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Weak Response (weak + response)
Selected AbstractsPorous Silicon-Based Optical Microsensors for Volatile Organic Analytes: Effect of Surface Chemistry on Stability and SpecificityADVANCED FUNCTIONAL MATERIALS, Issue 17 2010Anne M. Ruminski Abstract Sensing of the volatile organic compounds (VOCs) isopropyl alcohol (IPA) and heptane in air using sub-millimeter porous silicon-based sensor elements is demonstrated in the concentration range 50,800 ppm. The sensor elements are prepared as one-dimensional photonic crystals (rugate filters) by programmed electrochemical etch of p++ silicon, and analyte sensing is achieved by measurement of the wavelength shift of the photonic resonance. The sensors are studied as a function of surface chemistry: ozone oxidation, thermal oxidation, hydrosilylation (1-dodecene), electrochemical methylation, reaction with dicholorodimethylsilane and thermal carbonization with acetylene. The thermally oxidized and the dichlorodimethylsilane-modified materials show the greatest stability under atmospheric conditions. Optical microsensors are prepared by attachment of the porous Si layer to the distal end of optical fibers. The acetylated porous Si microsensor displays a greater response to heptane than to IPA, whereas the other chemical modifications display a greater response to IPA than to heptane. The thermal oxide sensor displays a strong response to water vapor, while the acetylated material shows a relatively weak response. The results suggest that a combination of optical fiber sensors with different surface chemistries can be used to classify VOC analytes. Application of the miniature sensors to the detection of VOC breakthrough in a full-scale activated carbon respirator cartridge simulator is demonstrated. [source] Hydroxyproline-rich glycoprotein accumulation in tobacco leaves protected against Erysiphe cichoracearum by potato virus Y infectionPLANT PATHOLOGY, Issue 2 2000V. Raggi Tobacco cv. Havana 425 acquired resistance to a compatible isolate of Erysiphe cichoracearum after infection by a strain of potato virus Y (PVYN) that causes veinal necrosis; another common strain (PVYO) that does not cause necrosis gave less protection. Hydroxyproline-rich glycoproteins (HRGPs), believed to be involved in resistance, were determined by analysing hydroxyproline (Hyp) in purified cell walls. Hyp content increased significantly in PVYN -protected leaves, compared with untreated controls, 2,4 days after necrotic lesion symptoms developed. No further increase in Hyp was noted in PVYN -protected leaves after E. cichoracearum challenge. Hyp increases were significantly higher in protected leaves of plants showing symptoms on day 7 than on day 10. Infection with the PVYO strain caused significant decrease in Hyp content, compared with uninoculated controls. Inoculation of virus-free plants with E. cichoracearum induced moderate and transitory Hyp increases on day 2 or 3, followed by a quick decrease associated with a weak response by the compatible host. It is suggested that HRGP accumulation induced by PVYN (but not by PVYO) causes changes in the host cell wall that result in resistance to E. cichoracearum. [source] Lineage-specific overexpression of the P2Y1 receptor induces platelet hyper-reactivity in transgenic miceJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2003B. Hechler Summary., In order to investigate the role of the platelet P2Y1 receptor in several aspects of platelet activation and thrombosis, transgenic (TG) mice overexpressing this receptor specifically in the megakaryocytic/platelet lineage were generated using the promoter of the tissue-specific platelet factor 4 gene. Studies of the saturation binding of [33P]2MeSADP in the presence or absence of the selective P2Y1 antagonist MRS2179 indicated that wild-type (WT) mouse platelets bore 150 ± 31 P2Y1 receptors and TG platelets 276 ± 34, representing an 84% increase in P2Y1 receptor density. This led to a well defined phenotype of platelet hyper-reactivity in vitro, as shown by increased aggregations in response to adenosine 5,-diphosphate (ADP) and low concentration of collagen in TG as compared with WT platelets. Moreover, overexpression of the P2Y1 receptor enabled ADP to induce granule secretion, unlike in WT platelets, which suggests that the level of P2Y1 expression is critical for this event. Our results further suggest that the weak responses of normal platelets to ADP are due to a limited number of P2Y1 receptors rather than to activation of a specific transduction pathway. TG mice displayed a shortened bleeding time and an increased sensitivity to in vivo platelet aggregation induced by infusion of a mixture of collagen and epinephrine. Overall, these findings emphasize the importance of the P2Y1 receptor in hemostasis and thrombosis and suggest that variable expression levels of this receptor on platelets might play a role in thrombotic states in human, which remains to be assessed. [source] Bladder control, urgency, and urge incontinence: Evidence from functional brain imaging,NEUROUROLOGY AND URODYNAMICS, Issue 6 2008Derek Griffiths Abstract Aim To review brain imaging studies of bladder control in subjects with normal control and urge incontinence; to define a simple model of supraspinal bladder control; and to propose a neural correlate of urgency and possible origins of urge incontinence. Methods Review of published reports of brain imaging relevant to urine storage, and secondary analyses of our own recent observations. Results In a simple model of normal urine storage, bladder and urethral afferents received in the periaqueductal gray (PAG) are mapped in the insula, forming the basis of sensation; the anterior cingulate gyrus (ACG) provides monitoring and control; the prefrontal cortex makes voiding decisions. The net result, as the bladder fills, is inhibition of the pontine micturition center (PMC) and of voiding, together with gradual increase in insular response, corresponding to increasing desire to void. In urge-incontinent subjects, brain responses differ. At large bladder volumes and strong sensation, but without detrusor overactivity (DO), most cortical responses become exaggerated, especially in ACG. This may be both a learned reaction to previous incontinence episodes and the neural correlate of urgency. The neural signature of DO itself seems to be prefrontal deactivation. Possible causes of urge incontinence include dysfunction of prefrontal cortex or limbic system, suggested by weak responses and/or deactivation, as well as abnormal afferent signals or re-emergence of infantile reflexes. Conclusions Bladder control depends on an extensive network of brain regions. Dysfunction in various parts may contribute to urge incontinence, suggesting that there are different phenotypes requiring different treatments. Neurourol. Urodynam. 27:466,474, 2008. © 2007 Wiley-Liss, Inc. [source] |