Discriminative fabric defect detection using adaptive wavelets

We propose a new method for fabric defect detection by incorporating the design of an adaptive wavelet-based feature extractor with the design of an Euclidean distance-based detector. The proposed method characterizes the fabric image with multiscale wavelet features by using undecimated discrete wavelet transforms. Each nonoverlapping window of the fabric image is then detected as defect or nondefect with an Euclidean distance-based detector. Instead of using the standard wavelet bases, an adaptive wavelet basis is designed for the detection of fabric defects. Minimization of the detection error Is achieved by incorporating the design of the adaptive wavelet with the design of the detector parameters using a discriminative feature extraction (DFE) training method. The proposed method has been evaluated on 480 defect samples from five types of defects, and 480 nondefect samples, where a 97.5% detection rate and 0.63% false alarm rate were achieved. The evaluations were also carried out on unknown types of defects, where a 93.3% detection rate and 3.97% false alarm rate were achieved in the detection of 180 defect samples and 780 nondefect samples. © 2002 Society of Photo-Optical Instrumentation Engineers.published_or_final_versio

Sex-specific assessment of reduced coronary sinus flow in non-hypertensive patients with coronary artery disease at rest

Background: Access to data on the coronary flow in the coronary sinus (CS) can aid in the diagnosis of coronary artery disease (CAD). We tested the hypothesis that assessing the CS flow by transthoracic Doppler echocardiography (TTE) at rest can detect coronary artery stenosis in non-hypertensive patients.Methods: The antegrade phase of coronary flow in the CS was analyzed and compared in 140 male and 135 female non-hypertensive subjects who had all undergone coronary angiography.Results: There were statistically significant differences noted between males and females for the CS flow both in normal subjects and patients with CAD. Compared with normal subjects, patients with CAD had significantly lower blood flow in the CS both in males (196.69174.31 vs. 367.659168.04 ml/min, PB0.01) and females (183.04965.46 vs. 244.139135.43 ml/min PB0.01). For males, the diagnostic sensitivity, specificity, and accuracy of the cutoff value of the CS flow (206 ml/min) for predicting a significant coronary artery stenosis (70%) were 91.67%, 81.25%, and 85.71%, respectively. For females, those of the cutoff value of the CS flow (195 ml/min) were 85.71%, 75%, and 80%, respectively.Conclusion: TTE can effectively detect coronary hemodynamically significant stenosis in non-hypertensive male and female patients at different cutoff values.Keywords: coronary flow; coronary sinus; coronary artery stenoses; males and females; non-hypertensive patients; transthoracic Doppler echocardiograph

Comparison of the degradations of diphenamid by homogeneous photolysis and heterogeneous photocatalysis in aqueous solution

2009-2010 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Effects of dissolved oxygen, pH, and anions on the 2,3-dichlorophenol degradation by photocatalytic reaction with anodic TiO?nanotube films

2008-2009 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

A RAMP marker linked to the tobacco black shank resistant gene

Bulk segregant analysis (BSA) and randomly amplified microsatellite polymorphism (RAMP) were employed to analyze F2 individuals of the Yunyan 317×Hubei 517 to screen and characterize molecularmarkers linked to black shank resistant gene. A total of 800 arbitrary decamer oligonucleotide primerpairs were used for RAMP analysis. Primer pair GT (CA) 4/S89, producing one RAMP marker GT (CA)4/S89550, was tightly linked to the black shank resistant gene. Results of Southern blot suggest that the fragment GT (CA) 4/S89550 was existed in Yunyan 317 and resistant plants, and absent in Hubei 517.Linkage analysis was carried out using marker GT (CA) 4/S89550 on 752 black shank high-resistant individuals of F2 progenies from crossing between Yunyan 317 and Hubei 517. Our results indicated thatthe genetic distances between GT (CA) 4/S89550 and black shank resistant gene was 1.4cM

Inhibited carrier transfer in ensembles of isolated quantum dots

We report significant differences in the temperature-dependent and time-resolved photoluminescence (PL) from low and high surface density InxGa1-xAs/GaAs quantum dots (QDs). QD's in high densities are found to exhibit an Arrhenius dependence of the PL intensity, while low-density (isolated) QD's display more complex temperature-dependent behavior. The PL temperature dependence of high density QD samples is attributed to carrier thermal emission and recapture into neighboring QD's. Conversely, in low density QD samples, thermal transfer of carriers between neighboring QD's plays no significant role in the PL temperature dependence. The efficiency of carrier transfer into isolated dots is found to be limited by the rate of carrier transport in the InxGa1-xAs wetting layer. These interpretations are consistent with time-resolved PL measurements of carrier transfer times in low and high density QD's. [S0163-1829(99)04748-7]

Ethanolic Extract of Aconiti Brachypodi Radix Attenuates Nociceptive Pain Probably Via Inhibition of Voltage-Dependent Na+ Channel

Aconiti Brachypodi Radix, belonging to the genus of Aconitum (Family Ranunculaceae), are used clinically as anti-rheumatic, anti-inflammatory and anti-nociceptive in traditional medicine of China. However, its mechanism and influence on nociceptive threshold are unknown and need further investigation. The analgesic effects of ethanolic extract of Aconiti Brachypodi Radix (EABR) were thus studied in vivo and in vitro. Three pain models in mice were used to assess the effect of EABR on nociceptive threshold. In vitro study was conducted to clarify the modulation of the extract on the tetrodotoxin-sensitive (TTX-S) sodium currents in rat’s dorsal root ganglion (DRG) neurons using whole-cell patch clamp technique. The results showed that EABR (5-20 mg/kg, i.g.) could produce dose-dependent analgesic effect on hot-plate tests as well as writhing response induced by acetic acid. In addition, administration of 2.5-10 mg/kg EABR (i.g.) caused significant decrease in pain responses in the first and second phases of formalin test without altering the PGE2 production in the hind paw of the mice. Moreover, EABR (10 μg/ml -1 mg/ml) could suppress TTX-S voltage-gated sodium currents in a dose-dependent way, indicating the underlying electrophysiological mechanism of the analgesic effect of the folk plant medicine. Collectively, our results indicated that EABR has analgesic property in three pain models and useful influence on TTX-S sodium currents in DRG neurons, suggesting that the interference with pain messages caused by the modulation of EABR on TTX-S sodium currents in DRG neurones may explain some of its analgesic effect

Paradoxical effect of rapamycin on inflammatory stress-induced insulin resistance in vitro and in vivo

Insulin resistance is closely related to inflammatory stress and the mammalian target of rapamycin/S6 kinase (mTOR/S6K) pathway. The present study investigated whether rapamycin, a specific inhibitor of mTOR, ameliorates inflammatory stress-induced insulin resistance in vitro and in vivo. We used tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) stimulation in HepG2 hepatocytes, C2C12 myoblasts and 3T3-L1 adipocytes and casein injection in C57BL/6J mice to induce inflammatory stress. Our results showed that inflammatory stress impairs insulin signaling by reducing the expression of total IRS-1, p-IRS-1 (tyr632), and p-AKT (ser473); it also activates the mTOR/S6K signaling pathway both in vitro and in vivo. In vitro, rapamycin treatment reversed inflammatory cytokine-stimulated IRS-1 serine phosphorylation, increased insulin signaling to AKT and enhanced glucose utilization. In vivo, rapamycin treatment also ameliorated the impaired insulin signaling induced by inflammatory stress, but it induced pancreatic β-cell apoptosis, reduced pancreatic β-cell function and enhanced hepatic gluconeogenesis, thereby resulting in hyperglycemia and glucose intolerance in casein-injected mice. Our results indicate a paradoxical effect of rapamycin on insulin resistance between the in vitro and in vivo environments under inflammatory stress and provide additional insight into the clinical application of rapamycin

Use of moxibustion to treat primary dysmenorrhea at two interventional times: study protocol for a randomized controlled trial

published_or_final_versio

Sterol-resistant SCAP Overexpression in Vascular Smooth Muscle Cells Accelerates Atherosclerosis by Increasing Local Vascular Inflammation through Activation of the NLRP3 Inflammasome in Mice

Atherosclerosis is a serious age-related pathology, and one of its hallmarks is the presence of chronic inflammation. Sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) is a cholesterol sensor that plays an essential role in regulating intracellular cholesterol homeostasis. Accordingly, dysregulation of the SCAP-SREBP pathway has been reported to be closely associated with an increased risk of obesity, hypercholesterolemia, and cardiovascular disease. In this study, we explored whether sterol-resistant SCAP (D443N mutation) in vascular smooth muscle cells (VSMCs) of mice promotes vascular inflammation and accelerates the occurrence and progression of atherosclerosis. We established a transgenic knock-in mouse model of atherosclerosis with an activating D443N mutation at the sterol-sensing domain of SCAP (SCAPD443N) by microinjection. Next, SCAPD443N/ApoE-/- mice were generated by crossing SCAPD443N mice with apolipoprotein E-/- (ApoE-/-) background mice. We found that sterol-resistant SCAP markedly amplified and accelerated the progression of atherosclerotic plaques in SCAPD443N/ApoE-/- mice compared with that in control ApoE-/- mice. Similarly, in SCAPD443N mice, aortic atherosclerotic plaques both appeared earlier and were greater in number than that in control SCAP+/+ mice, both of which were fed a Western diet for 12 or 24 weeks. Moreover, we observed that sterol-resistant SCAP significantly increased local inflammation and induced endothelial dysfunction in the aortas of SCAPD443N mice and SCAPD443N/ApoE-/- mice. In vitro, we also found that sterol-resistant SCAP overexpression in VSMCs increased the release of inflammatory cytokines and induced endothelial cell injury when both cell types were cocultured. Furthermore, we demonstrated that sterol-resistant SCAP overexpression in VSMCs promoted SCAP and NLRP3 inflammasome cotranslocation to the Golgi and increased the activation of the NLRP3 inflammasome pathway. These findings suggested that sterol-resistant SCAP in VSMCs of mice induced vascular inflammation and endothelial dysfunction, consequently accelerating atherosclerosis by activating the NLRP3 inflammasome pathway