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Differences in response

In addition to examining pre-exposure effects, the slow strain-rate testing technique has been used increasingly to examine and compare the stress-corrosion susceptibility of aluminium alloys of various compositions, heat treatments and forms. A recent extensive review draws attention to differences in response to the various groups of commonly employed alloys which are summarised in Fig. 8.57. The most effective test environment was found to be 3 Vo NaCl -F 0.3 Vo HjOj. The most useful strain rate depends upon the alloy classification. [Pg.1282]

There are a number of basic forms of energy loads or impingement on products to which plastics react in a manner different from other materials. These dynamic stresses include loading due to impact, impulse, puncture, frictional, hydrostatic, and erosion. They have a difference in response and degree of response to other forms of stress. Analyzing these differences provides... [Pg.89]

Lipoxygenase AVNTR polymorphism in 100 bp upstream from the ATG start codon is associated with transcription efficiency. Differences in response to 5-lipoxygenase inhibitors and leucotriene receptor antagonists. [Pg.950]

Tables (3-1, 3-2, and 3-3) and figures (3-1 and 3-2) are used to summarize health effects and illustrate graphically levels of exposure associated with those effects. These levels cover health effects observed at increasing dose concentrations and durations, differences in response by species, minimal risk levels (MRLs) to humans for noncancer end points, and EPA s estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to locate data for a specific exposure scenario. The LSE tables and figures should always be used in conjunction with the text. All entries in these tables and figures represent studies that provide reliable, quantitative estimates of No-Observed-Adverse-Effect Levels (NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels (CELs). Tables (3-1, 3-2, and 3-3) and figures (3-1 and 3-2) are used to summarize health effects and illustrate graphically levels of exposure associated with those effects. These levels cover health effects observed at increasing dose concentrations and durations, differences in response by species, minimal risk levels (MRLs) to humans for noncancer end points, and EPA s estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to locate data for a specific exposure scenario. The LSE tables and figures should always be used in conjunction with the text. All entries in these tables and figures represent studies that provide reliable, quantitative estimates of No-Observed-Adverse-Effect Levels (NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels (CELs).
In Fig. 4.39, results for spiked placebo and for the verum tablets are given for compound A (bold lines) and B all horizontal bars should be at 100%, and the vertical lines should be centered at the same height. The gray trendlines, particularly for the LO- and Hl-range A-values indicate a systematic difference in response between tbe calibration solutions and the spiked placebo tablets (extraction efficiency, interference, etc.). For same ranges, the verum-tablets assays either underestimate the content of A by 4—5%, or A is underdosed. For compound A the repeatability figures are as follows (%-of-nom-inal, see file Fig4 39.dat), see Table 4.36. [Pg.288]

As with sweetness, an enantiomeric difference in response is observed in the bitter-taste quality. Isodonal (113) and dihydroisodonal (114) are bitter. [Pg.312]

Utilizing the stark difference in response of wildtype astrocytes (increased apoptosis) and astrocytes (decreased apoptosis), Warrington et al. (2007)... [Pg.261]

Kent DM, Price LL, Ringleb P, Hill MD, Selker HP. Sex-based differences in response to recombinant tissue plasminogen activator in acute ischemic stroke A pooled analysis of randomized clinical trials. Stroke. 2005 36 62-65. [Pg.58]

Green T, Prout MS. 1985. Species differences in response to trichloroethylene. 11. Biotransformation in rats and mice. Toxicol Appl Pharmacol 79 401-411. [Pg.269]

All clinical trials should have a pre-specified research question, which may be stated in the form of a primary hypothesis (or possibly a few primary hypotheses). An objective outcome measure or measures should also be clearly identified, such as the results of a biochemical test or the score on a validated scale. This allows statistical tests to be applied in order to assess the likelihood that any differences in response between treatment groups resulted from the active treatment and were not due to chance. [Pg.240]

The significance level relates to the risk of designating a chance occurrence as statistically significant. Usually a 5% level is utilized for testing treatment effects. If a p-value of 0.04 is reported for a treatment effect, this means that there is only a 4% chance that the difference in response between the active and control treatments occurred due to chance. Keep in mind, however, that if many tests are run in a trial, it is entirely possible that one or two might be significant due to chance. As an extreme example, consider a study in which 100 statistical tests are run. We would expect five of those tests to show significance with a p-value of 0.05 or less due to chance. Therefore, it is essential to specify the main tests to be run in the protocol. Any tests that are conducted after the trial has been completed should be clearly labeled as post hoc exploratory analyses. [Pg.243]

Fig. 5.9(b) Sex differences in responsiveness to female hamster vaginal fluid (FHVS) androgen (T) effects on central transmission pathways (from Swann and Fiber, 1997). [Pg.113]

Fig. 7.7 Discrimination by F. (a) of estrous, vs. non-estrous, urine frequency in feral goats (from O Brien, 1982) and (b) within social groups, species-differences in responsiveness of male antelopes to urinary and/or genital signals (from Hart and Hart, 1987). Fig. 7.7 Discrimination by F. (a) of estrous, vs. non-estrous, urine frequency in feral goats (from O Brien, 1982) and (b) within social groups, species-differences in responsiveness of male antelopes to urinary and/or genital signals (from Hart and Hart, 1987).
There was little difference in response between the two weed species to gHBA (a 30% inhibition at 8 mM for (Z. album versus 27% for A. retroflexus). There was no significant interaction effect on HL between the two compounds (F = 0.97, P > F 0.50). The difference in sensitivity of the weed species to the two compounds could have been due to the duration of the experiments (8 days for C. album versus 60 hr for A. retroflexus). The longer duration may have resulted in a lower concentration of the compound because of microbial degradation. [Pg.264]

It is clear that ethnic differences in response to antipsychotics exist (Emsley et al, 2002 Frackiewicz et al, 1997). Whereas there has been some work examining first-generation antipsychotics (FGAs) (for reviews, see Frackiewicz etal, 1997 Poolsup et al, 2000), there remains a considerable dearth of research that has examined ethnic differences with respect to the second-generation antipsychotics (SGAs). [Pg.47]

An open-label study of paroxetine and fluoxetine (Alonso et al, 1997) in depressed Hispanic (Mexican descent, n = 13) and non-Hispanic females (n = 13) showed no differences in response rates. At variance with the tricyclic data, Hispanic subjects complained of fewer side effects (2.2 2.0 vs. 5.1 2.5 p < 0.005), but twice as many terminated participation prior to study completion due to non-compliance, intolerable side effects or pregnancy. [Pg.98]

A small, flexible dose study of citalopram (dosage range = 10-40 mg/day) in 14 Hispanic and 6 non-Hispanic (non-White) depressed HIV-positive patients conducted in Miami also showed no differences in response rate or effective dose between ethnicities (Currier etal., 2004). In addition, Hispanic patients did not have a significantly higher attrition rate compared to non-Hispanics. [Pg.98]

The results from an open-label, pilot study evaluating the efficacy of fluvoxamine for hypochondriasis were recently published (Fallon et al, 2003). The study sample included six Hispanics (subgroup unknown). Significant improvement (57.1%) was noted for the intent-to-treat group (eight out of fourteen) based on physicianrated and self-rated scales. The sample size was too small to identify differences in response or adverse effects by ethnicity. [Pg.99]

Wagner, G. J., Mague, S. Rabkin, J. G. (1998). Ethnic differences in response to fluoxetine in a controlled trial with depressed HIV-positive patients. Psychiatr. Serv., 9, 239-40. [Pg.110]

Carson, R, Ziesche, S., Johnson, G. et al. (1999). Racial differences in response to therapy for heart failure analysis of the vasodilator-heart failure trials. /. Card. Pail., 5, 178-87. [Pg.115]

Gautier Can you do the experiment to check whether this difference in responsiveness between G1 and G2 is dependent on transcription Another explanation would be that the passage into S phase changes the transcriptional competence of the cell. [Pg.218]


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See also in sourсe #XX -- [ Pg.241 ]




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