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E Hatta

Publications and source records attributed to E Hatta.

14 recordsLinked to original sources
PubMed2005

String defects connecting pairs of half-integer disclinations and tilting transition of a langmuir monolayer.

The static and dynamic string defect textures connecting pairs of half-integer disclinations have been observed by Brewster angle microscopy in the solid phase of pentacosadiynoic acid Langmuir monolayers. The static string defect structures have appeared coexisting with two kinds of point disclinations that have four and two black brushes. The use of local laser heating has allowed one to observe kinetics of creation and annihilation of string defects connecting the two-half-integer disclinations in the splitting process of an s = 1 point disclination into fractional disclinations. These kinetics have been analyzed by studying the competition between the orientational elasticity of the molecules and the line tension of the string and the drag force of the disclinations.

Journal Article↗
PubMed2004

Sequential collapse transitions in a Langmuir monolayer.

Unusual sequential collapse transitions are investigated in a lignoceric acid Langmuir monolayer. The nucleation of monolayer collapse is first initiated in the solid, S, phase but at remarkably low surface pressure where small three-dimensional (3D) granular dots appear. The density of nucleation centers increases, and the 3D dots prevail over the monolayer (surface roughening regime) as the surface pressure increases, but individual dots neither grow very much in size nor evolve into other shapes such as stripes or elongated dots. On further compression the second collapse mode manifests itself by highly anisotropic, global crack arrays (anisotropic cracking regime) where the surface pressure "kink" appears in the isotherm. In the latter regime, various forms of 3D curved filaments develop in the crack regions, and they break into smaller fragments with a typical relaxation time (approximately 60 ms).

Journal Article↗
PubMed2003

Topological manifestations of surface-roughening collapse in Langmuir monolayers.

A transition from surface-roughening collapse to a random network collapse has been investigated in fatty acid Langmuir monolayers. In contrast to the random network crack pattern, the surface-roughening crack pattern grows on a much longer time scale and on a much shorter length scale. A change in the isotherm from a surface pressure "spike" to a "plateau" occurs at the transition. In the surface-roughening regime, the pattern is manifested by the emergence of a three-dimensional (3D) disordered stripe phase with locally aligned, anisotropic stripe clusters. The individual stripes coalesce less with each other even at a late stage of the collapse process and there is a characteristic length for the stripe width and the nearest neighbor spacing. The pattern includes a high density of topological defects such as single open ends, twin open ends, branches, and loops. The effects of shear deformation on the observed patterns are discussed.

Journal Article↗
PubMed2003

[Infected false aneurysm due to methicillin-resistant staphylococcus aureus after proximal aortic grafting].

A 70-year-old man developed meticillin-resistant staphylococcus aureus (MRSA) mediastinitis after prosthetic graft replacement of the ascending aorta. The sternal wound was reexplored and a single-stage procedure of irrigation, debridement, and omental transposition was performed. Ten months after the first operation, he suffered recurrence of pyrexia and the presence of false aneurysm originated from the distal suture line was diagnosed by the chest computed tomography (CT) scan. Re-replacement of the ascending aorta and proximal hemiarch with rifampicin soaked Gelseal was successfully performed. Hypothermic perfusion with circulatory arrest through peripheral cannulation and left ventricular venting via a left anterior thoracotomy was useful to obtain safe reentry in the operation of retrosternal false aneurysm.

Aged↗
PubMed2002

Cavitation of Langmuir monolayers.

Cavitation in liquid expanded and liquid condensed Langmuir monolayers induced by laser heating or microbubble coalescence is studied experimentally using fluorescence and Brewster angle microscopy. The kinetics of hole closure of two-dimensional (2D) gaseous cavitation bubbles exhibits a decelerated dynamics for cavities surrounded by a liquid expanded phase and an accelerated dynamics for cavities in a liquid condensed phase. Most of the cavities in liquid condensed phases possess a nonconvex shape and do not close. The results are compared with theoretical predictions derived for 2D cavitation of liquid monolayers of different surface shear viscosities, and for solid monolayers with diffusive flux of vacancies and interstitials. While part of the theory is in qualitative agreement with the experiment, the experimentally observed hole persistence within the liquid condensed phases and the hole closure within liquid expanded phases remains to be explained. The technique of microbubble coalescence might be particularly useful for the study of the rheological properties of hexatic phases.

Journal Article↗
PubMed2001

[Mixed type of total anomalous pulmonary venous return: a rare pattern of pulmonary venous drainage].

The occurrence of multiple drainage sites in total anomalous pulmonary venous return (TAPVR) has important implication in preoperative diagnosis and surgical treatment. We report a rare pattern of pulmonary venous drainage with the right upper pulmonary vein draining into the innominate vein and the other three pulmonary veins into the portal vein (Ib + III type). The preoperative diagnosis was made by echocardiography and confirmed by angiography. In operation, an anastomosis was made between the common pulmonary vein and the left atrium through posterior approach, but the right upper pulmonary vein was left uncorrected because the anomalously draining blood flow of a single pulmonary vein was about 20% of total pulmonary blood flow. The postoperative course was uneventful, however, the long-term follow-up is mandatory because of the right upper pulmonary vein being left uncorrected.

Anastomosis, Surgical↗
PubMed2000

Angiotensin-converting enzyme-independent angiotensin formation in a human model of myocardial ischemia: modulation of norepinephrine release by angiotensin type 1 and angiotensin type 2 receptors.

Angiotensin II (Ang II) promotes norepinephrine (NE) release from cardiac sympathetic nerve endings. We assessed in a human model in vitro whether locally formed Ang II contributes to NE release in myocardial ischemia. Surgical specimens of human right atrium were incubated in anoxic conditions. After 70 min of anoxia, NE release (carrier-mediated; caused by NE transporter reversal) was 8-fold greater than normoxic release. Angiotensin-converting enzyme inhibition with enalaprilat failed to reduce anoxic NE release. In contrast, prevention of chymase-dependent Ang II formation with chymostatin, Bowman-Birk inhibitor, or alpha(1)-antitrypsin significantly inhibited anoxic, but not exocytotic, NE release. Two mast-cell stabilizers, cromolyn and lodoxamide, markedly reduced NE release, implicating cardiac mast cells as a major source of chymase. Angiotensin type 1 receptor (AT(1)R) blockade with EXP3174 inhibited NE release, whereas angiotensin type 2 receptor (AT(2)R) blockade with PD123319 did not. Interestingly, PD123319 reversed the inhibitory effect of EXP3174. Furthermore, synergisms were uncovered between EXP3174 and an AT(2)R agonist, and between EXP3174 and a Na(+)/H(+) exchanger inhibitor. Thus, angiotensin-converting enzyme-independent Ang II formation via chymase is important for carrier-mediated ischemic NE release in the human heart. Locally generated Ang II promotes NE release by acting predominantly at AT(1)Rs, which are likely coupled to the Na(+)/H(+) exchanger. Effects of Ang II at AT(2)Rs, seemingly opposite to those resulting from AT(1)R activation, are uncovered when AT(1)Rs are blocked. Because NE release is associated with coronary vasoconstriction and arrhythmias, and mast-cell density and chymase content increase in the ischemic heart, the notion that chymase-generated Ang II plays a major role in carrier-mediated NE release may have important clinical implications.

Aged↗
PubMed1999

Partial median sternotomy as a minimal access for the closure of subarterial ventricular septal defect. Feasibility of transpulmonary approach.

BACKGROUND: Minimally invasive techniques in congenital heart surgery have evolved steadily over the past few years, but documentation in the literature is rare. The majority of reported techniques involve thoracoscopic approach and partial sternotomy. We have employed a lower partial sternotomy as a minimal-access procedure for the closure of subarterial ventricular septal defect, for situation where this approach would be unsuitable for adequate exposure of the pulmonary artery. The purpose of this study is to demonstrate the feasibility and safety of this technique and report its superior cosmetic result. SUBJECTS AND METHODS: Beginning in 1997, we began approaching the closure of subarterial ventricular septal defect through a lower sternal split incision using a 6 to 10 cm skin opening, associated with a reversed L incision at the left second intercostal space. A total of consecutive 12 patients (6 male and 6 female) have been operated on using this approach. The patients ranged in age from 6 to 21 years (mean, 12.8 +/- 5.0 years). The straight cannula with stylet was used for aortic cannulation. RESULTS: There was no mortality or morbidity, except for late pericardial effusion in 4 cases. The durations of cardiopulmonary bypass and aortic cross-clamping ranged from 94 to 206 (mean, 131 +/- 33) minutes and from 40 to 122 (mean, 70 +/- 26) minutes, respectively. Ten of 12 patients were extubated in the operating room, and no patient required blood transfusion. The postoperative hospital stay ranged from 8 to 21 (mean, 13.4 +/- 4.2) days. No patient developed deterioration of aortic regurgitation or residual ventricular septal defect. CONCLUSIONS: Our experience demonstrates that the lower partial sternotomy for the closure of subarterial ventricular septal defect is technically feasible and can be used with excellent cosmetic results and safety. Although experience is limited and follow-up is relatively short, this less invasive surgical technique may become a beneficial option for the management of subarterial ventricular septal defect.

Adolescent↗
PubMed1999

Norepinephrine release and ventricular fibrillation in myocardial ischemia/reperfusion: roles of angiotensin and bradykinin.

Exogenous bradykinin (BK), acting at B2-receptors, enhances norepinephrine (NE) release and exacerbates arrhythmias (VF) in myocardial ischemia/reperfusion. Inhibition of BK formation (with serine proteinase inhibitors) alleviates NE release and VF, whereas prevention of BK degradation (with kininase inhibitors) potentiates them. Yet serine proteinase and kininase inhibitors also prevent the formation of angiotensin (AII), a potent NE-release enhancer. Thus we assessed the respective contribution of AII and BK to NE release and VF by using selective B2- and AT1-receptor antagonists. Isolated guinea pig hearts were subjected to 10- and 20-min global ischemia and 45-min reperfusion. NE overflow (pmol/g) was approximately 8 (exocytotic) and approximately 750 (carrier mediated). VF, associated with carrier-mediated NE release, lasted approximately 2 min. The B2-receptor antagonist Hoe 140 (30 nM) affected neither NE overflow nor VF. In contrast, the AT1-receptor antagonist EXP3174 (100 nM) markedly reduced exocytotic and carrier-mediated NE release and shortened VF. When EXP3174 was combined with Hoe 140, NE overflow and VF were decreased even further. Thus in myocardial ischemia, local AII production contributes to NE release and VF via AT1-receptors. Although BK production increases in myocardial ischemia, the effects of BK on adrenergic nerve terminals are uncovered only when BK half-life is prolonged and/or when AII effects are suppressed.

Angiotensin Receptor Antagonists↗
PubMed1999

Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts.

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

[Long-term results of mitral valve regurgitation after surgical repair of incomplete atrioventricular septal defect].

Although the postoperative outcome in patients with incomplete atrioventricular septal defect (iAVSD) is excellent, deterioration of mitral valve regurgitation (MR) is still remained to be resolved. Therefore, this study was undertaken to compare surgical procedures for mitral cleft repair with their long-term results of MR. From 1991 to 1996, 52 patients underwent surgical repair of iAVSD. Age at operation ranged from 2 months to 62 years old with mean age of 14.2 years. Mean follow-up period was 8.6 +/- 4.4 years. All patients underwent patch closure of ostium primum defect. Two patients did not have cleft (Group A). Seven patients did not close the cleft at all (Group B), while 40 patients had the repair of valve by closing cleft near septal attachment only (Group C). The latest 3 patients had the complete closure of cleft from annulus to margin of leaflet where chorda is attached. MR was evaluated by echocardiography grading 0 to IV and regurgitation more than grade II was considered to be significant. In Group A, MR remained grade I. In Group B, MR was deteriorated in 5 patients (71%). Consequently, 6 patients (86%) had grade II or more regurgitation and 4 patients (57%) revealed grade III/IV regurgitation including one (14%) reoperation. In Group C, MR was deteriorated in 10 patients (55%). Consequently, 22 patients (86%) had grade II or more regurgitation and 5 patients (13%) had grade III/IV regurgitation including 3 (7.5%) reoperations. In Group D, no deterioration of MR was noted and all had grade I or less regurgitation. These results suggest that the closure of cleft near septal attachment is not sufficient to prevent MR in late phase and the complete closure of cleft from annulus to margin of leaflet, where chorda is attached, would be useful to prevent the deterioration of MR in late phase.

Adolescent↗
PubMed1998

Application of the reversed elephant trunk technique during total thoracoabdominal replacement in patients with Marfan's syndrome.

The reversed elephant trunk operation has been applied in patients with extensive aortic involvement as a scheduled staged operation. We report application of the same technique in two patients with Marfan's syndrome. The two patients underwent total replacement of the thoracoabdominal aorta for a DeBakey IIIb aortic dissection. The proximal end of the prosthetic graft was invaginated to facilitate future proximal operation. No complication related to the trunk had been observed during the follow-up period.

Adult↗
PubMed1997

Activation of histamine H3 receptors inhibits carrier-mediated norepinephrine release in a human model of protracted myocardial ischemia.

During protracted myocardial ischemia, ATP depletion promotes Na+ accumulation in sympathetic terminals and prevents vesicular storage of norepinephrine (NE). This forces the reversal of the neuronal uptake1 transporter, and NE is massively released (carrier-mediated release). We had shown that histamine H3 receptors (H3Rs) modulate ischemic NE release in animals. We have now used a human model of protracted myocardial ischemia to investigate whether H3Rs may control carrier-mediated NE release. Surgical specimens of human atrium were incubated in anoxic conditions. NE release increased approximately 7-fold within 70 min of anoxia. This release was carrier mediated because it was Ca++ independent and inhibited by the uptake1 inhibitor desipramine. Furthermore, the Na+/H+ exchanger (NHE) inhibitors ethyl-isopropyl-amiloride and HOE 642, and the Na+ channel blocker tetrodotoxin inhibited NE release, whereas the Na+ channel activator aconitine potentiated it. The selective H3R agonist imetit decreased NE release, an effect that was blocked by each of the H3R antagonists thioperamide and clobenpropit. Notably, imetit acted synergistically with ethyl-isopropyl-amiloride, HOE 642 and tetrodotoxin to reduce anoxic NE release. Thus, activation of H3R appears to result in an inhibition of both NHE- and voltage-dependent Na+ channels. Most importantly, endogenous histamine was released from the anoxic human heart, and thioperamide and clobenpropit each alone increased NE release, indicating that H3R become activated in myocardial ischemia. Our findings indicate that H3Rs are likely to mitigate sympathetic overactivity in the ischemic human heart and suggest new therapeutic strategies to alleviate dysfunctions associated with myocardial ischemia.

Aged↗