Real-time processing system of a two-color CO2 laser interferometer for density feedback control in JT-60SA.

A real-time processing system for the two-color CO2 laser interferometer on the JT-60SA has been developed for density feedback control. The system has a novel feature that can detect fringe jumps due to off-normal events, such as loss detection due to displacement of the beam axis and changes in the laser wavelengths. Because a phase change due to the JT-60SA plasma is smaller than π/2, corresponding to the line-integral electron density NL of ∼6×1019 m-2 in a short interval of 500 ns, the threshold of the fringe jump detection is decided to be π/2. Hence, off-normal events can be detected from a fringe jump, leading to the abort of the real-time feedback control. In the density feedback control of the JT-60SA plasma, the system is employed as a density monitor, with NL being successfully controlled at 16.8% ± 6.6% lower than the reference.

Small ion-temperature-gradient scale length and reduced heat diffusivity at large hydrogen isotope mass in conventional H-mode plasmas.

The dependence of the ion-temperature-gradient scale length on the hydrogen isotope mass was examined in conventional H-mode plasmas in JT-60U tokamak. While identical profiles for density and temperature were obtained for hydrogen and deuterium plasmas, the ion conductive heat flux necessary for hydrogen to sustain the same ion temperature profile was two times that required for deuterium, resulting in a clearly higher ion heat diffusivity for hydrogen at the same ion-temperature-gradient scale length. On the other hand, the ion-temperature-gradient scale length for deuterium is less than that for hydrogen at a given ion heat diffusivity.

Observation of a complex multistage transition in the JT-60U H-mode edge.

A complex multistage transition of the edge radial electric field is observed in JT-60U H-mode phase without edge localized mode. An interesting feature is that the poloidal rotation velocity of the carbon impurity ions changes in the later H-phase without a comparable change in the main ion pressure gradient, indicating a change in the parallel momentum (and particle) balance channel.

Enhanced external counterpulsation improves exercise tolerance, reduces exercise-induced myocardial ischemia and improves left ventricular diastolic filling in patients with coronary artery disease.

OBJECTIVES: We examined whether enhanced external counterpulsation (EECP) improves myocardial ischemia, exercise tolerance and cardiac function in patients with coronary artery disease (CAD). BACKGROUND: Enhanced external counterpulsation reduces angina and improves exercise tolerance in patients with CAD. Some objective improvements of ischemia by EECP have been reported, but they should be confirmed further. Detailed hemodynamic effects of EECP have been less well documented. METHODS: Enhanced external counterpulsation was performed for a total of 35 h in patients with stable CAD (n = 12) who showed evidence of exercise-induced myocardial ischemia despite conventional medical or surgical therapies. All patients had significant stenotic lesions in major coronary arteries. RESULTS: Enhanced external counterpulsation improved all exercise test parameters (p < 0.05): exercise duration, time to 1-mm ST segment depression, rate-pressure product at peak exercise and rate-pressure product at 1-mm ST segment depression. Moreover, the prevalence of exercise-induced reversible perfusion defects by thallium scintigraphy decreased after treatment (p < 0.01). Enhanced external counterpulsation did not alter systolic function but improved diastolic filling, left ventricular (LV) end-diastolic pressure (p < 0.05) by cardiac catheterization and LV peak filling rate end-diastolic volume/s (p < 0.01) and time to peak filling rate (p < 0.05) by radionuclide scintigraphy. These hemodynamic improvements were associated with decreased plasma brain natriuretic peptides levels after EECP (p < 0.05). CONCLUSIONS: Thus, EECP treatment improves exercise tolerance and reduced myocardial ischemia by thallium scintigraphy in association with improved LV diastolic filling in patients with stable CAD.

Assessment of the accuracy of plasma shape reconstruction by the Cauchy condition surface method in JT-60SA.

For the purpose of stable plasma equilibrium control and detailed analysis, it is essential to reconstruct an accurate plasma boundary on the poloidal cross section in tokamak devices. The Cauchy condition surface (CCS) method is a numerical approach for calculating the spatial distribution of the magnetic flux outside a hypothetical surface and reconstructing the plasma boundary from the magnetic measurements located outside the plasma. The accuracy of the plasma shape reconstruction has been assessed by comparing the CCS method and an equilibrium calculation in JT-60SA with a high elongation and triangularity of plasma shape. The CCS, on which both Dirichlet and Neumann conditions are unknown, is defined as a hypothetical surface located inside the real plasma region. The accuracy of the plasma shape reconstruction is sensitive to the CCS free parameters such as the number of unknown parameters and the shape in JT-60SA. It is found that the optimum number of unknown parameters and the size of the CCS that minimizes errors in the reconstructed plasma shape are in proportion to the plasma size. Furthermore, it is shown that the accuracy of the plasma shape reconstruction is greatly improved using the optimum number of unknown parameters and shape of the CCS, and the reachable reconstruction errors in plasma shape and locations of strike points are within the target ranges in JT-60SA.

Transforming growth factor beta 1 and beta 2 induce down-modulation of thrombomodulin in human umbilical vein endothelial cells.

To investigate the effects of transforming growth factor-betas (TGF-betas) on endothelial anticoagulant activity, we assayed thrombomodulin (TM) activity and antigen levels of human umbilical vein endothelial cells (HUVECs) incubated with TGF-betas in vitro. TGF-beta 1 suppressed surface TM activity and surface TM antigen levels maximally 12 h after incubation in dose-dependent manners. TGF-beta 2 was almost equipotent with TGF-beta 1 for the suppression of them. Both TGF-betas suppressed total TM antigen level in HUVECs, and the time course of the suppression was similar to that of the cell surface TM antigen level. The maximal reductions of TM mRNA levels by TGF-betas were observed at several hours ahead of those observed in both surface and total TM antigens levels, suggesting that the TGF-beta-mediated suppression of TM antigen of HUVECs is primarily regulated at the TM mRNA level. Our present work suggests that the down-modulation of TM level induced by TGF-betas in HUVECs contributes in vivo to promoting the thrombogenesis either at the sites of injury of vessel walls, such as atherosclerotic lesions where TGF-beta 1 is released from platelets, smooth muscle cells and monocytes, or at neovascular walls in tumors secreting TGF-beta 2.

Prothrombin and its derivatives stimulate motility of melanoma cells.

Several studies indicated that activation of the clotting system may promote the growth and the invasive behavior of tumor cells. In the present study, we evaluated the migratory response of various melanoma cell lines to several clotting factors and prothrombin derivatives (thrombin, fragment 1, fragment 2 and kringle 1 fragment). Prothrombin, thrombin and fragment 1 stimulated chemotaxis of the murine (K-1735 M2, X21) and human A375 (SM) melanoma cell lines. Prothrombin and prothrombin fragment 1 showed their maximal chemotactic activity at 0.5 approximately 1 microM. Chemotaxis induced by thrombin was inhibited by hirudin, but not that induced by prothrombin or fragment 1. Other clotting proteins and the fragment 2 and kringle 1 fragment of prothrombin did not elicit chemotactic activity. Checkerboard analysis indicated that motility was directional with a significant chemokinetic component. The K-1735 M2 cells also migrated in a concentration-dependent manner to substratum-bound insoluble prothrombin, thrombin or fragment 1. Ligand binding assays showed that both prothrombin and fragment 1 bound to K-1735 M2 cells with apparent Kds of 0.5 microM. This binding was inhibited by an excess concentration of unlabeled prothrombin and fragment 1 but not by similar concentrations of other prothrombin fragments. These findings suggest that prothrombin and its fragment 1 exert chemotactic activity on melanoma cells by different mechanisms and different binding sites from that induced by thrombin.

Adenosine regulates tissue factor expression on endothelial cells.

The aim of this study was to evaluate the inhibitory activity of adenosine on tumor necrosis factor-alpha (TNF), thrombin-, or phorbol 12-myristate 13-acetate (PMA)-induced tissue factor (TF) expression on human umbilical vein endothelial cells (HUVECs). This inhibitory effect of adenosine was found to be counteracted by the non-selective adenosine receptor (AR) antagonist, 8-(p-sulfophenyl) theophylline. To clarify the role of ARs (A1, A2a, A2b, and A3) in this regulation, we evaluated the effect of several agonists and antagonists specific for AR-subclass on TF expression. The selective A2aAR agonist, 2-p-(2-carboxyethyl) phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride (CGS 21680), the A3AR agonist, N6-2-(4-aminophenyl) ethyladenosine (APNEA), and the A1AR antagonist, 1,3-dipropyl-8-(2-amino-4-chlorophenyl) xanthine (PACPX) each inhibited TF activity expression induced by TNF, thrombin, or PMA on HUVECs. In contrast, the selective A1AR agonist, chloro-N6-cyclopentyladenosine (CCPA) and the A2AR antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX) enhanced each stimulant-induced TF activity expression. All agonist or antagonist alone did not alter the basal TF expression on HUVECs. Our results suggest that stimulation of A2aAR and A3AR down-regulates and that of A1AR up-regulates the endothelial cell TF expression induced by TNF, PMA, or thrombin. Thus, it appears that adenosine itself may exert anticoagulant activity on vascular endothelial cells via its A2a and A3 receptors, particularly during ischemic or atherosclerotic processes which are known to be associated with local increased levels of adenosine.

Aggressive non-Hodgkin's lymphoma after successful eradication of Helicobacter pylori and regression of gastric lymphoma of mucosa-associated lymphoid tissue.

A 57-year-old woman presented to our clinic with low-grade gastric lymphoma of mucosa-associated lymphoid tissue (stage IE) and Helicobacter pylori infection. She received a 2-week course of omeprazole and clarithromycin, resulting in eradication of H. pylori and histological disappearance of the lymphoma. However, 9 months later (May 1996), multiple mass lesions were found around the pancreas and hepato-duodenal ligament on abdominal computed tomography. Inguinal lymph node biopsy revealed aggressive nodal type B-cell non-Hodgkin's lymphoma, diffuse large cell type. She received chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisolone, but failed to achieve remission and died in December 1996. There was no evidence of recurrent gastric lymphoma. This case emphasizes the importance of performing follow-up examinations to detect other neoplasms in patients with gastric lymphoma of mucosa-associated lymphoid tissue.

Facilitation of cleaning of alumina surfaces fouled with heat-treated bovine serum albumin by ozone treatment.

Facilitation of cleaning of alumina (A12O3) particles fouled with heat-treated bovine serum albumin (BSA), which contains sulfhydryl groups on the molecule, by gaseous ozone was studied. With increasing temperature of heat treatment, the amount of adsorbed BSA onto A12O3 surfaces increased, whereas the rate of BSA desorption during alkali cleaning decreased markedly, resulting in the larger amounts of BSA remaining on 12O3 surfaces. No significant amounts of BSA were removed from A12O3 surfaces by alkali cleaning alone when treated at temperatures above 120 degrees C. Before alkali cleaning, the heat-treated, BSA-fouled AI2O3 at 150 degrees C were treated with 0.05 to 0.30% (vol/vol) gaseous ozone at room temperature. Ozone pretreatment markedly accelerated the rate of BSA desorption during subsequent alkali cleaning. The effect of ozone pretreatment on BSA removal depended on the concentration of ozone and treatment time and hence on the total amount of ozone supplied. The molecular weight (MW) of desorbed BSA during alkali cleaning without ozone pretreatment coincided with the MW of the native BSA, whereas the MW of desorbed BSA during the combined ozone-alkali cleaning was lower than the MW of the native BSA. This indicated that the heat-treated BSA molecules adsorbed on A12O3 were partially decomposed into some fragments by ozone pretreatment, resulting in the facilitation of the removal of BSA during alkali cleaning.

Conformation of adsorbed bovine serum albumin governing its desorption behavior at alumina-water interfaces.

The mode of initial adsorption of bovine serum albumin (BSA) onto positively charged Al2O3 particles was studied as a function of surface coverage (theta). The adsorption isotherm of BSA exhibited saturation (theta = 1) and the existence of an inflection point at theta of 0.82. The relative numbers of ionic groups on a BSA molecule interacting with the Al2O3 surface at various theta were monitored by measuring the relative adsorption density of H+ and OH-, ([gamma(H+) - gamma(OH-)]), for BSA-adsorbed Al2O3 using potentiometric titration. The [gamma(H+) - gamma(OH-)] curves for Al2O3, BSA, and BSA-adsorbed Al2O3 at various KNO3 concentrations showed a common intersection point (cip) which was the pH giving the acid-base equivalence point, respectively. Compared with the cip's of Al2O3 (5.6) and BSA (5.2), the cip's of BSA-adsorbed Al2O3 were situated at points corresponding to more alkaline pH values over the theta range of 0.13 to 1.0. These results suggested that negatively charged groups, mainly carboxyl groups, on the BSA molecule electrostatically interacted with the Al2O3 surface. The degree of shift in the cip increased gradually with increasing theta from 0.13 to 0.70, while it decreased markedly over the theta range of 0.82 to 1.0. The variation in the cip reflected the change in the total number of ion pairs formed between BSA molecules and Al2O3. The initial rates of BSA desorption during alkali cleaning were low and almost constant over the theta range of 0.13 to 0.70, but increased markedly at theta higher than 0.82. It is suggested that the conformational changes of BSA adsorbed on Al2O3, involving changes in the relative magnitude of electrostatic interaction forces, occur discretely at theta of approximately 0.8.

Effect of ozone pretreatment on alkali cleaning of alumina fouled with bovine serum albumin.

Pretreatment of alumina particles fouled with bovine serum albumin (BSA) by 0.3% (v/v) gaseous ozone markedly accelerated the removal of BSA during alkali cleaning through partial decomposition of the BSA molecule. The results suggest that ozone pretreatment can reduce the NaOH concentration required for adequate alkali cleaning by at least one order of magnitude.

Increases of thrombomodulin activity and antigen level on human umbilical vein endothelial cells treated with asbestos and man-made mineral fibers.

The potential influences of crocidolite asbestos fibers and man made mineral fibers (potassium titanate whisker and magnesium sulfate whisker) on a procoagulant system of human umbilical vein-endothelial cells (HUVECs) were investigated by measuring the activity and antigen level of thrombomodulin (TM) on the cell surface. Statistically significant increases in both the TM activity and TM antigen level were observed on HUVECs treated with crocidolite asbestos fibers for 48 h and 72 h compared to untreated cells at low concentrations of the fibers which showed no sign of a cytotoxic effect on the cells. An extensive increase in both the TM activity and TM antigen level was also observed on HUVECs treated with potassium titanate whisker or magnesium sulfate whisker for 48 h and 72 h. A statistical analysis revealed that these fibers had almost the same effects on the increases in both TM activity and the TM antigen level of HUVECs treated with the fibers for 48 h and 72 h, but a treatment of magnesium sulfate whisker at more than 1.25 micrograms/ml for 24 h was slightly more effective in increasing TM activity on HUVECs compared to other fibers (p < 0.05). The [3H]leucine incorporation in HUVECs increased when the cells were treated with crocidolite asbestos or man-made mineral fibers (MMMFs), indicating that the increases in TM activity and the TM antigen level on HUVECs directly exposed to those fibers may not reflect the sole induction of anticoagulant activities, but the general cell damage induced by the fibers.

Successful management of tracheo-innominate artery fistula using interposition of a thymus pedicle flap.

Tracheo-innominate artery fistula is usually a fatal complication of tracheostomy. The trachea and innominate artery were successfully reconstructed in an 11-year-old girl who presented with this complication. The thymus was interposed between these two structures in order to prevent further long-term complications.

[Progress in research of the blood coagulation system].

Blood coagulation is an amplification system consisting of reactions between enzymes and zymogens. It has been illustrated as a cascade model. However, the exact mechanism by which haemostasis is achieved under physiological conditions remains to be clarified. The solving of structure-function relation of each coagulation factor, analysis of the enzymological characteristics of each reaction, analysis of the regulation mechanism of the reactions and identification of novel factors involved in coagulation reactions contribute to the understanding of this complex system. Based on these findings, some new conceptions of blood coagulation are proposed. In the model introduced in this review, the extrinsic pathway and the intrinsic pathway of the 'classical' cascade model of the blood coagulation system could not be separated, and the suppression of fibrinolysis by TAFI (thrombin activatable fibrinolysis inhibitor) during coagulation reactions is thought to be a critical process for effective haemostasis.

The association of the platelet count and the peripheral CD8+ cell count in Japanese HIV-infected hemophiliacs.

To determine the factors involved in the pathogenesis of thrombocytopenia frequently found in human immuno-deficiency virus (HIV) infection, we studied the clinical and laboratory findings of 35 Japanese HIV-infected hemophiliacs regarding their association with thrombocytopenia. Seventeen HIV-positive patients were thrombocytopenic. They had fewer CD4+ cells and were in more advanced stages of the disease, compared with the 18 patients without thrombocytopenia. We carried out the stepwise regression analysis on 32 patients in the early stage of HIV infection, with the platelet count as the dependent variable, and with the CD8+ cell count, serum cholinesterase, alanine aminotransferase (ALT), CD4+ cell count and white blood cell count as explanatory variables. The CD8+ cell count, serum cholinesterase, and ALT were entered into the regression model as explanatory variables of the platelet count with statistical significance. A positive linear correlation in these 32 patients between the CD8+ cell count and platelet count (r = 0.50, P < 0.01) was noted. We conclude that the decrease of the CD8+ cell count may play a role in the pathogenesis of thrombocytopenia in Japanese hemophiliacs in the early stage of HIV-infection.

[A family with multiple thrombosis including infancy occurrence].

Since the first patient with antithrombin deficiency was reported, various hereditary thrombophilia have been discovered. However, we experienced a family line of multiple thrombosis in which known hereditary thrombophilia were all refuted. Case 1 died of inferior vena cava thrombosis at the age of 56 days. Case 2, the elder sister of Case 1, developed deep vein thrombosis of the left leg at age 2. She was started on warfarin but contracted deep vein thrombosis of the right leg at the age of 7. In the family of these cases there have been another five cases of thrombosis, spanning three generations, giving a total of seven cases. Six of the cases developed at an early age, below 50 years. Antithrombin, protein C, protein S, heparin cofactor II, soluble thrombomodulin, plasminogen, alpha 2 plasminogen inhibitor, and tissue factor pathway inhibitor were measured but there were no abnormalities, nor was there any resistance to activated protein C. The onset of thrombosis in this family is becoming younger with the passing of generations, and clinical symptoms have been showing a worsening tendency.