Designer germanium quantum dot phototransistor for near infrared optical detection and amplification.

We demonstrated a unique CMOS approach for the production of a high-performance germanium (Ge) quantum dot (QD) metal-oxide-semiconductor phototransistor. In the darkness, low off-state leakage (Ioff ∼ 0.27 pA µm(-2)), a high on-off current ratio (Ion/Ioff ∼ 10(6)), and good switching behaviors (subthreshold swing of 175 mV/dec) were measured on our Ge-QD phototransistor at 300 K, indicating good hetero-interfacial quality of the Ge-on-Si. Illumination makes a significant enhancement in the drain current of Ge QD phototransistors when biased at both the on- and off-states, which is a great benefit from Ge QD-mediated photoconductive and photovoltaic effects. The measured photocurrent-to-dark-current ratio (Iphoto/Idark) and the photoresponsivities from the Ge QD phototransistor are as high as 4.1 × 10(6) and 1.7 A W(-1), respectively, under an incident power of 0.9 mW at 850 nm illumination. A superior external quantum efficiency of 240% and a very fast temporal response time of 1.4 ns suggest that our Ge QD MOS phototransistor offers great promise as optical switches and transducers for Si-based optical interconnects.

Purulent pericarditis, multi-site abscesses and ketoacidosis in a patient with newly diagnosed diabetes: a rare case report.

BACKGROUND: Purulent pericarditis is an acute and fulminant disease characterized by pus accumulation in the pericardial space. Its incidence has declined substantially and the common pathogen has changed since the beginning of the antibiotic era; however, it is still found in some patients with immunocompromised conditions. CASE REPORT: We report a rare case in which the onset of diabetes mellitus presented as extremely high HbA1c concentration, ketoacidosis, multi-site abscesses and purulent pericarditis. After antibiotic therapy and pericardiocentesis, the purulent pericarditis still did not resolve and further intrapericardial thrombolytic therapy also failed. Finally, this patient was treated successfully by surgical debridement and pericardiectomy. CONCLUSION: In the immunocompromised state of severe hyperglycaemia, purulent pericarditis is a possible complication of uncontrolled infection. If purulent pericarditis cannot be cured using non-surgical treatments, such as antibiotic therapy, pericardiocentesis and intrapericardial thrombolytic therapy, a surgical pericardiectomy should be considered to avoid morbidity and mortality.

The A1166C polymorphism of angiotensin II Type 1 receptor as a predictor of renal function decline over 4 years follow-up in an apparently healthy Chinese population.

AIM: The angiotensin II Type 1 receptor (AT1R) A1166C (rs5186) genez polymorphism is equivocally associated with the patients' susceptibility to chronic kidney disease or end-stage renal disease. We conducted a prospective study to investigate the influence of AT1R A1166C gene polymorphism on the quantitative changes of renal function. METHOD: Of 1500 people screened, 112 non-diabetic normotensive elderly Chinese were recruited and received biochemistry examination at the baseline, at the second and fourth year follow-up. Serum creatinine and calculated renal parameters, using Cockroft-Gault (CG) formula, Modification of Diet in Renal Disease (MDRD) Study and abbreviated MDRD (abMDRD) equation, were used to evaluate renal function and their progression. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. RESULT: Age was 71.9 +/- 3.7 years (range 60 - 81). Serum creatinine, CG creatinine clearance (CrCl), MDRD and abMDRD glomerular filtration rate (GFR) were significantly decreased at the 2 and 4-year follow-up (all p < 0.001). The magnitude of 4-year decline of above four renal parameters was significantly higher in subjects carrying the AT1R AA genotype than C-allele carriers (p = 0.014, 0.033, 0.008 and 0.014 for creatinine, CG CrCl, MDRD and abMDRD GFR, respectively). This association was still significant in multivariate analyses (p = 0.019, 0.045, 0.035 and 0.018, respectively). CONCLUSION: This longitudinal study showed that the aging process was associated with decline of renal function in the healthy elderly. The AT1R A1166C gene polymorphism might modulate these changes in the Chinese. This provides further knowledge essential in the assessment of renal disease and determination of renal function in the older subjects.

Probiotics exert reciprocal effects on autophagy and interleukin-1ß expression in Salmonella-infected intestinal epithelial cells via autophagy-related 16L1 protein.

This study aimed to examine how probiotics affect autophagy and interleukin-1ß (IL-1ß) expression in Salmonella-infected intestinal epithelial cells (IECs). The original Caco-2 cells and ATG16L1 siRNA-transfected Caco-2 cells were pretreated or left untreated with probiotics, including Lactobacillus rhamnosus GG (LGG; ATCC 53103) and Bifidobacterium longum (BL; ATCC15697), and these cells were infected with wild-type Salmonella enterica serovar Typhimurium (S. Typhimurium strain, SL1344). Western blot analysis was used to detect the conversion of microtubule-associated proteins 1A/1B light chain 3B (LC3)-I to LC3-II. Immunofluorescence was used to analyse LC3+ autophagosomes. Membrane proteins were analysed by western blot for protein (ATG16L1, NOD2), and total RNA by RT-PCR for mRNA expression [ATG16L1, vitamin D receptor (VDR)]. We demonstrated that probiotics enhanced both VDR mRNA, and nucleotide-binding oligomerisation domain-containing protein 2 (NOD2) and autophagy-related protein 16-like 1 (ATG16L1) protein expression. The enhanced expression resulted in autophagic LC3-II protein expression and formation of LC3 punctae in Salmonella-infected Caco-2 cells. It was observed that ATG16L1 siRNA could attenuate this mechanism, and ATG16L1-mediated IL-1ß expression was suppressed by probiotics. These results suggest that probiotics enhance autophagy and also suppress inflammatory IL-1ß expression in Salmonella-infected IECs via membrane ATG16L1 protein expression. Probiotics may enhance autophagic clearance of Salmonella infection and modulate inflammatory responses to protect the hosts. Hence, we can assume that probiotics could treat infectious and autoimmune diseases through mechanisms involving ATG16L1.

Adipocytokines and proinflammatory mediators from abdominal and epicardial adipose tissue in patients with coronary artery disease.

OBJECTIVE: Epicardial and abdominal adipose tissues have recently been demonstrated to play inflammatory roles in coronary atherosclerosis. We sought to compare tissue adipocytokine levels of these two anatomically distinct adipose stores in patients with and without coronary artery diseases (CAD). DESIGN: Samples of abdominal and epicardial fat tissues were harvested to detect the levels of adipocytokines and proinflammatory mediators. SUBJECTS: Forty-six patients with CAD who underwent coronary artery bypass surgery and 12 non-CAD control subjects who underwent other types of open-heart surgery. MEASUREMENTS: Tissue levels of adipocytokines (adiponectin, leptin and visfatin) and proinflammatory mediators (tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)) were determined by enzyme-linked immunosorbent assay. RESULTS: Tissue levels of TNF-alpha, IL-6, leptin and visfatin were significantly higher in CAD patients relative to control subjects. In addition, significantly higher tissue levels of these four cytokines from abdominal fat depots were found compared to those from epicardial fat in CAD patients. Conversely, in comparison with control subjects, tissue levels of adiponectin were significantly reduced in CAD patients with a significantly lower tissue levels of abdominal than epicardial fat depots demonstrated. CONCLUSION: Abdominal adiposity may play more significant role than epicardial fat in the pathogenesis of coronary atherosclerosis.

B-cell lymphoma/leukemia 10 promotes oral cancer progression through STAT1/ATF4/S100P signaling pathway.

This corrects the article DOI: 10.1038/onc.2014.43.

Acute effect of ionic high osmolar contrast medium on renal antioxidant enzyme activity in streptozotocin-induced diabetic rats.

Acute contrast medium-induced nephrotoxicity was estimated in 3%-12% of patients receiving cardiac angiography, especially in advanced age, renal insufficiency and diabetic patients. As intrinsic renal antioxidant enzyme activities may play a crucial role in defence against renal oxidant injury, this study was designed to investigate the acute effect of ionic high osmolar diatrizoate meglumine/diatrizoate sodium on renal antioxidant activities in normal or streptozotocin (STZ)-induced diabetic rats at two time points (1 h and 24 h). A total of 40 Wistar rats were separated to normal and STZ-induced diabetic groups. Ten of each group were injected with diatrizoate (10 ml/kg) via tail vein and 10 with 10 ml/kg of 0.9% NaCl as control. This study shows that diabetic rats had higher renal glutathione peroxidase (GPx) activities than those of normal rats. GPx activities decreased significantly after diatrizoate injection at the first hour (717.4+/-104.0 to 578.6+/-92.1 mU/mg in the diabetic group, 466.4+/-30.6 to 371.4+/-75.5 mU/mg in the normal group, all P=0.032) but the difference faded 24 h later. The increase of superoxide dismutase (SOD) activities was enhanced (673.5+/-100.2 to 750.4+/-129.8 U/mg, P=0.04) in the normal group, but not in the diabetic group (624.1+/-156.6 to 671.1+/-136.7 U/mg, P=0.15) after diatrizoate injection at the first hour. At 24 h, renal SOD activities were still significantly higher in the diatrizoate injection group. In summary, intrinsic renal antioxidant activities are adapted in STZ-induced diabetes and ionic high osmolar diatrizoate could modify their activities. Furthermore, diabetics have abnormal response of renal antioxidant activities by contrast media and are at risk for contrast-mediated nephrotoxicity.

B-cell lymphoma/leukemia 10 promotes oral cancer progression through STAT1/ATF4/S100P signaling pathway.

B-cell lymphoma/leukemia 10 (BCL10) is an apoptotic regulatory protein related to advanced TNM stage and disease recurrence in oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of BCL10 in OSCC progression is still unknown. Here, we showed that knockdown of endogenous BCL10 could significantly reduce cell migration and invasion abilities, retard cell proliferation by G0/G1 phase accumulation and inhibit tumorigenicity in vivo. In molecular level, we identified S100P as a crucial downstream effector of BCL10-inhibited OSCC progression by high-throughput microarray analysis. S100P messenger RNA and protein expression levels were significantly diminished in silenced-BCL10 clones, and transfected S100P expression plasmids restored migration, invasion, proliferation abilities and tumorigenicity in shBCL10 transfectants. Furthermore, we provided evidence that BCL10 regulated S100P expression through signal transducers and activators of transcription 1 (STAT1) and activating transcription factor 4 (ATF4). Knockdown of BCL10 decreased S100P promoter activity, but showed no effect in truncated STAT1/ATF4 S100P promoter.  In addition, we also found that the P50/P65 signaling pathway was involved in BCL10-enhanced OSCC progression. Restored S100P in silenced-BCL10 clones could markedly reverse P65 activation via outside-in signaling. Taken together, we discovered a novel axis of BCL10-regulated OSCC progression via STAT1/ATF4/S100P/P65 signaling, which could predict the prognosis of OSCC and will be beneficial for developing therapeutic strategy against advanced OSCC.

Role of left ventricular activation sequence in the genesis of isovolumic relaxation flow in the Wolff-Parkinson-White syndrome.

In patients with left Kent bundle, the initial phase of isovolumic relaxation flow was directed basally at pre-excited beats, but apically at nonpreexcited beats or after successful ablation of the Kent bundle. This suggests an important role of the left ventricular activation sequence in the direction of isovolumic relaxation flow.

Negative dromotropism of adenosine under beta-adrenergic stimulation with isoproterenol.

Adenosine depresses atrioventricular (AV) nodal function by binding to specific A1 receptors which activate the acetylcholine, adenosine-regulated potassium current. In addition, adenosine can act to antagonize the effects of beta-adrenergic stimulation on AV nodal function. To assess the negative dromotropic effects of adenosine under beta-adrenergic stimulation, 15 patients were studied during clinical electrophysiologic study. During high right atrial pacing at a cycle length of 400 to 600 ms, adenosine was injected intravenously at an initial dose of 0.5 mg followed by a stepwise increment of 0.5 or 1.0 mg given at 5-minute intervals until a maximal dose of 12 mg was achieved or AV block developed. Intravenous isoproterenol (1 to 3 micrograms/min) was then infused to accelerate sinus rate by 20 to 30% during which intravenous injection of incremental doses of adenosine as described was repeated. The AV nodal conduction time (AH interval) was measured at each dose of adenosine. Dose-response curves of AV nodal conduction time (expressed as percent increase in AH interval) were studied during the control state and during isoproterenol infusion. The dose of adenosine required to produce AV nodal Wenckebach block, the increase in the AH interval by 50% (ED50) and the maximal response (Emax) were 3.4 +/- 0.9 mg, 1.8 +/- 0.9 mg and 60 +/- 4%, respectively, in the control state, and 3.7 +/- 0.8 mg, 2.0 +/- 0.7 mg and 56 +/- 4%, respectively, during isoproterenol infusion. No significant changes in ED50, Emax and the dose of adenosine yielding AV nodal Wenckebach block could be demonstrated between the control state and during isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of intravenous isoproterenol in the electrophysiologic induction of atrioventricular node reentrant tachycardia in patients with dual atrioventricular node pathways.

To assess the role of intravenous isoproterenol for the facilitation of electrophysiologic induction of atrioventricular (AV) node reentrant tachycardia, 20 patients with dual AV node pathways who lacked inducible AV node reentrant tachycardia at control study had a constant isoproterenol infusion administered and underwent repeat study. Six (30%) of 20 patients (group I) had inducible AV node reentrant tachycardia during isoproterenol infusion whereas the other 14 (70%) patients (group II) did not. Paroxysmal supraventricular tachycardia was clinically documented in all 6 group I patients compared to 3 (21%) of 14 group II patients (p = 0.002). The sensitivity and specificity of isoproterenol-facilitated induction of AV node reentrant tachycardia were 67 and 100%, respectively. The isoproterenol-facilitated induction of sustained AV node reentry was mediated by resolution of the weak link in anterograde slow pathway in 2 (33%) patients, in retrograde fast pathway in 3 (50%) and in both anterograde slow and retrograde fast pathways in 1 (17%) patient. Four group I patients were given intravenous propranolol, 0.2 mg/kg body weight, and had complete suppression of isoproterenol-facilitated induction of AV node reentry. Thus, intravenous isoproterenol is a rather sensitive and highly specific adjunct to electrophysiologic induction of AV node reentrant tachycardia in patients with dual AV node pathways but without inducible sustained AV node reentry.

Electrophysiologic manifestations of the excitable gap of orthodromic atrioventricular reciprocating tachycardia demonstrated by single extrastimulation.

To assess the electrophysiologic characteristics of the excitable gap, 12 patients with orthodromic atrioventricular (AV) reciprocating tachycardia were studied. During tachycardia, 8 patients used a left-sided and 4 patients a right-sided anomalous bypass tract for retrograde conduction. QRS complex-synchronized single extrastimuli were delivered from high right atrium, right ventricular apex and coronary sinus, respectively, scanning the whole cycle length of tachycardia. An excitable gap was determined to be present if tachycardia resetting or tachycardia termination occurred. The duration of the excitable gap varied among different pacing sites and occupied 0 to 48% (mean 17 +/- 16) of basic tachycardia cycle length (240 to 480 ms, mean 327 +/- 70). Three patterns of tachycardia resetting were observed: the sum of coupling interval and return cycle being (1) less than a fully compensatory pause in 12 of 12 patients, (2) more than a fully compensatory pause in 5 of 12 patients and (3) equal to a fully compensatory pause in 2 of 12 patients, depending on extent of AV nodal conduction delay exhibited in return cycle. Tachycardia termination was possible when extrastimuli were delivered from right ventricular apex and coronary sinus but not from high right atrium, and only when basic tachycardia cycle length was greater than or equal to 290 ms in 7 of 12 patients. Tachycardia termination was accounted for by development of orthodromic conduction block in AV node in 7 of 7 patients and in bypass tract in 2 of 7 patients. Therefore, site of extra-stimulation and basic tachycardia cycle length affect electrophysiologic manifestations of excitable gap. Further, functional properties of the AV node influence patterns of tachycardia resetting and are primarily responsible for tachycardia termination during programmed single extrastimulation.

Spectrum of electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease.

Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamil-sensitive VT in 32 patients (aged 38 years +/- 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81% of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p <0.05) and adenosine sensitive (p <0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p >0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.

Comparison of the electrophysiologic effects of oral sustained-release and intravenous verapamil in patients with paroxysmal supraventricular tachycardia.

The electrophysiologic effects of intravenous verapamil (0.15 mg/kg) and oral sustained-release verapamil (verapamil-SR) (240 mg once daily for 7 days) were studied in 17 patients with paroxysmal supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) nodal reentrant tachycardia and 7 had AV reciprocating tachycardia involving an accessory AV pathway. Both preparations significantly prolonged anterograde effective refractory period of the AV node and depressed the retrograde AV nodal conduction system. The sinus cycle length, and atrial and ventricular effective refractory periods were prolonged after oral verapamil-SR. Furthermore, oral verapamil-SR depressed retrograde accessory pathway conduction which was not interfered with by intravenous verapamil. Intravenous verapamil and oral verapamil-SR prevented induction of sustained SVT in 12 of 17 (71%) and 10 of 17 (59%) patients, respectively. Follow-up study with oral verapamil-SR 240 mg once daily in 15 patients for 19 +/- 6 months revealed that among the 8 patients without induction of sustained SVT, 7 have been free of symptomatic arrhythmia; only 1 patient had occasional SVT attacks. For the 7 patients with induction of sustained SVT, 3 patients failed to respond to oral verapamil-SR, 1 patient became symptom free, and the remaining 3 patients had less frequent SVT attacks. Thus, immediate intravenous verapamil testing predicts the electrophysiologic results of oral verapamil-SR therapy, and oral verapamil-SR once daily may be used for long-term prophylaxis of SVT with better patient compliance.

Is sick sinus syndrome an adenosine-mediated disease? Effects of intravenous aminophylline on sick sinus node function after pharmacologic autonomic blockade.

To assess the effects of intravenous aminophylline on the sinus node, 12 patients with clinical and Holter monitor-documented sick sinus syndrome were studied (1) during the control state, (2) after pharmacologic autonomic blockade and (3) 5 min after intravenous administration of aminophylline. The effects of aminophylline on sinus node function were compared with those after pharmacologic autonomic blockade. No significant improvement of sinus node function was found after intravenous aminophylline administration with a mean sinus cycle length and a mean maximum CSRT of 968 +/- 218 and 1832 +/- 1036 ms, respectively. The mean serum theophylline level was 10.9 +/- 1.7 micrograms/ml. Since aminophylline is an adenosine receptor antagonist, these findings suggest that intrinsic adenosine may not play an important role in pathogenesis in patients with chronic and advanced sick sinus syndrome.

Surgical correction of giant patent ductus arteriosus.

In reviewing the literature, there was only one report having the ductus over 30 mm in width. Recently, we utilized cardiopulmonary bypass, hypothermia, and low flow through a transpulmonary approach to close 2 cases of giant patent ductus arteriosus. Both cases complicated with systemic pulmonary hypertension. Its outside diameters were 31 mm and 36 mm respectively based on the measurement from magnetic resonance imaging. To our knowledge, its seem the biggest ductus in comparison to previous reports. Both cases survived the operation and doing well for a follow-up time of 5 years and 4 years 10 months respectively.

Impression cytology of pterygium.

The purpose of this study was to study the morphology and cytokeratin expression in the epithelia of pterygia. Impression cytology and immunohistochemical staining with antikeratin antibodies were performed in 32 eyes of 16 patients with pterygia. TUNEL stain and electron microscopy were also performed in surgical specimens ofpterygium. Squamous metaplasia-like epithelial cells were found in all specimens of impression cytology, especially in the head part. These specimens had positive immunostaining by antipancytokeratin antibodies, but not by anti-K12 AK2 mAb. Goblet cells were found around the area of these abnormal epithelial cells. TUNEL-positive cells were found in the epithelia of the pterygial head, but not in the body of pterygia and normal conjunctiva. The expressional patterns of keratin by these epithelial cells ofpterygia are consistent with the notion that they are derived from conjunctival epithelium and mimic the process of squamous metaplasia.

3D time of flight MR angiography: acquisition with small field of view and low phase encodes.

The aim of the study was to evaluate and compare the image quality of the 3D TOF MRA acquired with a small FOV and low phase encodes with those MR angiographic images acquired with standard pulse sequence parameters. Twenty patients who were referred to our institution for MR imaging of the brain and strictly satisfied the selection criteria were included in this study. Apart from the routine protocol for MR imaging of the brain, 3D TOF MRA of the circle of Willis with a small FOV and a standard FOV were performed. The image quality of all MRA was evaluated by two independent observers who were blind to the pulse sequence parameters. From the standard FOV MRA, 22.5, 12.5, and 5% of the patients were graded as mild, moderate, and severe stenosis of the internal carotid artery, respectively. On the contrary, no apparent stenosis was observed from the small FOV MRA with low phase encodes. Regarding the reduction in MR artifacts and acquisition time achieved with the small FOV 3D TOF MRA with low phase encodes, this might be a useful MR angiographic technique to be used in routine clinical practice.

Supraventricular tachyarrhythmias. Mechanisms, types, and management.

Advances in the area of clinical electrophysiology have allowed definition of the mechanisms of most forms of supraventricular tachyarrhythmias. Reentry, automaticity, and triggered activity are the three basic mechanisms. Treatment of the arrhythmias is based on frequency and hemodynamic severity. After accurate diagnosis, empirical therapy with currently available medications usually controls symptomatic supraventricular tachyarrhythmias. Nonpharmacologic therapy with permanent antitachycardia pacemakers, percutaneous catheter ablation, or surgery is indicated for selected patients with medically recalcitrant supraventricular tachyarrhythmia.

Serial changes of cardiac troponin-I in acute myoischemia induced by exercise treadmill test.

Cardiac troponin-I (cTn-I) is a sensitive and specific marker for the diagnosis of acute myocardial infarction (AMI). However, elevation of serum cTn-I has been observed in some unstable angina patients who have a worse prognosis than those with normal serum cTn-I levels. It is unknown whether serum cTn-I can elevate in stable angina patients with acute ischemic burden. Therefore, the purpose of this study was to determine a serial change of cTn-I in patients with acute ischemia induced by a treadmill exercise test. Thirty-five patients suspected of having coronary artery disease and five healthy medical students were enrolled into this study. Every patient received a treadmill exercise test. Cardiac troponin-I was measured by fluorescent immunoassay before the treadmill test and at 5 minutes, 1 hour, 3 hours, and 6 hours after the treadmill test. Patients with cTn-I levels of less than 0.5 ng/ml were considered normal, and those with cTn-I levels of greater than 2.0 ng/ml was considered to have AMI. The exercise test was positive in 19 of the 35 patients and negative in 16 of the 35 patients and 5 medical students. Among the 19 patients with positive treadmill exercise test, the cTn-I concentrations were abnormally increased in 7/19 (37%) patients (mean: 1.1 +/- 0.4 ng/ml; range: 0.5 to 2.0 ng/ml). One of the 16 patients with negative treadmill test showed an increase of serum cTn-I. Normal cTn-I levels were found in the other 15 patients and the 5 medical students. In conclusion, serum cTn-I levels were found to increase to some extent in one third of stable angina patients who have an acute ischemic episode induced by treadmill exercise test.