Search

Reduction of silica (SiO2) in the bulk form is quite challenging because the bulk silica in both the amorphous and crystalline states is a highly stoichiometric material. In this work, a solution-based synthesis route is developed to produce off-stoichiometric amorphous silica (SiOx with x < 2) by using sonochemical reduction of silica-based materials in the presence of sodium. The resulting amorphous SiOx materials are found to crystallize after annealing at temperatures higher than ∼800 °C under Ar or vacuum environment, resulting in off-stoichiometric silica crystals. The main crystal phase is cristobalite, and a small amount of tridymite was also included. The thus obtained silica crystals exhibit a broad photoluminescence (PL) emission peaking at ∼500 nm, characterized by the PL decay constant on the time scale of microseconds. The spin forbidden emission of oxygen vacancies in a silica crystal lattice is likely to be responsible for the observed broad visible PL emission. The present sonochemical re...

To assess the effects of thyroid hormone and cardiac function on senile dementia, relations between serum thyroid hormone concentrations, hemodynamic parameters and dementia rating scale scores were studied in 83 subjects aged 70 and over. Age and serum-free T3 concentrations had a significantly negative correlation in all subjects and in subjects without dementia, but not when analysed only in dementia subjects. Regarding the genesis of dementia, serum free T3 concentrations and cardiac index were both significantly lower in cerebrovascular dementia than in those without dementia. Moreover, subjects with cerebrovascular dementia showed significantly lower serum free T3 concentrations and cardiac index than those with senile dementia of Alzheimer's type in all age groups. These findings suggest that cognitive function is closely related to serum free T3 and cardiac function in subjects with cerebrovascular dementia and that serum free T3 concentrations may be a good indicator, reflecting health and cognitive status.

Radiometric surveys have been conducted in support of a project investigating the potential of biofuel power generation coupled with remediation of forests contaminated with radionuclides following the Fukushima Daiichi accident. Surveys conducted in 2013 and 2014 were used to determine the distribution and time dependence of radionuclides in a cedar plantation and adjacent deciduous forestry subject to downslope radionuclide migration, and a test area where litter removal was conducted. The radiocaesium results confirmed enhanced deposition levels in the evergreen areas compared with adjacent areas of deciduous forestry, implying significant differences in depositional processes during the initial interception period in 2011. Surveys were conducted both with and without a collimator on both occasions, which modified the angular response of the detector to separate radiation signals from above and below the detector. The combined data have been used to define the influence of radionuclides in the forest canopy on dose rate at 1 m, indicating that, in evergreen areas, the activity retained within the canopy even by 2013 contributed less than 5% of ground level dose rate. The time dependent changes observed allow the effect of remediation by litter removal in reducing radionuclide inventories and dose rates to be appraised relative natural redistribution processes on adjacent control areas. A 15 × 45 m area of cedar forest was remediated in September 2013. The work involved five people in a total of 160 person hours. It incurred a total dose of 40-50 μSv, and generated 2.1 t of waste comprising forest litter and understory. Average dose rates were reduced from 0.31 μSv h-1 to 0.22 μSv h-1, with nuclide specific analyses indicating removal of 30 ± 3% of the local radiocaesium inventory. This compares with annual removal rates of 10-15% where radionuclide migration down-slope over ranges of 10-50 m could be observed within adjacent areas. Local increases were also observed in areas identified as sinks. The results confirm the utility of time-series, collimated, radiometric survey methods to account for the distribution and changes in radionuclide inventory within contaminated forests. The data on litter removal imply that significant activity transfer from canopy to soil had taken place, and provide benchmark results against which such remediation actions can be appraised.

We investigated the relationship between the common cold and restenosis after percutaneous coronary intervention (PCI) in Japanese patients with angina pectoris, because suffering from a common cold during the follow-up period after PCI may be involved in the development of restenosis. In addition, we measured the soluble (s) L-selectin level early after PCI in patients with and without restenosis. The study group included 104 effort angina pectoris patients. We examined whether or not they had had a common cold in the 6 months following angioplasty. Finally, 88 patients, whose common cold status was known, were selected as the study subjects. Twelve patients caught a common cold after PCI. All of these patients were given antibiotics and/or anti-inflammatory agents and recovered within 2 weeks. None had clinically detectable influenza infection. Thirty-three patients suffered from restenosis and 55 did not. There was no significant difference in the restenosis frequency between effort angina pectoris patients with and without a common cold. The sL-selectin level was significantly increased in patients with restenosis early after PCI, whereas in patients without restenosis, sL-selectin remained unchanged. These findings suggest that restenosis development after PCI in patients with effort angina pectoris may involve leukocyte activation early after PCI, while suffering from a common cold during the follow-up period after PCI has no effect.

Minimal deviation endometrioid adenocarcinoma (MDA-E) of the endometrium is a rare pathological entity, and its radiological features are rarely documented. A 73-year-old Japanese woman was referred to the authors when an endometrial biopsy revealed moderately differentiated endometrioid adenocarcinoma. Preoperative radiological examinations, including ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) showed no evidence of cancer nests. In the hysterectomy specimen, mildly atypical glands were scattered throughout the entire depth of the myometrium, without stromal desmoplastic reaction, and a tiny focus of typical, ruptured, endometrioid adenocarcinoma glands was found in the atrophic endometrium. MRI had not been able to identify this unusual, scattered, myometrial invasion. It should be kept in mind that in cases showing Stage IA endometrial carcinoma without endometrial thickening on MRI, this rare form of invasion may be present.

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors. Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and TGF-beta in cardiac fibroblasts. Ang II stimulated fibronectin mRNA levels dose-dependently with a maximal increase (approximately 5-fold) observed after 12 h of incubation. Ang II-, or calcium ionophore-induced fibronectin synthesis was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. Ang II-induced fibronectin mRNA was not affected by PKC inhibitors or PKC depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. We isolated the rat fibronectin gene including the 5'-flanking region and found that the AP-1 binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. Gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-ATF-2 antibodies. Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin. Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function. The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis. We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase, and that Ang II-induced fibronectin mRNA expression is regulated by two different mechanisms; transcriptional control by binding of c-fos/c-jun complex to the AP-1 site, and post-transcriptional control by mRNA stabilization due to autocrine and/or paracrine effects of TGF-beta. Thus, this study suggested that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

To evaluate the effect of weight carrying on dynamic exercise response, 12 normal subjects were studied during treadmill exercise using ear densitography in two ways: (1) no weight, (2) 10 kg weight in one hand. Although there were no significant differences in diastolic time (DT), tension-time index [TTI: systolic blood pressure x heart rate (HR) x left ventricular ejection time (LVET)] was significantly higher throughout the weight carrying exercise compared to dynamic exercise. The amount of change (delta) in TTI was significantly larger in the initial stage (control to 1 min) of weight carrying exercise compared to dynamic exercise, but there were no significant differences in the later stages (1-3 min and 3-6 min). A prolongation in LVET was observed despite increasing HR during the first minute of exercise in both type of exercise, but LVET was longer at any given HR in weight carrying compared to dynamic exercise. Thus, despite higher TTI throughout the weight carrying exercise, delta TTI was larger only in the initial stage which was caused by prolongation of LVET resulting from disproportionate increase in venous return of early exercise.

Computer simulation and myocardial cell models were used to evaluate a low-energy defibrillation technique. A generated spiral wave, considered to be a mechanism of fibrillation, and fibrillation were investigated using two myocardial sheet models: a two-dimensional computer simulation model and a two-dimensional experimental model. A new defibrillation technique that has few side effects, which are induced by the current passing into the patient's body, on cardiac muscle is desired. The purpose of the present study is to conduct a basic investigation into an efficient defibrillation method. In order to evaluate the defibrillation method, the propagation of excitation in the myocardial sheet is measured during the normal state and during fibrillation, respectively. The advantages of the low-energy defibrillation technique are then discussed based on the stimulation timing.

To evaluate whether renal blood flow (RBF) can be monitored during acute change in cardiac index, ureter urine oxygen tension (PuO2) and bladder urine oxygen tension (PbO2) were measured in six mongrel dogs. PuO2, cardiac index, and RBF increased after dobutamine infusion and decreased after propranolol infusion. PuO2 had an excellent correlation with RBF (r = 0.94) and a fair correlation with cardiac index (r = 0.50) and mean blood pressure (r = 0.56); RBF had a fair correlation with mean blood pressure (r = 0.52, P < 0.05) but was not related to cardiac index. With multiple-regression analysis, PuO2 was found to be the significant factor related to RBF. PbO2 had a good correlation with PuO2 (r = 0.94) at control levels. Furthermore, when two dogs were added to evaluate relationships among PbO2, PuO2, and RBF, PbO2 had an excellent correlation with PuO2 (r = 0.92) and RBF (r = 0.91). These data indicate that PuO2 is a more sensitive predictor of RBF than cardiac index and mean blood pressure and that PbO2 can be a noninvasive indicator reflecting RBF during acute circulatory change in dogs.

The histopathological changes related to chlormadinone acetate (CMA) implantation were examined using female beagle dogs given 10mg/kg for four years. All control animals showed sign of estrus during the experiment, with periods of anestrus of normal duration. In contrast, estrus was completely inhibited in the CMA-implanted animals. Histopathologically, uterine sections from the CMA-implanted animals showed cystic glandular hyperplasia, but no histologic evidence of endometritis, myometritis, and pyometra was found. In the ovaries of the CMA-implanted animals, developing ovarian follicles were observed but no mature follicles were noted in addition to an absence of corpus luteum. No remarkable changes were observed in the liver, adrenal, mammary gland, gallbladder and implanted site. Furthermore, the intensity of staining and number and size of ACTH-and LH-positive cells in the pituitary sections of CMA-implanted animals were not different from control animals. It was concluded, therefore, that subcutaneous implantation of CMA is a potential drug-delivery system for reducing changes due to antigonadotropic and glucocorticoid-like activities and characteristic histopathological changes in the uterus due to progestagenic activity.

The prognosis for patients with chronic critical leg ischemic is often poor. The treatment of peripheral vascular disease, although greatly improved over recent decades by drug medication, surgical and minimally-invasive techniques, remains limited by vascular proliferative lesions and by our inability to modulate the progression of native disease. The therapeutic angiogenesis is now the most expected therapy for peripheral vascular diseases. This review explores some of concepts and methods of therapeutic angiogenesis including gene therapy using angiogenic growth factor such as VEGF and basic FGF and an implantation of bone marrow derived endothelial progenitor cells.

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.

We measured platelet-derived microparticles, activated platelets, and various adhesion molecules in 48 patients with diabetes mellitus. We also performed a comparative study of these parameters before and after administration of sarpogrelate hydrochloride. The numbers of platelet-derived microparticles and activated platelets were increased significantly in diabetic patients, and CD63-positive platelets were increased in patients with diabetic complications and poorly controlled blood glucose. Soluble adhesion molecules and thrombomodulin were also increased significantly. After administration of sarpogrelate hydrochloride, not only CD62p- and CD63-positive platelets, but also platelet-derived microparticles were decreased significantly. Soluble adhesion molecules and thrombomodulin were also significantly decreased after the treatment. These data suggest that (a) in patients with diabetes, antiplatelet therapy with sarpogrelate hydrochloride is a useful antithrombin therapy because it suppresses the production of intrinsic coagulants by activated platelets; and (b) sarpogrelate hydrochloride decreases endothelial cell damage via adhesion molecules.

We previously demonstrated that iodothyronine 5'-deiodination (5'D) activity is present and increased by triiodothyronine (T3) and angiotensin II (Ang II) in cultured rat cardiac myocytes. To further elucidate the stimulatory mechanism of Ang II, we investigated the effect of intracellular Ca2+ and protein kinase C on myocardial 5'D activity. Moreover, to elucidate the molecular mechanism of the stimulatory effect of T3 and Ang II, we detected the mRNA levels by means of a reverse-transcriptase polymerase chain reaction (RT-PCR). 5'D activity was increased by adding Bay-k 8644, Ca2+ channel agonist and the effect of Bay-k 8644 was completely blocked by nifedipine, a Ca2+ channel antagonist. 12-O-tetradecanoylphorbol-13-acetate, a protein kinase C activator, similarly stimulated 5'D activity. The addition of a high concentration (20-40 mM) of K+, which caused the depolarization of the membrane had significant stimulatory effects on 5'D activity. Type 1 deiodinase (D1) mRNA was evident in myocardial cells by RT-PCR in a single 758 bp band similar to that in the liver. Cardiac fibroblasts did not express the D1 mRNA. A significant increase in D1 mRNA was also evident after adding T3 and Ang II. These findings indicate that 5'D activity in myocardial cells is increased by activating the voltage sensitive Ca2+ channel, protein kinase C, and membrane depolarization, and that the D1 mRNA is present in cardiac myocytes and is increased by T3 and Ang II. This study therefore suggests that Ang II could affect the action of thyroid hormone on the heart by increasing the D1 gene expression.

Measurement of anti-thyroglobulin antibody(TgAb) is used for diagnosis of autoimmune thyroid disease(AITD). Approximately 82-100% of patients with Hashimoto's thyroiditis and 60-70% of patients with Graves' disease are TgAb positive using high sensitive radioimmunoassay. In patients with subacute thyroiditis(SAT), TgAb is usually negative. Therefore, measurement of TgAb is useful to diagnose painless thyroiditis or acute worsening of Hashimoto's thyroiditis from SAT. To predict the post-partum thyroid dysfunction and thyroid dysfunction after interferon treatment, TgAb measurement is important, since patients with positive TgAb are apt to progress thyroid dysfunction.

Animal models for chronic thyroiditis include (1) experimental autoimmune thyroiditis induced by immunizing rabbits or rodents with thyroid extracts or thyroglobulin and (2) spontaneous thyroiditis in certain species of rodents and chickens. For Graves' disease, no spontaneous animal models are reported. An animal model for Graves' disease has been developed by xenotransplantation of Graves' thyroid tissue plus autologous immune cells to immunodeficient mice. Another animal model for Graves' disease is made by immunizing TSH receptor-peptide or protein to mice. Animal models are very useful for studying etiology of autoimmune thyroid diseases, although no current animal models are satisfactory for human autoimmune thyroid disease.

To assess clinically whether alterations of autonomic tone precede left ventricular dilatation, heart rate variability and early left ventricular dilatation after a first myocardial infarction were assessed. Low-frequency power (LF), high-frequency power (HF), and total power (TP) were obtained by ambulatory electrocardiogram on day 1 in 53 patients with a first acute myocardial infarction. Left ventricular end-diastolic volume determined by echocardiography was obtained on day 1 and day 14. Stepwise linear regression analysis was used to assess the associations of early left ventricular dilatation with heart rate variability adjusted for clinical variables. Higher LF and TP were significantly associated with early left ventricular dilatation after adjustment for age, sex, site of myocardial infarction, acute revasucularization, peak creatine kinase level, history of hypertension, and use of angiotensin-converting enzyme inhibitors and beta-blockers. Higher LF and TP preceded early left ventricular dilatation after myocardial infarction.

Leptin, the product of the obese gene, is produced exclusively in fat cells.To evaluate the clinical significance of measuring serum leptin in 56 patients with chronic renal failure on hemodialysis (HD), we measured leptin levels using radioimmunoassay in 34 normal volunteers and in 56 patients on HD.Normal serum leptin averaged 5.7 +/- 0.7 (mean +/- SEM) ng/ml, which correlated significantly (p0.001) with the body fat percentage as measured by bioelectrical impedance analysis. Serum leptin in HD patients ranged from 1.3 to 142 ng/ml. The mean serum leptin analyzed after the logarithmic conversion was 5.6 ng/ml, which was not significantly different from the normal control value, although the body fat percentage was significantly lower than normal volunteers. There was a significant (p0.01) positive correlation between body fat percentage and serum leptin in both normal controls and HD patients. The slope of the regression curve was steeper in HD patients than in normal controls.(1) serum leptin levels to body fat mass are significantly higher in HD patients than controls; (2) the variability is much wider in HD patients; and (3) a significant relation exists between percent body fat and log serum leptin, the relation being steeper in HD patients than in controls.

The aim of this study was to determine the optimum threshold value of the left ventricular border and the extent of myocardial infarction using quantitative 201Tl single photon emission tomography (SPET). We used the unfolded map method to determine the size of the left ventricle and the extent of myocardial infarction in 10 patients, because it has been shown to be superior to the conventional polar map method. The relative differences in the size of the left ventricle and extent of infarction between 201Tl SPET and post-mortem examination were calculated. The optimum threshold value was determined when the relative difference = 0%. There was an excellent correlation between scintigraphic and post-mortem left ventricular size at a threshold value of 53% (r = 0.91, P0.001); an excellent correlation was also observed between scintigraphic and post-mortem infarct size at a threshold value of 55% (r = 0.93, P0.03). The optimum threshold value in determining left ventricular size using 201Tl SPET is 53% and that in determining infarct size is 55%.

Angiotensin II (Ang II) C-terminal hexapeptide (referred to as Ang IV) possesses the characteristics of a real hormone with specific receptors and biological effects. Clinical application of Ang II type 1 receptor (AT1-R) antagonists cause an increase in plasma Ang II level, which may result in enhanced production of Ang IV.In this study, we measured plasma Ang IV and Ang II levels in patients with chronic renal failure (CRF), and also examined the changes in Ang IV and Ang II levels after administration of an ATI-R antagonist.Ang II and Ang IV levels in CRF patients untreated with hemodialysis (n = 16) were 15.8+/-3.6 and 6.0+/-1.1 pg/ml, respectively, which did not differ significantly from Ang II (20.6+/-2.4) and Ang IV levels (8.6+/-1.1) in normal controls (n = 23). The ratio of Ang IV to Ang II was 38%, similar to that in the controls (41%). Ang II or Ang IV levels in CRF patients treated with hemodialysis (n = 12) were also similar to the control values. Ang IV levels had a significant correlation with Ang II levels (r = 0.59). When hypertensive patients were treated with an AT1-R antagonist candesartan for 7 days, Ang II and Ang IV levels were increased 5.5- and 4.1-fold relative to the control levels, respectively. Ang II levels 28 and 56 days after treatment were significantly lower than those 7 days after treatment, whereas Ang IV levels did not differ significantly from those 7 days after treatment. Similar differential kinetics in Ang II and Ang IV levels after long-term (90 days) treatment with an AT1-R antagonist was also confirmed in experiments using rats. Significant decrease in blood pressure continued during long-term treatment with an AT1-R antagonist.These findings demonstrated that plasma Ang IV levels in patients with CRF did not differ significantly from those in normal subjects, and that treatment with an AT1-R antagonist caused marked increases in both Ang II and Ang IV levels. In contrast, during long-term treatment plasma Ang II levels were more rapidly decreased than Ang IV levels, suggesting longer-lasting enhancement of the action of Ang IV rather than that of Ang II after treatment with an AT1-R antagonist.

Annuloaortic ectasia is often accompanied by Marfan syndrome and associated with infective endocarditis usually involving the mitral valves. We treated a patient with annuloaortic ectasia due to idiopathic cystic medial necrosis who developed congestive heart failure with aortic valvular vegetation. A 56-year-old man had dyspnea on effort since the beginning of January, 1997 and was admitted to our hospital on April 6, 1997 because of orthopnea. The diagnosis was congestive heart failure due to severe aortic regurgitation with annuloaortic ectasia detected by echocardiography. Medication and rest after hospitalization relieved his symptoms but congestive heart failure deteriorated after he had a high fever. At this time, a vegetation attached to the noncoronary cusp of the aortic valve was found which had not been detected on admission. Blood culture yielded Streptococcus sanguis. The diagnosis was infective endocarditis involving the aortic valve. Surgical correction (Bentall method) improved congestive heart failure and he was discharged on August 4, 1997 without recurrence of endocarditis. Infective endocarditis involving the aortic valves is a possible cause of development or deterioration of congestive heart failure in patients with annuloaortic ectasia.

A 61-year-old male was referred to our hospital for rapidly progressive azotemia. He was also found to have huge vegetation at the aortic valve causing regurgitation. Biochemical examinations revealed the presence of an immunocomplex associated with decreased circulating complements. In biopsy samples from the kidney, we found the presence of fibrillar crescents, proliferation of mesangial cells, increase in extracellular matrix proteins, atrophy of tubules, infiltration of mononuclear cells in the interstitial regions, high density deposits in the mesangial area and mesangial interposition. Since the patient strongly rejected operative treatment by valvular replacement, we continued non-invasive treatment such as hemodialysis and treatment with penicillin G. This transiently improved the condition of the patient, including biochemical data and cardiac function, but there was no reduction in the size of vegetation at the aortic valve and the bacteria responsible for infective endocarditis were not identified. About three months after admission, overt signs of congestive heart failure emerged and the patients was subjected to intensive care with a respirator and hemodynamic monitoring. Although the cardiac function was improved, concomitant severe pneumonia occurred and the patient died of septic shock. Thus, we report a rare case in whom immune complex-mediated glomerulonephritis was associated with infective endocarditis with aortic valve vegetation.

Aims Transient atrial fibrillation is a relatively common arrhythmia in the early phase of acute Q-wave myocardial infarction. However, the role of infarction-associated pericarditis on the genesis of atrial fibrillation is controversial. This study was designed to examine the relative importance of infarction-associated pericarditis among other clinical variables on the genesis of transient atrial fibrillation in patients with acute myocardial infarction. Methods and results Three hundred and ninety-eight patients with acute Q-wave myocardial infarction were examined carefully by means of auscultation, ECG, two-dimensional echocardiography and haemodynamic measurements. The diagnosis of pericarditis was made on the basis of pericardial rub detected during the first 3 days after admission. At least 0·5mm of PQ-segment depression from a TP segment lasting more than 24h in both limb and precordial leads was considered diagnostic of PQ-segment depression. Atrial fibrillation was present in 76 patients (19%). Sixteen (42%) of 38 patients with PQ-segment depression had atrial fibrillation, whereas 23 (30%) of 77 patients with pericardial rub had atrial fibrillation. Based on ten clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of atrial fibrillation. PQ-segment depression (chi-square=4·10, P

The safety, findings and clinical usefulness of magnetic resonance (MR) imaging were assessed in patients with a prosthetic carbon valve in the mitral position. In vitro deflection, heating and image distortion due to the magnetic field of a 1.5 tesla MR machine were examined in three carbon valves (CarboMedics, St. Jude Medical and Björk-Shiley valves). In vivo MR imaging of the left ventricular horizontal long-axis, vertical long-axis and short-axis views was performed by electrocardiographically synchronized spin echo and field (gradient) echo techniques in eight patients with prosthetic mitral carbon valves, consisting of six CarboMedics valves, one St. Jude Medical valve and one Björk-Shiley valve. No deflection and significant heating was seen in all three valves in vitro. Although little image distortion was shown in the CarboMedics and St. Jude Medical valves, a small distortion toward the frequency encoded direction was seen in the Björk-Shiley valve but caused no difficulty in assessing the surrounding images. Four of the eight patients had normal sinus rhythm and the other four had atrial fibrillation. The prosthetic valves were depicted as signal voids in the images taken by both spin echo and field echo techniques in vivo. Clear structural information with little image distortion of the adjacent tissues of the prosthetic valves were obtained in all patients, although the image of the Björk-Shiley valve which contained stainless steel in the frame had a slightly stronger distortion than those of the CarboMedics and St. Jude Medical valves which contained titanium. The stainless wire suture material used to close the sternal incision was depicted as a signal void, and the areas of the signal loss were larger in the images taken by the field echo technique than those by the spin echo technique. The images taken by the spin echo technique in patients with atrial fibrillation had reduced quality due to the irregularity of repetition time. Cine MR imaging by the field echo technique showed physiological mitral regurgitant jets as signal loss within the flowing blood, which appeared as high signal intensity, bidirectionally in the bileaflet mechanical valve and unidirectionally in the monoleaflet mechanical valve. An abnormal cavity was seen behind the basal left ventricular myocardium in one patient with a CarboMedics valve. The wall of the abnormal cavity was disrupted abruptly and the rest of the wall consisted of pericardium and adjacent tissue in the image taken by the spin echo technique. The image taken by the field echo technique showed an abnormal jet flow from the basal part of the left ventricular cavity into the abnormal cavity, which was compatible with left ventricular pseudoaneurysm. Two-dimensional echocardiography and Doppler color flow mapping disclosed the abnormal cavity and the abnormal flow inside, but failed to show the connection between the left ventricle and the cavity due to reverberation of the ultrasound signal by the prosthetic valve. These findings suggest that MR imaging is a safe and promising method to assess the complications and valvular function in patients with a prosthetic carbon valve in the mitral position.

Resting [123I]MIBG and 201TI imaging were performed at 2 wk and 4 and 12 mo after successfully reperfused myocardial infarction. Although [123I]MIBG uptake of the infarcted segments revealed significant improvement in the early image at 4 mo, delayed image displayed decreased [123I]MIBG uptake. However, decreased [123I]MIBG uptake of the delayed image became almost uniform at 12 mo. These observations suggest that reinnervation initially occurs in norepinephrine uptake and then in retention ability. On the other hand, a 201TI defect remained in the infarcted segments at 12 mo. Thus, reinnervation can occur not only in the peri-infarct area but also in the infarcted area.

This study investigated the clinical significance of abnormally high signal intensity in the left ventricular myocardium on gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA) enhanced magnetic resonance (MR) imaging in patients with dilated cardiomyopathy. Gd-DTPA enhanced MR imaging, Tl-201 myocardial single photon emission computed tomography (SPECT), Tc-99m radionuclide angiocardiography, M-mode echocardiography, electrocardiography and chest radiography were performed in 18 patients with dilated cardiomyopathy. The left ventricle was divided into five areas, the anteroseptal, anterolateral, inferoseptal, posterolateral and apical areas. Five patients (group A) had 0-2 and 13 patients (group B) had 3-5 high signal intensity areas. High signal intensity areas were demonstrated in 19 of 90 areas (21%) before Gd-DTPA enhancement and 50 of 90 areas (56%) after enhancement. Fifteen of 34 areas (44%) with abnormal Tl-201 uptake showed high signal intensity before Gd-DTPA enhancement and 31 (91%) showed high signal intensity after enhancement. Fifteen areas without abnormal Tl-201 uptake also showed high signal intensity after enhancement. Left ventricular ejection fraction (LVEF) and percent fractional shortening (%FS) in group B were lower than those in group A. LVEF(r = 0.78) and %FS (r = 0.82) were significantly correlated with the number of high signal intensity areas. Systolic left ventricular dimension was larger in group B than that in group A, and a significant correlation (r = 0.62) between systolic left ventricular dimension and the number of high signal intensity areas was found. There was no significant difference in right ventricular ejection fraction, left ventricular peak filling rate, diastolic left ventricular dimension, left ventricular thickness, cardiothoracic ratio or SV1+RV5 or 6 between group A and B. There was no correlation of peak filling rate, diastolic left ventricular dimension, cardiothoracic ratio or SV1+RV5 or 6 with the number of high signal intensity areas. These results suggest that abnormal high signal intensity on Gd-DTPA enhanced MR imaging may reflect myocardial degeneration, necrosis or fibrosis, and the high signal intensity predicts the severity of left ventricular dysfunction in dilated cardiomyopathy.

A very rare case of directly penetrating injury of the head, neck and chest caused by a nail-gun was reported. A 56-year-old male was admitted to our critical care center due to chest injury. On admission, he showed numbness of the handleg, left hemiparesis and hypalgesia. Physical examination disclosed three nails on the left anterior chest, but other wounds or nails were not found. Chest films showed three nails penetrating the lung without reaching the heart, but other nails were found by skull and neck films. One nail had penetrated the cervical canal at the C1 level through the posterolateral cervical region. Two other nails were demonstrated at the right temporal and the left frontal region, Computed tomography revealed no massive cerebral hemorrhage and cerebral angiography showed no extravasation and no passage through main vessels. Emergency surgery was performed uneventfully and the nails in the chest, neck and head were totally removed. He was discharged one month after surgery. Some injuries caused by a nail-gun have been reported in the world literature but in Japan this multiple injury case was the first reported. Since nail-gun injuries can cause multiple damage, systemic X-ray examination was very important.

The significance of abnormal high signal intensity observed in left ventricular myocardium by gadolinium-diethylenetriaminepenta-acetic acid (Gd-DTPA) enhanced magnetic resonance (MR) imaging in hypertrophic cardiomyopathy (HCM) patients was assessed by comparison with T1-weighted MR imaging, thallium-201 (201Tl) myocardial scintigraphy, radionuclide angiocardiography, M-mode echocardiography, electrocardiography, and chest radiography. The 16 patients were divided into three groups: 8 patients (group I) with abnormal high signal intensity before and after Gd-DTPA enhancement, 4 (group II) with abnormal high signal intensity only after enhancement and 4 (group III) without abnormal high signal intensity. Thallium-201 myocardial single photon emission computed tomography (SPECT) showed 4 of the 8 patients in group I, 3 of the 4 patients in group II and only 1 of the 4 patients in group III had abnormalities of regional 201Tl uptake in the left ventricular myocardium. No significant difference in left ventricular ejection fraction (LVEF) was seen between groups I, II, and III (64 +/- 13%, 67 +/- 17% and 71 +/- 7%, respectively) although three patients of group I had LVEF of less than 55%. Left ventricular peak filling rates (PFR) of groups I and II were significantly lower than that of group III (1.90 +/- 0.44, 2.41 +/- 0.43 and 3.37 +/- 0.48 EDV/sec, respectively). Group I had larger end-diastolic left ventricular dimension (LVDd), significantly larger end-systolic left ventricular dimension (LVDs), and smaller % fractional shortening (%FS) than group III (49 +/- 4 vs 42 +/- 6 mm, 31 +/- 5 vs 22 +/- 4 mm, and 38 +/- 8 vs 49 +/- 4%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The significance of exercise-induced S-T elevation in aVR was studied in 57 patients with recent anterior infarction and single-vessel disease. S-T elevation in aVR was found at peak exercise in 24 patients. Although the initial defect area was similar in the groups with and without S-T elevation in aVR, the redistribution area was larger in the former group (p0.01). When three electrocardiographic criteria were used in the multivariate analysis, S-T elevation in aVR was the significant variable related to redistribution in the anterior wall. Thus, S-T elevation in aVR may indicate ischemia of the anterior wall.

21-hydroxylase deficiency was described as a fatal disease in infancy manifested by severe adrenal insufficiency with lack of differentiation of the external genitalia in males. Patients are in adrenal insufficiency or receiving long term corticosteroid therapy and are unable to respond normally to surgery or other forms of stress. Therefore, supplementation with corticosteroids and various regimens are required for surgery and anesthetic management. A 3 year 10 months correction of 6] old phenotypic female [correction of male] with 21-hydroxylase deficiency and congenital adrenal hyperplasia was scheduled for critroplasty. Anesthesia was induced with sevoflurane, nitrous oxide and oxygen. After endotracheal intubation, a caudal epidural catheter was placed. At the induction of anesthesia, the patient received a bolus of hydrocortisone 30 mg i.v. followed by a continuous infusion of hydrocortisone. The patient's general condition was good during surgery without any major complications. Caudal epidural anesthesia is considered to be effective for anesthetic management of these patients.

Using ear densitography, consisting of photoelectric plethysomography and Holter electrocardiography, we measured systolic time intervals (STI) in 21 patients, ASA class 1 and 2, undergoing laparoscopic cholecystectomy using CO2 insufflation under general anesthesia (neuroleptanesthesia with isoflurane in air, FIO2 0.5). The patients were divided into two groups: Y-group (10 patients under 59 years of age) and O-group (11 patients over 60 years of age). We investigated the influence of age on cardiac pump function during pneumoperitoneum non-invasively. Y-group showed improvement of cardiac pump function (reduction of PEP/LVET) from 30 minutes after the beginning of insufflation and quick recovery of cardiac function immediately after deflation. O-group showed a tendency of increasing PaCO2 and arterial diastolic pressure, and delayed recovery of cardiac function (elongation of PEP at 60 minutes, and increase of PEP/LVET at 60 and 90 minutes, respectively, after insufflation). Hypertension and tachycardia were apparent immediately after pneumoperitoneum in the O-group. We conclude that special care and monitoring are mandatory for the aged patients with impaired cardiac or respiratory function during laparoscopic surgery.

To investigate the differences in local immune response between persistent and regressive cervical dysplasia.We conducted a quantitative study of Langerhans cells, pan-T cells, and helper-inducer T cells in the subepithelial connective tissue using immunohistochemical techniques with S-100 protein antibody, UCHL1, and OPD4, respectively, in 52 paraffin sections. The subjects were patients with persistent cervical dysplasia and a comparable control group of 46 patients with regressive dysplasia.In the subepithelial stroma, the mean (+/- standard deviation) numbers of S-100- and OPD4-positive cells in the persistent group were 8.6 +/- 8.1 and 84.6 +/- 66.3, respectively, compared with 15.1 +/- 9.4 and 147.0 +/- 67.7, respectively, in the regression group. These data demonstrate a significant reduction of Langerhans cells and helper-inducer T cells (P.0002 and P.0001, respectively) with persistent dysplasia.The decreased numbers of S-100-positive Langerhans cells and helper-inducer T cells in persistent dysplasia compared to those of regressive dysplasia strongly support a decreased local immune response in persistent cervical dysplasia.

OBJECTIVE Left ventricular remodeling occurs immediately after MI, involving structural changes in noninfarcted segment. However, the residual left ventricular pump function in NIDDM patients after acute MI has not been clarified. The purpose of this study was to evaluate the difference in the process of left ventricular remodeling between NIDDM and nondiabetic patients. RESEARCH DESIGN AND METHODS Left ventricular regional EF images obtained by radionuclide angiography were investigated in 20 NIDDM and 29 nondiabetic patients the 3rd wk after acute MI. RESULTS Regional EF of the noninfarcted area and P/V had a significant hyperbolic relation with left ventricular EDV in both groups of patients. Despite no difference in the extent of myocardial necrosis and the number of coronary vessels diseased between NIDDM and nondiabetic patients, regional EF of the noninfarcted area and P/V were significantly lower when left ventricular EDV increased in NIDDM patients compared with nondiabetic patients. CONCLUSIONS Pathogenetic changes of the residual myocardium associated with NIDDM may adversely influence the process of left ventricular remodeling after MI, especially in patients with increased left ventricular EDV.

To evaluate whether the response of left ventricular pump function during low-level exercise in the early postinfarction period can anticipate its change during the first year after acute myocardial infarction (MI), global and regional ejection fractions (EF) were investigated using radionuclide angiography in 52 consecutive patients with negative predischarge exercise test. The changes in left ventricular EF and regional EF of the noninfarcted area during the early exercise test had a good linear relation with the changes during the first year after MI (r = 0.86, p less than 0.001 and r = 0.81, p less than 0.001, respectively). Our results indicate that the mobilization of the Frank-Starling mechanism and myocardial contractility were the important factors related to the change of left ventricular EF, and that the changes of left ventricular EF during exercise in the patient with a negative predischarge exercise test can predict the direction of change (concordant rise or fall) during the first year after MI.

To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.

In this study, the differences in hemodynamic changes during paroxysmal supraventricular tachycardia (PSVT) between A-V nodal re-entry and A-V re-entry were evaluated. In 8 patients with A-V nodal re-entrant tachycardia and 10 with A-V re-entrant tachycardia, electrophysiological studies were performed to measure systolic time intervals (pre-ejection period: PEP, ejection time: ET, PEP/ET ratio: PEP/ET). These measurements were obtained in the control state (atrial pacing at 90/min) and during PSVT with simultaneous recordings of electrocardiogram and femoral arterial pulse tracing. During PSVT, there was no difference in the heart rate between the 2 groups, but ventriculo-atrial conduction time was shorter in A-V nodal re-entry than in A-V re-entry. There was a marked fall in the ET and an increase in PEP/ET in all the patients when PSVT was induced. PEP increased significantly in A-V nodal re-entry, but did not change in A-V re-entry. This resulted in a greater increase in the PEP/ET suggesting a greater deterioration of the hemodynamic consequences in A-V nodal re-entry than in A-V re-ent y. Thus, the hemodynamic changes of PSVT differ between these 2 types of re-entrant circuits, which are mainly influenced by the ventriculo-atrial conduction time.

To evaluate the effect of microangiopathic complications and autonomic dysfunction on diastolic time (DT) during dynamic exercise, 19 patients with type 2 diabetes and ten normal subjects were studied using ear densitography. All subjects had neither an ischemic electrocardiographic response nor chest pain during maximal treadmill exercise. The DT and heart rate (HR) had an inverse nonlinear relation, and electromechanical systole (QS2) and HR had an inverse linear relation during exercise. When the exercise DT-HR and QS2-HR relations were compared, a significant lengthening of QS2, with a consequent shortening of DT, was observed in diabetic patients with retinopathy, compared to patients without retinopathy and normal subjects (p less than 0.005), while no significant differences were found between diabetic patients without retinopathy and normal subjects; however, there were no significant differences in the exercise DT-HR and QS2-HR relations among diabetic patients with and without autonomic dysfunction and normal subjects. A more prominent abbreviation in the diastolic perfusion time observed in patients with retinopathy would be meaningful because microangiopathy might already have limited subendocardial blood flow. Thus, patients with type 2 diabetes who have retinopathy have a potential risk of aggravation of left ventricular function through the deterioration of myocardial blood flow.

To evaluate the effect of percutaneous transvenous mitral commissurotomy (PTMC), equilibrium radionuclide angiocardiography was performed in eight patients with mitral stenosis who had atrial fibrillation. Accurate cardiac function in patients with atrial fibrillation is difficult to assess, since the wide fluctuation of cardiac cycle makes the ventricular hemodynamics variable. A new processing algorithm was devised to make multiple gated images discriminated from a heart rate distribution histogram. We obtained about 1,000 beats data by list mode acquisition, and processed a heart rate distribution histogram. The data in the area +/- 5% of the most frequent heart rate were converted into frame mode and a representative time activity curve was derived. Mitral valve area calculated by echocardiography increased from 1.3 +/- 0.5 to 2.0 +/- 0.6 (cm2) significantly (p less than 0.01). The mean transmitral pressure gradient measured by catheterization decreased from 12.4 +/- 5.9 to 4.9 +/- 3.7 (mmHg) significantly (p less than 0.01) and the clinical symptoms improved in all patients. The change in left ventricular ejection fraction from 43 +/- 9 to 48 +/- 13 (%) was not statistically significant, but peak filling rate (PFR) derived from the time activity curve increased from 1.5 +/- 0.3 to 2.0 +/- 0.4 (EDV/sec) significantly (p less than 0.01). Thus PFR is a noninvasive parameter that can evaluate the effect of PTMC.