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In this paper, we present a new information leakage threat combining intentional electromagnetic interference (IEMI) and observations of EM leakage. In previous studies, the analysis of secret key information in cryptographic modules using fault injection has led to methods whereby faults can be injected via low-voltage IEMI. However, the timing of fault injections cannot be controlled with this approach, and it is difficult to obtain faulty ciphertexts for use in secret key analysis by differential fault analysis (DFA). To overcome this problem, we propose a method for estimating the fault-injection timing by detecting characteristic fluctuations in the EM leakage from the device. As a result, it may be possible to implement a realistic secret information analysis method applicable to a wide range of devices. First, to show the feasibility of the proposed method, we describe an experiment using an on-chip fault-injection circuit that can control the injection timing. Furthermore, we apply a fault analysis method that combines the injection timing estimation method and fault injection by IEMI in a practical experimental environment. We select useful faulty ciphertexts using the proposed method, and then perform secret key analysis by DFA. Experimental results demonstrate that the secret key can be successfully analyzed.

The Coffee Shop called Kopi Tiam in Malaysia is an interesting system of eating house as assembly of hawkers. The independent hawkers with each special meal are assembled by the shop's owner, and the owner provides drink stall and tables for eat. It is similar to Hawker Centre in Singapore or modern food court, but It seems to became a spontaneous system to sustain the quality of foods. The Coffee Shop in Malaysia is analyzed by compared with Hawker Centre in Singapore to clarify the system and know a type of the plan.

Although ferroelectric random access memory (FRAM) has superior electric properties, its downside is that it has a relatively larger cell area in comparison other non-volatile memories. We tried to apply TiOx, and AlOx to an underlying layer (TiOx-UL, AlOx-UL) instead of our previously used Ti underlying layer (Ti-UL) for the La-doped lead zirconate titanate (PLZT) capacitor to obtain a high polarization value aiming to a lowering cell area. The failed bit ratio of the FRAM with TiOx-UL was found to be higher than that with AlOx-UL even though polarization values of the PLZT capacitor with both underlying layers are almost the same and much higher than that with Ti-UL. It is strongly suggested that the imprint induced in PLZT by charged defect is a main cause of bit failure by fail-bit analysis. X-ray diffraction and atomic force microscopy observations shows that charged defect density in PLZT over TiOx-UL is possibly higher than that in PLZT over AlOx-UL due to surface roughness of underlying layers.

Ferroelectric random access memory (FRAM) has been commercialized for about 20 years and its reliability has been well proven all over the world. In the recent Internet of Things (IoT) era, it also plays important roles to particularly in edge computing because of its high writing speed, high rewriting endurance, and low writing energy consumption. We review the history of semiconductor memories using ferroelectrics and overview the progresses of the new ferroelectrics and promising ferroelectric applications in the future.

There is an “Illegality” on people's activity like hawkers on street. In that case, the law lose effect and people's unspoken agreement regulate their activity instead of the law. It can be considered coexistence of the spontaneous order as “Local code” and free behavior without restriction from the law. With that background, Hawker's “Illegality” and their behavior In Bangkok's Chinatown were analyzed on following 3 aims.1. To show the effective utilization through a classification of eating activities on the street as an urban public space.2. To consider the “Illegality” for urban design as a new aspect of architectural planning.3. To discover the “Local code” developed from hawker's relations between themselves as a making spontaneous rules with their unspoken agreement.

Creatol (CTL) is a hydroxyl radical adduct of creatinine (Cr). The serum methylguanidine (MG) level and the MG/Cr molar ratio are reported to be biomarkers for oxidative stress. The aim of this study was to examine whether urinary excretion of CTL, another oxidative stress-related marker, is increased in patients with chronic renal failure (CRF). One hundred twenty-four non-dialyzed patients with chronic renal failure (serum Cr level, 1.3-10.0 mg/dL) were recruited from our hospitals. Urine and serum levels of CTL and MG were determined by high-performance liquid chromatography with the use of 9, 10- phenanthrenequinone as a fluorogenic reagent. The CTL/Cr and (CTL+MG)/Cr molar ratios in spot urine samples were also compared with those in 24-h urine samples. The urinary CTL/Cr and (CTL+MG)/Cr molar ratios increased with decreases in Cr clearance in patients with CRF. Correlations between serum and spot urine (CTL+MG)/Cr and between serum and spot urine CTL/Cr were quite similar to those in 24-h urine samples. CTL/Cr and (CTL+MG)/Cr molar ratios in both 24-h urine and spot urine samples appear to be useful indices of the severity of CRF.

The existing intentional electromagnetic interference (IEMI) fault injection method based on continuous sinusoidal wave has a difficulty in injecting faults at a specific operation or time. This means that the obtained faulty outputs do not always satisfy a specific condition (e.g., time or number of error bytes) for performing fault analysis such as differential fault analysis (DFA). This paper presents a method for estimating the timing of fault occurrences caused by the above IEMI-based method, which make it possible to examine if an obtained faulty output is available for fault analysis. The idea of this method is to observe side-channel information such as EM leakage and estimate fault injection time from the detection of a characteristic change in the obtained waveform. To validate this method, we performed an IEMI fault injection experiment on actual cryptographic hardware (a side-channel attack standard evaluation board). From the obtained faulty encryption outputs and waveforms, we confirm that the fault injection time estimated by back-calculation of faulty outputs corresponded to that obtained by waveform analysis. We also demonstrate the validity of several non-invasive observation techniques for obtaining waveforms.

We have developed a ferroelectric RAM (FRAM) with a low operation voltage of 1.2 V and a high switching endurance up to 1017 cycles. Our newly developed tripleprotection structured cell array, has constructed without an additional mask step, effectively protects 0.4-μm2 ferroelectric capacitors from hydrogen and moisture degradation. We have designed our capacitor-over-bit-line (COB) structure to have a small cell size of 0.5 μm2.

We can summarize our results as follows: (1) A pair of fluorescent crosslines were isolated from the Maillard reaction mixture; (2) AGE-proteins contained crossline-like structures, and (3) crossline-like immunoreactivities were accumulated in renal tissues of diabetic rats. From these results we concluded that fluorophores in AGE proteins have crossline-like structures and we had the first indication that XLs could be markers for renal disorders.

1. The aim of the present study was to determine whether the vasorelaxant effect of atrial natriuretic peptide (ANP) is, in part, endothelium dependent in humans. 2. We used veno-occlusive plethysmography to measure forearm blood flow (FBF) during intra-arterial infusions of ANP (4, 8, 16, 32 pmol/min per dL forearm tissue volume) before and after the inhibition of nitric oxide (NO) synthesis by N(G)-monomethyl-L-arginine (L-NMMA; 100 micromol) in seven normal healthy subjects. 3. Atrial natriuretic peptide caused a dose-dependent increase in FBF both before and after L-NMMA and significantly reduced the plasma concentration of angiotensin (Ang) II. Administration of L-NMMA significantly diminished the increase in FBF in response to ANP infusion (P < 0.05). 4. These results suggest that the forearm vasodilative response to ANP is modulated, in part, by an endothelium-derived NO-mediated mechanism associated with a decrease in AngII caused by ANP.

Exercise capacity is often reduced in patients with atrial fibrillation (AF), but very few studies have focused on changes in endothelial function as a potential mechanism for the exercise limitation. The present study used using venous occlusion plethysmography to investigate whether nitric oxide (NO)-mediated vasodilatation is attenuated during exercise in patients with AF by measuring forearm blood flow (FBF) in 10 patients at rest and immediately after 2 levels of rhythmic handgrip exercise, before and after inhibition of NO synthesis with N(G)-monomethyl-L-arginine (L-NMMA, 100 micromol). The measurements were repeated 1 day after restoration of sinus rhythm by cardioversion. FBF responses to graded doses of acetylcholine (ACh) were also observed before and after cardioversion. Heart rate decreased after cardioversion, but blood pressure did not change. FBF at rest was not affected by cardioversion, but at the highest level of exercise it increased from 28.4+/-2.3 ml x min(-1) x dl(-1) before to 39.4+/-3.2 ml x min(-1) x dl(-1) after cardioversion (p

Recent studies have demonstrated that proinflammatory cytokines induce large amounts of nitric oxide (NO) and that the amount increases in patients with congestive heart failure (CHF). There are, however, few reports regarding the relationships between NO production, cytokines and the severity of heart failure, so the plasma concentrations of nitrite and nitrate (NOx), tumor necrosis factor-α (TNF-α) and brain natriuretic peptide (BNP) were measured in 43 patients with CHF caused by dilated cardiomyopathy and 26 age- and sex-matched normal control subjects. Forearm blood flow (FBF) was measured using plethysmography during infusions of acetylcholine and nitroglycerin and after the administration of the NO synthesis inhibitor L-NMMA (NG-monomethyl-L-arginine). Plasma concentrations of both NOx and TNF-α were significantly higher in the patient group than in the control group (p

We have developed ferroelectric capacitor fabrication technique and a new sensing amplifier circuit to realize low-voltage and high-density FRAM. Improvement of IrO, top electrode near the ferroelectric interface successively lowers operation voltage. And our developed “Dual Reference Sensing Amplifier” enables to commercialize highly-reliable FRAM with memory density of 4Mb or larger.

Crossline is one of the structurally defined adducts of advanced glycation endproducts (AGEs) which has both a crosslink and fluorescence similar to AGE-protein in vivo. Crossline was measured in serum and erythrocyte membrane proteins (EMP) from 52 type 2 diabetic patients using a specific enzyme-linked immunosorbent assay system. Serum and EMP crossline levels in the diabetic patients were significantly higher than those in normal control. The patients with advanced diabetic nephropathy (serum creatinine levels of more than 1.2 mg/dl) had markedly elevated serum crossline levels compared to those with moderate diabetic nephropathy (clinical proteinuria) (180. 7+/-51.7 vs. 71.8+/-18.4 pmol/ml; P0.01). On the other hand, there were no significant differences in EMP crossline levels between the two. EMP crossline levels in the patients with moderate diabetic nephropathy (8.8+/-2.9 pmol/mg protein) and those with advanced diabetic nephropathy (9.7+/-3.0 pmol/mg protein) were significantly higher than those without clinical proteinuria (6.4+/-1.9 pmol/mg protein; P0.01). The present study demonstrated that EMP crossline levels were associated with the presence of nephropathy in patients with type 2 diabetes mellitus. Serum crossline levels were significantly influenced by remaining renal function. The measurement of crossline from a blood sample could provide us with important information for the study of clinical evaluation and pathogenesis of diabetic complications.

Objectives. We sought to assess the clinical significance of peak negative myocardial velocity gradient (MVG) in early diastole as a noninvasive indicator of left ventricular (LV) diastolic function. Background. Peak systolic MVG has been shown useful for the quantitative assessment of regional wall motion abnormalities, but limited data exist regarding the diastolic MVG as an indicator of LV diastolic function. Methods. Peak negative MVG was obtained from M-mode tissue Doppler imaging (TDI) in 43 subjects with or without impairment of systolic and diastolic performance: 12 normal subjects, 12 patients with hypertensive heart disease (HHD) with normal systolic performance and 19 patients with dilated cardiomyopathy (DCM), and was compared with standard Doppler transmitral flow velocity indices. In a subgroup of 30 patients, effects of preload increase on these indices were assessed by performing passive leg lifting. In an additional 11 patients with congestive heart failure at the initial examination, the measurements were repeated after 26 ± 16 days of volume-reducing therapy. Results. Peak negative MVG was significantly depressed both in HHD (−3.9 ± 1.3/s, p Conclusions. Peak negative MVG derived from TDI may be a noninvasive indicator of LV diastolic function that is less affected by preload alterations than the transmitral flow velocity indices, and thereby could be used for the follow-up of patients with nonischemic LV dysfunction presenting congestive heart failure.

It is still unclear whether echocardiography with an automated boundary detection technique (ABD) can accurately determine the left ventricular (LV) volume and function particularly in the presence of LV wall asynergy. We intended to re-evaluate the reliability and application of the ABD, which was based on the acoustic quantification technique (Sonos 2500, Hewlett Packard) for the LV volume measurement in patients without or with LV wall asynergy. A total of 80 patients (mean age 56 years) who underwent left ventriculography (LVG) were divided into two groups. The group A consisted of 29 patients with normal LV wall motion and the group B consisted of 51 patients with generalized or regional LV wall motion abnormality. In group A patients, the LV end-diastolic volume (LVEDV) was 96 ± 25 ml by ABD and 112 ± 33 ml by LVG and those of LV end-systolic volume (LVESV) were 44 ± 14 ml by ABD and 48 ± 17 ml by LVG, thus resulting in the underestimation of LV volume by 12% in average. Under these conditions, the LV ejection fraction (LVEF) by ABD, 54 ± 8%, correlated well with that by LVG, 58 ± 7%. Although underestimation of LV volume by 17% in average also occurred in groups B (N.S.), LVEF was found to correlate well with that by LVG; 27 ± 8% vs 30 ± 11% (r=0.87, SEE=3.1%) for 21 patients with the generalized LV asynergy; 39 ± 10% vs 39 ± 12% (r=0.86. SEE=3.3%) for 30 patients with the regional LV asynergy. These results demonstrate the feasibility of the ABD in determining the LVEF, although underestimation can occur in measuring the absolute LV volume in patients with or without LV asynergy.

Recent studies have suggested that advanced glycation end products (AGEs) are involved in the development of diabetic complications. To assess the pathogenic role of AGEs and vascular endothelial growth factor (VEGF) in the development of retinal neovascularization in diabetic retinopathy, we investigated the effect of AGEs on induction of VEGF by retinal Muller cells and measured AGE and VEGF concentrations in the vitreous of patients with proliferative diabetic retinopathy (PDR) and nondiabetic patients. The expression of VEGF mRNA and the production of VEGF protein by cultured Muller cells were enhanced by the presence of AGEs. The vitreous concentrations of AGEs and VEGF were both elevated in patients with PDR compared with patients without diabetes (P < 0.01). There was a moderate positive correlation between the levels of crossline and VEGF (r=0.698, P < 0.01). Elevation of AGEs in the vitreous may promote intraocular neovascularization in diabetic retinopathy through production of VEGF from Muller cells.

A novel creatinine metabolite, creatol (5-hydroxycreatinine), is a key precursor in the synthesis of the uremic toxin methylguanidine (MG). Creatinine is converted to creatol within the mammalian body and this conversion is mediated specifically by hydroxyl radicals. We investigated the production of creatol and MG from creatinine in rats with renal failure induced by the lipid peroxide produced as a consequence of vitamin E deficiency and depletion of the reduced form of glutathione (GSH). In addition, we examined serum levels of other guanidino compounds, namely guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA). The injury to kidneys induced by the depletion of GSH in combination with vitamin E deficiency caused markedly elevated serum levels of creatol, MG and GSA and decreased serum GAA. The molar ratio of creatol to creatinine in the serum, which should be an index of the oxygen stress mediated by hydroxyl radicals, increased with time. Therefore, the enhanced production of creatol in vitamin-E-deficient rats that have been depleted of GSH might be due to the enhanced production of oxygen radicals in this system.

A methylguanidine-synthesizing enzyme localized in rat liver microsomes produces methylguanidine via the intermediates creatone A and creatone B from the substrate, creatol, a substance produced from

Methylguanidine (MG)-synthesizing enzyme was purified from rat kidney lysosomes and peroxisomes. The enzyme was a flavoprotein with a molecular weight of about 37,000 and oxidized creatol to produce MG. The present results suggest that the reaction mechanism of this enzyme is different from that of L-gulono-gamma-lactone oxidase (EC 1.1.3.8) isolated from rat liver microsomes.

Creatinine (Cr), creatol and methylguanidine (MG), which accumulate in the body with the progress of renal failure after adenine administration, were given separately to rats in order to compare their toxicities. Food containing adenine was given to rats for 20 days to induce renal failure. Then each of the test substances was administered intraperitoneally, and renal function of the rats was determined. The changes in glomerular filtration rate, renal plasma flow and renal blood flow after administration of Cr were only slight in comparison with those of the control group. Creatol or MG administration induced a significant decrease in renal function. In addition, the level of MG in serum, liver and kidney was extraordinarily high in rats given creatol or MG. The toxic effects are discussed on the basis of these results.

SUMMARY 1. Serum hepatocyte growth factor (HGF) is considered to be a potent marker of vascular endothelial injury. The present study was designed to examine serum HGF levels in atrial fibrillation and after successful direct current (DC) cardioversion. 2. We measured serum HGF levels before and 7 days and 1 month after DC cardioversion in 39 patients with atrial fibrillation in whom sinus rhythm was maintained for at least 7 days after DC cardioversion and in 30 age- and sex-matched normal control subjects with sinus rhythm. We also measured acetylcholine-induced changes in forearm blood flow (FBF) using venous occlusive plethysmography in 10 patients. 3. Serum HGF levels were significantly higher in the atrial fibrillation patients (both lone atrial fibrillation and with underlying heart disease) than in the controls (0.16 ± 0.07 vs 0.10 ± 0.04 ng/mL; P

0.5 /spl mu/m design rule embedded 64 kbit SBT (SrBi/sub 2/(Ta,Nb)/sub 2/O/sub 9/) FeRAMs (ferroelectric RAM) are fabricated using a new low temperature SBT deposition technique. The developed deposition technique has successfully lowered SBT crystallization temperature from 800/spl deg/C to 700/spl deg/C, resulting in co-fabrication of FeRAM and fine CMOS logic devices with W plugs. The fabricated devices are proven to be fully functional.

An all-around in situ monitor for CMP was developed. It can detect the even surface during planarization, polishing pad wear, lack of uniformity on the surface of a wafer, and the interface of different materials. In this method, small vibrations of the polishing head were detected by using an accelerometer, and signal processing techniques were used to determine polishing events.

The origin of the pulmonary venous (PV) systolic flow wave is still unclear and could be the atrial relaxation and systolic descent of the atrioventricular plane, which decrease atrial pressure (suction) or raised PV pressure. In atrial fibrillation (AF), loss of atrial contraction and relaxation significantly modifies the systolic PV flow wave. The effect of recumbent positional changes on PV, however, has not yet been characterized in AF. The purpose of this study was to evaluate the effect of positional changes on systolic PV flow in patients with AF studied by transesophageal echocardiography. The study group consisted of 45 patients with AF (34 patients with AF, alone, and 11 patients with mitral stenosis [MS]). To assess the influence of left atrial pressure, we included patients with MS and AF. Pulsed wave Doppler transesophageal echocardiography of the left and right upper PV were performed in the left lateral recumbent position in all patients and repeated records were obtained with the subject in the supine position in 25 (AF alone: n = 20, MS: n = 5) of 45 patients. In the left lateral recumbent position, the systolic PV flow velocity and systolic fraction of the left PV, which were recorded on the recumbent subject's lower side, were significantly increased compared with those of the right PV in both AF alone and MS with AF (33.9 +/- 10.8 vs 13.8 +/- 6.4 cm/s, 0.45 +/- 0.09 vs 0.20 +/- 0.10 in AF alone; 30.2 +/- 11.7 vs 14.6 +/- 6.0 cm/s, 0.43 +/- 0.12 vs 0.20 +/- 0.07 in MS, respectively, P.01). By changing the position from the left lateral to the supine position, systolic PV flow velocity and systolic fraction of the left and right PV became the same (29.3 +/- 8.4 vs 27.9 +/- 8.4 cm/s, 0.39 +/- 0.09 vs 0.36 +/- 0.06 in AF alone, 23.5 +/- 8.8 vs 27.5 +/- 5.0 cm/s, 0.35 +/- 0.08 vs 0.35 +/- 0.09 in MS, respectively). These findings show that the PV volume (hydrostatic pressure) significantly modifies systolic PV flow wave in patients without atrial contraction and relaxation. We should take into consideration the body position on which PV flow is studied.

Background and Purpose — Assessment of left atrial appendage (LAA) function with transesophageal echocardiography is useful for detecting patients at high risk for thromboembolism as a result of atrial fibrillation (AF). A recent study reported that the atrium is the main source of brain natriuretic polypeptide (BNP) in AF patients without overt heart failure. The purpose of this study was to assess a possible relationship between LAA function and plasma BNP levels in nonvalvular AF. Methods — Thirty-four consecutive patients with chronic nonvalvular AF (age, 69±9 years) underwent transesophageal echocardiography and plasma BNP measurement. Thirteen patients with a history of thromboembolism or echocardiographic evidence of thrombus (E + group) were compared with 21 AF patients without complications (E− group). Results — The E+ group patients demonstrated greater impairment of LAA velocity and higher plasma BNP levels than the E− group patients (LAA velocity: 12±6 versus 31±17 cm/s, P P r =0.38, P Conclusions — The present data suggest the usefulness of measuring plasma BNP levels, which may reflect augmented atrial secretion of BNP from the impaired atrial myocardium, in detecting patients at high risk for thromboembolic complications in nonvalvular AF.

Background: Although there have been many studies on the effects of atrial fibrillation (AF) on cardiac function, few studies have been done on its effects on endothelial function. The present study was designed to examine the effects of AF on endothelial function in human subjects. Methods and Results: Changes in forearm blood flow (FBF) induced by acetylcholine and nitroglycerin were measured by using plethysmography in 14 patients with lone AF, 13 patients with AF and underlying heart disease, and 12 normal control subjects. In the patients, these measurements were repeated after cardioversion. Although baseline FBF was the same in the 3 groups, acetylcholine-induced increases in FBF were significantly smaller in both patient groups than in the control group, and FBF increases were particularly depressed in AF patients with underlying heart disease. After restoration of sinus rhythm by cardioversion, FBF response to the highest dose of acetylcholine increased by 46% in patients with lone AF (n = 10) and by 90% in AF patients with underlying heart disease (n = 11). Nitroglycerin-induced vasodilatation was the same in all 3 groups and was not affected by cardioversion. Conclusions: These findings suggest that endothelium-dependent vasodilatation is impaired by AF and improves after sinus rhythm is restored.

Recent in vitro experiments have shown that amrinone enhances the release of nitric oxide (NO) from the endothelium and induces NO mediated vasodilatation. This in vivo study examined whether amrinone causes vasodilatation mediated by endothelium-derived NO, and whether this effect is attenuated in patients with endothelial dysfunction. Eight patients with congestive heart failure and 10 age- and sex-matched healthy volunteers were studied. Forearm blood flow (FBF) was measured before and during infusion of drugs of acetylcholine, amrinone, and nitroglycerin in incremental doses. After the completion of these measurements, 100 micromol of N(G)-monomethyl-L-arginine (L-NMMA) was infused intraarterially. Thereafter, FBF measurement in response to incremental doses of amrinone was repeated. Infusion of incremental doses of amrinone caused a comparable increase in amrinone plasma concentration in both groups. Baseline FBF was 3.2+/-0.79 ml/min/100 ml in controls vs. 2.91+/-0.79 ml/min/100 ml in patients (p = 0.43). In both groups, FBF increased in response to acetylcholine, amrinone, and nitroglycerin. During infusion of the highest dose of nitroglycerin, FBF was not different between the two groups (p = 0.51); however, FBF during infusion of the highest doses of acetylcholine and amrinone was significantly less in patients than in controls: 9.75+/-2.69 vs. 24.87+/-8.65 ml/min/100 ml (p < 0.001) and 3.79+/-1.21 vs. 7.15+/-2.06 ml/min/100 ml (p < 0.001), respectively. L-NMMA significantly depressed the increase in FBF in response to amrinone in controls, but not in patients. In conclusion, the selective PDE III inhibitor, amrinone, has endothelium-derived NO-mediated vasodilating effects in addition to direct effects. This property may be impaired in patients with endothelial dysfunction.

Background Recent studies indicated that ischemic microvascular damage may be reversible or progressive after coronary reflow. Intramyocardial hemorrhage is a phenomenon that reflects severe microvascular injury. We examined the relationship between temporal changes in microvascular perfusion patterns detected by myocardial contrast echocardiography (MCE) and intramyocardial hemorrhage detected by magnetic resonance imaging (MRI) in patients with acute myocardial infarction (AMI). Methods and Results The study population consisted of 24 patients with anterior AMI. All patients underwent MCE shortly after reflow and in the chronic stage (a mean of 31 days after reflow). Wall motion score (WMS) was determined as the sum of 16 segmental scores (dyskinetic/akinetic=3 to normal=0) at days 1 and 31. Gradient-echo acquisition and gadolinium-DTPA–enhanced spin-echo MRI were performed within 10 days after reflow. In MCE shortly after reflow, 16 patients (67%) showed contrast enhancement and the other 8 patients (33%) showed a sizable contrast defect. In the chronic stage, a persistent contrast defect was observed in 7 of 8 patients with a contrast defect shortly after reflow. Consistent contrast enhancement was observed in 12 of 16 patients (75%) with contrast enhancement shortly after reflow, indicating that a contrast defect newly appeared in 4 patients (25%). Intramyocardial hemorrhage was detected in 9 patients (38%): 5 of 7 patients with a persistent contrast defect and in all 4 patients with a new appearance of a contrast defect during the chronic stage. The patients without hemorrhage showed a significant improvement in WMS compared with patients with hemorrhage at day 31 (5±5 versus 19±6, P Conclusions These results suggest that irreversible microvascular damage to the ischemic myocardium may cause intramyocardial hemorrhage after reflow, associated with impaired recovery of left ventricular function. Contrast enhancement within the risk area shortly after reflow does not necessarily indicate long-term microvascular salvage.

Diabetic patients (n = 23) with chronic renal failure (CRF) accumulate the creatinine (Cr) oxidative metabolites creatol (CTL) and methylguanidine (MG; a uremic toxin) in their sera. Analysis of serum CTL, a key intermediate in mammalian Cr catabolism into MG, is shown to offer some useful diagnostic information on CRF, especially in the determination of an initial stage of pathological renal failure. The sera of all diabetic (n = 23) and nondiabetic (n = 20) patients with CRF (s-Cr1.25 mg/dl) contained s-CTL (2 micrograms/dl), whereas those from normal subjects (n = 18) and diabetic patients (n = 18) without CRF contained no detectable s-CTL. A similar accumulation of s-MG was observed, but only when s-Cr was higher than 2.0 mg/dl. Although each s-CTL (Y: microgram/dl, Y': mol/l) and s-MG level (Z: microgram/dl, Z': mol/l) is highly correlated with s-Cr (X: mg/dl, X': mol/l) in a normal equation, Y or Z = AX + B, an alternative correlation in a second-order equation, Y or Z = alpha X2 + beta X, could also fit well. Since the quadratic equation can be convertible to Y/X or Z/X = alpha X + beta [Y'/X' or Z'/X' = alpha' X+ beta'] and active oxygen species, especially hydroxyl radicals, convert Cr into CTL, Y/X, Y'/X', Z/X and Z'/X' values which might be a kind of indices for oxygen stress (oxidative stress) increased in proportion to the increased severity of CRF in such patients. Although its meaning and interpretation are still debatable, diabetic CRF patients had a significantly higher alpha' value (2.2) than that (0.89) of nondiabetic CRF patients. All serum values for Cr, CTL and MG were measured with HPLC.

Analysis of creatol (CTL, 5-hydroxycreatinine), an oxidative creatinine (Cr) metabolite, in serum and urine of human subjects has indicated that CTL is a useful determinant of renal function. The existence itself of serum CTL (s-CTL) could be a diagnostic sign for chronic renal failure (CRF): in all normal subjects, s-CTL was undetectable, but s-CTL was detectable in sera of all patients with CRF (s-Cr: > 2.0 mg/dl). And the s-CTL values increased in proportion to the severity of CRF in such patients. Furthermore, the molar ratio (CTL/Cr) in both urine and serum increased significantly in proportion to the severity of CRF. Our results indicated not only hyperproduction of CTL but also higher oxygen stress in patients according to the progression of CRF. The diagnostic importance of the CTL value and the CTL/Cr ratio are discussed.

A rare case of eosinophilic granuloma of the orbit in a 3-year-old boy presented as right upper eyelid swelling and proptosis. Computed tomographic scanning revealed a soft-tissue dense mass in the lateral wall of the right orbit. Magnetic resonance (MR) imaging demonstrated tumor extension into the orbit, anterior and middle cranial fossae, and extracranial region. The tumor was completely removed. Histological diagnosis was eosinophilic granuloma. No evidence of recurrence was found 14 months later. MR imaging is useful for diagnosis of the lesion, and particularly for surgical management.

The chemical oxidative conversion of creatinine (Cr) into methylguanidine (MG) has been followed by 1H-NMR and HPLC. By using active oxygen species generated by Fenton's reagent (Fe2+ and H2O2) or the similar reagent (Fe3+ and H2O2), creatol (CTL), a metabolite newly isolated from the urine of uremic patients, and creatones A and B were experimentally detected in the reaction mixture and implicated as successive intermediates in the pathway from CR to MG. An alternative oxidation of Cr to demethylcreatinine (glycocyamidine) was also observed. The importance of CTL in this in vitro oxidation mechanism is discussed.

OBJECTIVESThe functional activation of inducible nitric oxide synthase (iNOS) was evaluated as a source of nitric oxide (NO) in the forearm of patients with heart failure.BACKGROUNDAlthough endogenous NO is normally produced by constitutive NO synthase (cNOS) in patients with congestive heart failure (CHF), expression of iNOS provides an additional source of NO. However, there are no in vivo studies showing functional activation of iNOS in humans.METHODSA nonselective NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA), and a selective inhibitor of iNOS, aminoguanidine, were administered intra-arterially in graded doses into the brachial arteries of 13 patients with CHF and 10 normal control subjects. Forearm blood flow (FBF) was measured simultaneously in the infused and noninfused arms by plethysmography. Arterial and venous plasma concentrations of nitrite/nitrate (NOx) were measured at baseline and at the highest dose of each drug.RESULTSL-NMMA significantly reduced the FBF ratio between the infused and noninfused arms in both the control and patient groups (35 ± 12% and 34 ± 10%, respectively; both p < 0.001). Aminoguanidine at the same concentration significantly reduced the ratio in the patient group (15 ± 9%, p < 0.01), with no change in the control group. The arterial NOx concentration was not affected by either drug; however, venous NOx concentrations were significantly decreased in both the control and patient groups by L-NMMA (18 ± 5% and 18 ± 17%, respectively; both p < 0.05) and in the patient group only by aminoguanidine (7 ± 6%, p < 0.05).CONCLUSIONSThese findings suggest that NO production in the forearms of patients with CHF is induced partly by iNOS activation, whereas in normal subjects, it can be ascribed to cNOS activation.