Conduit Flow Paths and Conduit/Matrix Interactions Defined by Quantitative Groundwater Tracing in the Floridan Aquifer

Author(s):  
Todd R. Kincaid ◽  
Christopher L. Werner
2016 ◽  
Vol 6 (3) ◽  
pp. 119 ◽  
Author(s):  
Nara Somaratne ◽  
Simon Mann

<p class="1Body">An integrated approach combining lithological logs, downhole geophysics, electromagnetic survey and the distribution of radiocarbon (<sup>14</sup>C) and the stable isotopes of water molecules (<sup>18</sup>O) were used to identify the conduit flow paths of a small freshwater lens. Lost circulation zones, where drilling fluid flows into geological formation instead returning up the annulus recorded during water well drilling, were considered as the major fracture zones. The presence of high porosity zones within boreholes were identified using caliper, gamma and neutron logs. These methods were used to identify the depth intervals at which cavities and the existence of conduit porosity within the boreholes. Transient electromagnetic (TEM) method was used to investigate resistivity anomalies in the profiles along nine pre-determined lines across the freshwater lens. Resistivity anomalies were related to borehole information and other surface features such as sinkholes. Low resistivity zones of the TEM tomography sections had excellent correlation to fracture zones identified during well drilling, and downhole geophysical logs. Similarly, high resistivity zones in the profiles correlate well with the zones of cemented or recrystallized limestone identified from the lithological logs. The interpreted resistivity anomaly accurately depicts depth to watertable at 15-18 m, presence of main fracture zone at 20-25 m, presence of possible conduits flow paths and the cemented or recrystallized limestone below 35 m depth. The <sup>14</sup>C, <sup>13</sup>C and <sup>18</sup>O signatures of the groundwater confirm the presence of conduits and potential pathways of preferential flows. This investigation illustrates the effectiveness using an integrated approach to trace the conduit flow paths in karst aquifers. The information gained from the study is currently being used for the management of the freshwater lens.</p>


Author(s):  
Marc Lenburg ◽  
Rulang Jiang ◽  
Lengya Cheng ◽  
Laura Grabel

We are interested in defining the cell-cell and cell-matrix interactions that help direct the differentiation of extraembryonic endoderm in the peri-implantation mouse embryo. At the blastocyst stage the mouse embryo consists of an outer layer of trophectoderm surrounding the fluid-filled blastocoel cavity and an eccentrically located inner cell mass. On the free surface of the inner cell mass, facing the blastocoel cavity, a layer of primitive endoderm forms. Primitive endoderm then generates two distinct cell types; parietal endoderm (PE) which migrates along the inner surface of the trophectoderm and secretes large amounts of basement membrane components as well as tissue-type plasminogen activator (tPA), and visceral endoderm (VE), a columnar epithelial layer characterized by tight junctions, microvilli, and the synthesis and secretion of α-fetoprotein. As these events occur after implantation, we have turned to the F9 teratocarcinoma system as an in vitro model for examining the differentiation of these cell types. When F9 cells are treated in monolayer with retinoic acid plus cyclic-AMP, they differentiate into PE. In contrast, when F9 cells are treated in suspension with retinoic acid, they form embryoid bodies (EBs) which consist of an outer layer of VE and an inner core of undifferentiated stem cells. In addition, we have established that when VE containing embryoid bodies are plated on a fibronectin coated substrate, PE migrates onto the matrix and this interaction is inhibited by RGDS as well as antibodies directed against the β1 integrin subunit. This transition is accompanied by a significant increase in the level of tPA in the PE cells. Thus, the outgrowth system provides a spatially appropriate model for studying the differentiation and migration of PE from a VE precursor.


1997 ◽  
Vol 27 (1) ◽  
pp. 22-27
Author(s):  
K. GOLDRING ◽  
J. A. WARNER

1968 ◽  
Vol 115 (3) ◽  
pp. 376 ◽  
Author(s):  
B.R. Myers ◽  
B.R. Myers ◽  
E.A. Davila
Keyword(s):  

2008 ◽  
Vol 31 (4) ◽  
pp. 23
Author(s):  
Rachel Vanderlaan ◽  
Rod Hardy ◽  
Golam Kabir ◽  
Peter Back ◽  
A J Pawson

Background: ShcA, a scaffolding protein, generates signalspecificity by docking to activated tyrosine kinases through distinct phosphotyrosine recognition motifs, while mediating signal complexity through formation of diverse downstream phosphotyrosine complexes. Mammalian ShcA encodes 3 isoforms having a modular architecture of a PTB domain and SH2 domain, separated by a CH1 region containing tyrosine phosphorylation sites important in Ras-MAPK activation. Objective and Methods: ShcA has a necessary role in cardiovascular development^1,2. However, the role of ShcA in the adult myocardium is largely unknown, also unclear, is how ShcA uses its signaling modules to mediate downstream signaling. To this end, cre/loxP technology was employed to generate a conditional ShcA allele series. The myocardial specific ShcA KO (ShcA CKO) and myocardial restricted domain mutant KI mice were generated using cre expressed from the mlc2v locus^3 coupled with the ShcA floxed allele and in combination with the individual ShcA domain mutant KI alleles^2. Results: ShcACKO mice develop a dilated cardiomyopathy phenotype by 3 months of life, typified by depressed cardiac function and enlarged chamber dimensions. Isolated cardiomyocytes from ShcA CKO mice have preserved contractility indicating an uncoupling between global heart function and single myocyte contractile mechanics. Force-length experiments suggest that the loss of shcAmediates the uncoupling through deregulation of extracellular matrix interactions. Subsequent, analysis of the ShcA myocardial restricted domain mutant KImice suggests that ShcA requires PTB domain docking to upstream tyrosine kinases and subsequent phosphorylation of the CH1 tyrosines important for downstream signaling. Conclusion: ShcA is required for proper maintenance of cardiac function, possibly regulation of extracellular matrix interactions. References: 1. Lai KV, Pawson AJ. The ShcA phosphotyrosine docking protein sensitizescardiovascular signaling in the mouse embryo. Genes and Dev 2000;14:1132-45. 2. Hardy WR. et al. Combinatorial ShcA docking interactions supportdiversity in tissue morphogenesis. Science2007;317:251-6. 3.Minamisawa, s. et al. A post-transcriptional compensatory pathway inheterozygous ventricular myosin light chain 2-deficient mice results in lack ofgene dosage effect during normal cardiac growth or hypertrophy. J Biol Chem 1999;274:10066-70.


1999 ◽  
Author(s):  
Ed O'Keefe ◽  
Matt Berge

1995 ◽  
Vol 50 (4) ◽  
pp. 551-571 ◽  
Author(s):  
G. Mensitieri ◽  
M. A. Del Nobile ◽  
A. Apicella ◽  
L. Nicolais

Stratigraphy ◽  
2019 ◽  
Vol 16 (1) ◽  
pp. 41-62
Author(s):  
Jean M. Self-Trail ◽  
Mercer Parker ◽  
John T. Haynes ◽  
Arthur P. Schultz ◽  
Paul F. Huddleston

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