SAMPLING BIAS IN EVALUATING THE PROBABILITY OF SEISMICALLY INDUCED SOIL LIQUEFACTION WITH SPT & CPT CASE HISTORIES

Several deterministic and probabilistic methods are used to evaluate the probability of seismically induced liquefaction of a soil. The probabilistic models usually possess some uncertainty in that model and uncertainties in the parameters used to develop that model. These model uncertainties vary from one statistical model to another. Most of the model uncertainties are epistemic, and can be addressed through appropriate knowledge of the statistical model. One such epistemic model uncertainty in evaluating liquefaction potential using a probabilistic model such as logistic regression is sampling bias. Sampling bias is the difference between the class distribution in the sample used for developing the statistical model and the true population distribution of liquefaction and non-liquefaction instances. Recent studies have shown that sampling bias can significantly affect the predicted probability using a statistical model. To address this epistemic uncertainty, a new approach was developed for evaluating the probability of seismically-induced soil liquefaction, in which a logistic regression model in combination with Hosmer-Lemeshow statistic was used. This approach was used to estimate the population (true) distribution of liquefaction to non-liquefaction instances of standard penetration test (SPT) and cone penetration test (CPT) based most updated case histories. Apart from this, other model uncertainties such as distribution of explanatory variables and significance of explanatory variables were also addressed using KS test and Wald statistic respectively. Moreover, based on estimated population distribution, logistic regression equations were proposed to calculate the probability of liquefaction for both SPT and CPT based case history. Additionally, the proposed probability curves were compared with existing probability curves based on SPT and CPT case histories.

INFLUENCE OF 24-HOUR SLEEP DEPRIVATION ON CARDIOVASCULAR AND NEURAL CONTROL AT REST AND DURING ACUTE STRESS IN HUMANS

Recent epidemiological studies report a consistent association between short sleep and incidence of hypertension, as well as short sleep and cardiovascular disease-related mortality. While the association between short sleep and hypertension appears to be stronger in women than men, the mechanisms underlying the relations between sleep deprivation, stress, risks of cardiovascular diseases, and sex remain unclear. We conducted two studies to investigate the underlying neural mechanisms of these relations. In study 1, we examined sympathetic neural and blood pressure responses to experimentally-induced sleep deprivation in men and women. We further investigated the influence of sleep deprivation on cardiovascular reactivity to acute stress. In study 2, we examined the neural and cardiovascular function throughout the ovarian cycle in sleep deprived women. Twenty-eight young healthy subjects (14men and 14 women) were tested twice in study 1, once after normal sleep (NS) and once after 24-h total sleep deprivation (TSD). We measured the blood pressure, heart rate (HR), muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) during 10min baseline, 5min of mental stress (MS) and 2 min cold pressor test (CPT). We demonstrated that TSD increased resting arterial blood pressure to a similar extent in both men and women, but MSNA decreased only in men following TSD. This MSNA response was associated with altered baroreflex function in women and divergent testosterone responses to TSD between men and women. Regarding TSD and cardiovascular reactivity, TSD elicited augmented HR reactivity and delayed recovery during both MS and CPT in men and women, and responses between sexes were not statistically different. Fourteen young healthy women participated in study 2. Subjects were tested twice, once during their early follicular (EF) phase after TSD, once during their mid-luteal (ML) phase after TSD. Blood pressure, HR, MSNA, and FBF were recorded during 10min baseline, 5 min MS, and 2 min CPT. We observed an augmented resting supine blood pressure during EF compared to ML in sleep deprived women. In contrast, resting MSNA, as well as cardiovascular responses to stressors, were similar between EF and ML after TSD. In conclusion, we observed sex differences in MSNA responses to TSD that demonstrate reductions of MSNA in men, but not women. TSD elicited augmented HR reactivity and delayed HR recovery to acute stressors similarly in men and women. We also reported an augmented supine blood pressure during EF compared to ML in sleep deprived women. These novel findings provide new and valuable mechanistic insight regarding the complex and poorly understood relations among sleep deprivation, sex, stress, and risk of cardiovascular disease.