Experiments were conducted to investigate the relationships of tissue damage with leaf age and location of tissue damage in relation to point of inoculation.
Altered electrode performance and hearing/speech outcomes do not always have an obvious causal relationship to damage of these delicate intracochlear structures and interpreting the role and impact of observed histopathological changes in hearing loss can be problematic.
With these statistical data, relationships of building damage indicator to repair to replacement cost ratio has been built from regression analysis.
Nevertheless, the general relationship of larger damage factor to probable building damage is confirmed, which indicates that the proposed methodology can be adopted confidently as a complementary assessment of building damage in catastrophe modeling.
In order to explain the causal relationship of wind damage to trees, most mechanistic model formulations require detailed information about physical as well as meteorological parameters (e.g. Peltola et al. 2013).
From observing the results in Figure 6 and Table 4 and understanding the trust model algorithms, we see a clear pattern between the relationship of trust damage and false alarms.
While there are limitations associated with retrospective analysis and the potential for bias resulting from selection, the relationship of intestinal damage to SCT complications was remarkable.
Integrating information about the structure-function relationship of glaucomatous damage through data fusion, presents some advantages over the simple combination of the two different types of data.
Although observational studies have demonstrated an alteration of heart rate variability (HRV) in septic patients, no single study has systematically addressed the relationship of heart damage by systemic inflammation and metabolic alterations.
Recent interest has been aroused in the relationship of renal damage with arterial stiffness evaluated by the augmentation index (AIx) and blood pressure including central blood pressure (cBP) and peripheral blood pressure (pBP).
Although much insight has been gained into the molecular mechanisms that regulate p53 pulses in response to DSBs [ 16] and their functional role [ 23], little is known about the quantitative relationship of DNA damage and p53 induction.
