4 days). The contribution of tumour necrosis factor alpha (TNFalpha) to the endotoxin-induced changes was also examined in rats pretreated with granulocyte colony-stimulating factor (G-CSF). The systemic clearance of antipyrine and the activity of hepatic cytochrome P450-dependent drug-metabolizing enzymes were dramatically reduced 24 h after a single injection of endotoxin, but had returned to control levels by 96h. The magnitudes of these decreases in these measurements after repeated doses of endotoxin were similar to those seen 24h after the single dose. The systemic clearance of antipyrine correlated significantly with cytochrome P450 content and aminopyrine N-demethylase activity. In histopathological experiments, moderate hypertrophy of Kupffer cells was observed, with no evidence of severe liver-tissue damage. G-CSF pretreatment suppressed the increased plasma concentrations of TNFalpha produced 2 h after single endotoxin injection, but did not eliminate the endotoxin-induced decrease in the systemic clearance of antipyrine, suggesting that TNFalpha is not the sole component responsible for the reduction of cytochrome P450-mediated drug-metabolizing enzyme activity. These results provide evidence that a single intraperitoneal injection of 1.0 mgkg(-1)K. pneumoniae endotoxin in rats reduces hepatic P450 and b5 levels, and reduces the activity of various cytochrome P450-mediated drug-metabolizing enzymes without causing severe liver-tissue damage. This suggests that the effect of endotoxin on hepatic cytochrome P450-mediated drug-metabolizing isozymes is non-selective.

Animals↗