Biological response curves

FIGURE 14.9 Shapes of the biological response curves in homologous series. 

The biological response line for acute respiratory disease is a dose-response curve, which for a constant concentration becomes a duration-response curve. The shape of such a curve reflects the ability of the human body to cope with short-term, ambient concentration respiratory exposures and the overwhelming of the body s defenses by continued exposure. 

Competitive antagonists affinity of, 261-264 description of, 75 IC50 correction factors for, 223 Schild analysis, 261-264 Concentration-dependent antagonism, 99 Concentration-response curve, 13 Confidence intervals, 228-229 Conformations, 13-14 Constitutive activity of receptors description of, 49—51 receptor density and, 56 Schild analysis, 108-111 Context-dependent biological effect, 188 Correction factors, 211-213, 223 Correlational research, 231 CP320626, 128... 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a specified magnitude of changes in a specified adverse response. For example, a BMDio would be the dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 10%. The BMD is determined by modeling the dose response curve in the region of the dose response relationship where biologically observable data are feasible. 

In view of the future development of sensors driven by increasing demand for accuracy and precision, and by the opening of new fields close to the biological area (which is oriented toward nano-biosensor fabrication), it appears even more important to properly use the most relevant sensor keywords, such as response curve, sensitivity, noise, drift, resolution, and selectivity. 

Nutrients enter into biological processes that are not characterized by a well-defined dose-response relationship. Therefore, in many cases, the dietary supplement itself is not expected to exhibit a characteristic dose-response curve. 

Ironically, SE or TSST-1 concentrations that cause T-cell proliferation do not always correlate with receptor affinity. For instance, SEE binds HLA-DR with 100-fold lower affinity relative to the very similarly structured SEA however, SEE stimulates T-cell proliferation to equivalent levels as SEA. The dose-response curves for cytokine and chemokine production in vitro by staphylococcal superantigen-stimulated cells are also very similar despite differences in affmity/specificity for major histocompatibility complex class II and T-cell receptor V/3 molecules. Overall, these observations suggest that the biological effects of staphylococcal superantigens are induced at rather low, nonsaturating occupancy rates not readily classified by typical biokinetics. 

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