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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Earth and Planetary Sciences, 1979. / Microfiche copy available in Archives and Science. / Bibliography: leaves 73-75. / by Steven J. Hellinger. / Ph.D.

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Earth and Planetary Sciences, 1981. / Microfiche copy available in Archives and Science. / Bibliography: leaves 102-106. / by Joann Miriam Stock. / M.S.

In historical, large-magnitude earthquakes, lateral spreading has been a very damaging type of ground failure. When a subsurface soil deposit liquefies, intact blocks of surficial soil can move downslope, or toward a vertical free face, even when the ground surface is nearly level. A lateral spread is defined as the mostly horizontal movement of gently sloping ground (less than 5% surface slope) due to elevated pore pressures or liquefaction in undelying, saturated soils. Here, lateral spreading is defined specifically to exclude liquefaction failures of steeper embankments and retaining walls, which can also produce lateral surface deformations. Lateral spreads commonly occur at waterfront sites underlain by saturated, recent sediments and are particularly threatening to buried utilities and transportation networks. While the occurrence of soil liquefaction and lateral spreading can be predicted at a given site, methods are needed to estimate the magnitude of the resulting deformations. In this research effort, an empirical model was developed for predicting horizontal and vertical surface displacements due to liquefaction-induced lateral spreading. The resulting model is called "EPOLLS" for Empirical Prediction Of Liquefaction-induced Lateral Spreading. Multiple linear regression analyses were used to develop model equations from a compiled database of historical lateral spreads. The complete EPOLLS model is comprised of four components: (1) Regional-EPOLLS for predicting horizontal displacements based on the seismic source and local severity of shaking, (2) Site-EPOLLS for improved predictions with the addition of data on the site topography, (3) Geotechnical-EPOLLS using additional data from soil borings at the site, and (4) Vertical-EPOLLS for predicting vertical displacements. The EPOLLS model is useful in phased liquefaction risk studies: starting with regional risk assessments and minimal site information, more precise predictions of displacements can be made with the addition of detailed site-specific data. In each component of the EPOLLS model, equations are given for predicting the average and standard deviation of displacements. Maximum displacements can be estimated using probabilities and the gamma distribution for horizontal displacements or the normal distribution for vertical displacements. / Ph. D.

To better understand the ground motion and associated seismic hazard of earthquakes in the central and eastern United States (CEUS), this dissertation focuses on the source parameters and wave propagation characteristics of both tectonic earthquakes and induced earthquakes in the CEUS. The infrequent occurrence of significant earthquakes in the CEUS limits the necessary observations needed to understand earthquake processes and to reduce uncertainty in seismic-hazard maps. The well-recored aftershock sequence of the 2011 Mineral, Virginia, earthquake offers a rare opportunity to improve our understanding of earthquake processes and earthquake hazard in this populous region of the United States. Moreover, the rapid increase of seismicity in the CEUS since 2009 that has been linked to wastewater injection has raised concern regarding the potential hazard. In this dissertation, I first present a detailed study of the aftershock sequence of the 2011 Mw 5.7 Mineral, Virginia earthquake. It involves the hypocenter locations of ~3000 earthquakes, ~400 focal mechanism solutions, statistics of the aftershock sequence, and the Coulomb stress modeling that explains the triggering mechnanism of those aftershocks. Second, I examine the S-wave attenuation at critical short hypocentral distances (< 60 km) using the aftershock data. The observed S-wave amplitudes decay as a function of hypocenter distance R according to R^-1.3 - R^-1.5, which is substantially steeper than R^-1 for a homogeneous whole space. Finally, I propose and apply a stable multi-window coda spectral ratio method to estimate corner frequencies and Brune-type stress drops for the 2011 Mineral, Virginia mainshock and aftershocks, as well as induced earthquakes in Oklahoma. The goal of this comparative study is to find out whether or not there are systematical differences in source parameters between tectonic earthquakes and induced earthquakes in the CEUS. I found generally much higher stress drops for the Mineral, Virginia sequence. However, the stress drops for those induced earthquakes in Oklahoma exhibit large varation among individual earthquake sequences, with the large mainshocks having high stress drops (20-30 MPa, Brune-type) except for the 2011 Mw 5.6 Prague, Oklahoma earthquake. And spatially varying stress drops indicates strong fault heterogeneity, which in the case of induced earthquakes may be influenced by the injection of fluids into the subsurface. / Ph. D.

Initial attachment to the extracellular matrix (ECM) and consequent spreading is a necessary process in the cell cycle of which little is known. Cell spreading has been well-recognized in 2D systems, however, the native fibrous ECM presents cells with 3D biophysical cues. Thus, using suspended fibers as model systems, we present the development of a novel platform (Cell-STEPs) capable of capturing cell attachment dynamics and forces from the moment a cell in suspension contacts the fiber. Cell-STEPs comprises of a custom glass-bottom petri dish with a lid to deliver a constant supply of CO2 to maintain pH. Fibrous scaffolds are attached in the dish to allow cellular investigations over extended periods of time. We find that cell-fiber attachment occurs in three progressive phases: initial attachment of cell to fiber (phase 0), rapid drop in circularity (phase 1), and increase in cell spread area (phase 2). Furthermore, using iterative inverse methods, forces involved in cell spreading through deflection of fibers were estimated. Our findings provide new insights in attachment biomechanics, including initial sensing and latching of cell to fiber with a negligible or protrusive force, followed by rapid loss in circularity through protrusion sensing at nearly constant spread area and minimal force generation, transitioning to a final phase of increased contractile forces until spread area and force saturation is observed. Also, anisotropic spreading of cells on single and two-fibers are closely related, while cells attached to several fibers take longer and spread isotropically. The Cell-STEPs platform allows, for the first time, detailed interrogations in the discrete and orchestrated adhesion steps involved in cell-fibrous matrix recognition and attachment along with simultaneous measurements of forces involved in cell attachment. / Master of Science

No / The purpose of this study was to ascertain whether or not spreading depression (CSD) propagates symmetrically along the anteroposterior axis of the cortex of mice, and to determine where CSD should be elicited to achieve a uniform exposure of the cortex to this phenomenon. Experiments were performed in halothane-anesthetized mice, with three different locations aligned 1.5 mm from the midline used for either KCl elicitation of CSD or the recording of its propagation. Our results demonstrated that, at least in the mouse cortex, CSD propagated much more effectively from posterior to anterior regions than in the opposite direction. This feature was due to a different efficacy of propagation in the two opposite directions, and not to a reduced susceptibility of occipital regions to CSD elicitation. Heterogeneous CSD propagation constitutes a potential pitfall for neurochemical studies of post-CSD changes in mice, as brain tissue samples collected for this purpose should be uniformly exposed to CSD. Occipital sites for CSD induction are clearly optimal for this purpose. If CSD propagation is confirmed to be more effective from posterior to anterior regions in other species, this may be relevant to the pathophysiology of classical migraine because the most frequent aura symptoms (i.e., visual disturbances) originate in the occipital cortex.

No / Two different theories of migraine aura exist: In the vascular theory of Wolff, intracerebral vasoconstriction causes migraine aura via energy deficiency, whereas in the neuronal theory of Leão and Morison, spreading depression (SD) initiates the aura. Recently, it has been shown that the cerebrovascular constrictor endothelin-1 (ET-1) elicits SD when applied to the cortical surface, a finding that could provide a bridge between the vascular and the neuronal theories of migraine aura. Several arguments support the notion that ET-1¿induced SD results from local vasoconstriction, but definite proof is missing. If ET-1 induces SD via vasoconstriction/ischemia, then neuronal damage is likely to occur, contrasting with the fact that SD in the otherwise normal cortex is not associated with any lesion. To test this hypothesis, we have performed a comprehensive histologic study of the effects of ET-1 when applied topically to the cerebral cortex of halothane-anesthetized rats. Our assessment included histologic stainings and immunohistochemistry for glial fibrillary acidic protein, heat shock protein 70, and transferase dUTP nick-end labeling assay. During ET-1 application, we recorded (i) subarachnoid direct current (DC) electroencephalogram, (ii) local cerebral blood flow by laser-Doppler flowmetry, and (iii) changes of oxyhemoglobin and deoxyhemoglobin by spectroscopy. At an ET-1 concentration of 1 µM, at which only 6 of 12 animals generated SD, a microarea with selective neuronal death was found only in those animals demonstrating SD. In another five selected animals, which had not shown SD in response to ET-1, SD was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment also resulted in a microarea of neuronal damage. In contrast, SD invading from outside did not induce neuronal damage in the absence of ET-1 (n = 4) or in the presence of ET-1 if ET-1 was coapplied with BQ-123, an ETA receptor antagonist (n = 4). In conclusion, SD in presence of ET-1 induced a microarea of selective neuronal necrosis no matter where the SD originated. This effect of ET-1 appears to be mediated by the ETA receptor.

Spreading depression (SD) is a slow propagating wave of depolarization that can spread throughout the cortex in the event of brain injury or any general energy failure of the brain. Massive cellular depolarization causes enormous ionic and water shifts and silences synaptic transmission in the affected tissue. Large amounts of energy are required to restore ionic gradients and are not always met. When these energetic demands are not met, brain tissue damage can occur. The exact mechanism behind initiation and propagation of SD are unknown, but a general model is known. It may be possible to prevent or delay the onset of SD using non-invasive electromagnetic techniques. Transcranial magnetic stimulation (TMS), electrical stimulation (ES), and transcranial direct coupled stimulation (tDCS) could be used to decrease neuronal excitability in different ways. In theory, any technique that can reduce cortical excitability could suppress SD initiating or propagating.