Statistical pattern modeling in vision-based quality control systems

Machine vision technology improves productivity and quality management and provides a competitive advantage to industries that employ this technology. In this article, visual inspection and quality control theory are combined to develop a robust inspection system with manufacturing applications. The inspection process might be defined as the one used to determine if a given product fulfills a priori specifications, which are the quality standard. In the case of visual inspection, these specifications include the absence of defects, such as lack (or excess) of material, homogeneous visual aspect, required color, predetermined texture, etc. The characterization of the visual aspect of metallic surfaces is studied using quality control chars, which are a graphical technique used to compare on-line capabilities of a product with respect to these specifications. Original algorithms are proposed for implementation in automated visual inspection applications with on-line execution requirements. The proposed artificial vision method is a hybrid between the two usual methods of pattern comparison and theoretical decision. It incorporates quality control theory to statistically model the pattern for defect-free products. Specifically, individual control charts with 6-sigma limits are set so the inspection error is minimized. Experimental studies with metallic surfaces help demonstrate the efficacy and robustness of the proposed methodology.Publicad

Detraining differentially preserved beneficial effects of exercise on hypertension: effects on blood pressure, cardiac function, brain inflammatory cytokines and oxidative stress.

AIMS: This study sought to investigate the effects of physical detraining on blood pressure (BP) and cardiac morphology and function in hypertension, and on pro- and anti-inflammatory cytokines (PICs and AIC) and oxidative stress within the brain of hypertensive rats. METHODS AND RESULTS: Hypertension was induced in male Sprague-Dawley rats by delivering AngiotensinII for 42 days using implanted osmotic minipumps. Rats were randomized into sedentary, trained, and detrained groups. Trained rats underwent moderate-intensity exercise (ExT) for 42 days, whereas, detrained groups underwent 28 days of exercise followed by 14 days of detraining. BP and cardiac function were evaluated by radio-telemetry and echocardiography, respectively. At the end, the paraventricular nucleus (PVN) was analyzed by Real-time RT-PCR and Western blot. ExT in AngII-infused rats caused delayed progression of hypertension, reduced cardiac hypertrophy, and improved diastolic function. These results were associated with significantly reduced PICs, increased AIC (interleukin (IL)-10), and attenuated oxidative stress in the PVN. Detraining did not abolish the exercise-induced attenuation in MAP in hypertensive rats; however, detraining failed to completely preserve exercise-mediated improvement in cardiac hypertrophy and function. Additionally, detraining did not reverse exercise-induced improvement in PICs in the PVN of hypertensive rats; however, the improvements in IL-10 were abolished. CONCLUSION: These results indicate that although 2 weeks of detraining is not long enough to completely abolish the beneficial effects of regular exercise, continuing cessation of exercise may lead to detrimental effects

Rat primers used for real-time RT-PCR.

<p>IL, Interleukin; TNF-α, Tumor necrosis factor-alpha; gp91^phox, NADPH oxidase subunit; iNOS, Inducible nitric oxide synthase; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase.</p

Effect of Exercise and Detraining on Weights, MAP, and HR of rats.

<p>Values are mean ±SE. Sal+Sed, saline+sedentary; Sal+Ex, saline+exercise; Sal+Det, saline+detraining; AngII+Sed, angiotensinII+sedentary; AngII+Ex, angiotensinII+exercise; AngII+Det, angiotensinII+detraining. BW(g), body weight (grams); HM (g), heart mass (grams); HM/BW (mg/g), heart mass to body weight ratio; MAP, mean arterial pressure (mmHg); HR, heart rate; bpm, beats per minute.</p>*<p>p<0.05 Sal+Sed vs AngII+Sed;</p>#<p>p<0.05 AngII+Sed vs AngII+Ex.</p

Baseline characteristic of studied rats: BW, MAP, and Echocardiographic Analysis of Cardiac Hypertrophy and Function.

<p>Values are mean ±SE. Sal+Sed, saline+sedentary; Sal+Ex, saline+exercise; Sal+Det, saline+detraining; AngII+Sed, angiotensionII+sedentary; AngII+Ex, angiotensinII+exercise; AngII+Det, angiotensinII+detraining. BW(g), body weight (grams); MAP, mean arterial pressure (mmHg). LVIDd and LVIDs indicate left ventricular internal diameter at diastole and systole, respectively; IVSTd and IVSTs, interventricular septal thickness at diastole and systole, respectively; LVPWTd and LVPWTd, left ventricle posterior wall thickness at diastole and systole, respectively; FS, fractional shortening (%); EF (%), ejection fraction; HR, heart rate; bpm, beats per minute.</p

A schematic depicting the proposed pathways of effects of exercise training and detraining on AngII-induced hypertensive response.

<p>Lines with arrow represent ‘activation’ and lines with no arrow represent ‘inhibition’. It has become clear from the past several years of research that an increased production of PICs in response to overactivated RAS within the cardiovascular regulatory centers of the brain (such as paraventricular nucleus) causes increased sympathetic outflow leading to increased arterial pressure and cardiac remodeling in experimental models of hypertension. At the cellular level, PICs activate reactive oxygen species which in turn can activate various intracellular signaling pathways, including that of NFκB. Activation of NFκB induces gene transcription of PICs fostering a positive feedback mechanism, and eventually leading to the progression of hypertension. A growing body of evidence suggests that the beneficial effects of exercise in hypertension could be attributed to reduced PICs, improved cellular redox homeostasis, and downregulation of NFκB activity. A step further, in the present study, we demonstrated that transient cessation of exercise (2 weeks of detraining) abolishes the exercise-induced improvements in cardiac hypertrophy, cardiac function, anti-inflammatory cytokine (IL-10) and oxidative stress in the PVN of hypertensive rats, although, positive effects in MAP and PICs remains unchanged. Further studies are still warranted to unravel the effects of exercise and detraining on other components of the AngII-induced signaling pathway such as downstream transcription factors and sympathetic activity.</p

Effects of exercise on TNF-α, IL-1β, and IL-10 in the PVN of normotensive and hypertensive rats.

<p><b>A,</b> mRNA expression of TNF-α. <b>B,</b> mRNA expression of IL-1β. <b>C,</b> mRNA expression of IL-10. <b>D</b>, a representative Western blot. <b>E,</b> densitometric analysis of protein expression. Detraining did not alter exercise-induced reduction in TNF-α and IL-1β levels in the PVN of AngII-infused animals; whereas, it did abolish exercise-mediated increase in IL-10 levels.Values are mean±SE. n = 9 per group for mRNA and n = 6 per group for protein analysis. *p<i><</i>0.05 Sal+Sed versus AngII+Sed; ^#p<0.05 AngII+Sed versus AngII+Ex and AngII+Sed versus AngII+Det; ^@p<0.05 AngII+Ex versus AngII+Det.</p

Effects of exercise on Cu/ZnSOD in the PVN of normotensive and hypertensive rats.

<p>Densitometric analysis of protein expression (upper panel) and a representative Western blot (lower panel) showed that detraining completely abolished exercise-mediated increase in Cu/ZnSOD levels.Values are mean±SE. n = 6 per group. *p<i><</i>0.05 Sal+Sed versus AngII+Sed; ^#p<0.05 AngII+Sed versus AngII+Ex and AngII+Sed versus AngII+Det; ^@p<0.05 AngII+Ex versus AngII+Det; ^$AngII+Sed versus AngII+Det.</p

Time course of mean arterial pressure (MAP, in millimeters of mercury) in normotensive and hypertensive rats.

<p>MAP was significantly increased in AngII+Sed compared with Sal+Sed rats from day 8 of AngII infusion (empty arrow). MAP was significantly reduced in AngII+Ex compared with AngII+Sed rats from day 16 of exercise (filled arrow). 2 weeks of detraining did not abolish the exercise-induced reduction in MAP in AngII-infused rats. Values are mean±SE; n = 6 per group. *p<i><</i>0.05 Sal+Sed versus AngII+Sed; ^#p<0.05 AngII+Sed versus AngII+Ex; ^$p<0.05 AngII+Sed versus AngII+Det.</p