Baseline resistance

First chemical test measurements have been conducted with the array chip. Figure 6.19 shows the results that have been obtained simultaneously from three microhotplates coated with different tin-dioxide-based materials at operation temperatures of 280 °C and 330 °C in humidified air (40% relative humidity at 22 °C). The first microhotplate (pHPl) is covered with a Pd-doped Sn02 layer (0.2wt% Pd), which is optimized for CO-detection, whereas the sensitive layer on microhotplate 3 contains 3 wt% Pd, which renders this material more responsive to CH4. The material on microhotplate 2 is pure tin oxide, which is known to be sensitive to NO2. Therefore, the electrodes on microhotplate 2 do not measure any significant response upon exposure to CO or methane. The digital register values can be converted to resistance values by taking into account the resistor bias currents [147,148]. The calculated baseline resistance of microhotplate 1 is approximately 47 kQ, that of hotplate 2 is 370 kQ and the material on hotplate 3 features a rather large resistance of nearly 1MQ. 

Consider checking baseline resistance patterns prior to initiating therapy. 

From the resistivity values obtained, the sensitivity of the measured materials in different test gas atmospheres could be calculated. Sensitivity is defined as the ratio of the resistance of a sensing material in the presence of an analyte to the baseline resistance measured in air. 

The baseline resistance of the sensors also depends on the posttreatment. There are various explanations for the mechanism behind the response behavior modification due to the posttreatment. The lower baseline resistance and the faster response transients after the acetone treatment could be caused by dissolving some of the acrylic matrix during this posttreatment. Dissolving the matrix can result in a closer contact between the conducting polymer grains and enhanced diffusion due to a smaller path length through the composite layer. 

Methanol and ethanol treatments do drastically increase the baseline resistance, which could be caused by the swelling of the polymer inhibiting the charge transfer between the conducting particles. Swelling can be permanent due to only partially reversible sorption of the treatment solvent at room temperature (therefore, the treatment also inhibits the response to the corresponding vapor). The remaining methanol or ethanol could, due to the polar character of these solvents, also be an explanation for the enhanced water response. 

Sista PR, Melby T, Davison D, Jin L, Mosier S, Mink M, Nelson EL, DeMasi R, Cammack N, Salgo MP, Matthews TJ, Greenberg ML (2004) Characterization of determinants of genotypic and phenotypic resistance to enfuvirtide in baseline and on-treatment HIV-1 isolates. Aids 18 1787-1794... 

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Measure blood glucose levels at baseline and every 3 months to assess for glucose intolerance and insulin resistance. Periodic measurement of glycosylated hemoglobin (HbAlc) also may be useful.34... 

For HIV HIV RNA, baseline HIV genotypic resistance test For HIV treatment Hepatitis B tests (hepatitis B surface antibody and antigen, hepatitis B envelope antigen, and HBV DNA), liver function tests... 

Nevertheless, a rapid disappearance of resistant bacteria was observed after stopping the antibiotic treatment (fig. 5). Different kinetics of disappearance were, however, observed. The aerobic species showed a more rapid return to the baseline sensitive status whereas the anaerobic bacteria, especially the Gram-negative rods, regained sensitivity to rifaximin more slowly. In any case, 3 months after the end of treatment resistant strains were no longer detectable in the feces [82], These results support the cyclic use of rifaximin that has been adopted by the investigators in the treatment of hepatic encephalopathy [77] and colonic diverticular disease [79]. 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

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