scholarly journals Corrigendum to “On the Role of Thermal Stresses during Hydraulic Stimulation of Geothermal Reservoirs”

Geofluids ◽  
2017 ◽  
Vol 2017 ◽  
pp. 1-1
Author(s):  
Gunnar Jansen ◽  
Stephen A. Miller
Keyword(s):  
Thermal Stresses ◽  
Hydraulic Stimulation ◽  
Geothermal Reservoirs ◽  
Stimulation Of

scholarly journals Fault slip in hydraulic stimulation of geothermal reservoirs: Governing mechanisms and process-structure interaction

2020 ◽  
Vol 39 (12) ◽  
pp. 893-900
Author(s):  
Inga Berre ◽  
Ivar Stefansson ◽  
Eirik Keilegavlen
Keyword(s):  
Fault Reactivation ◽  
Fluid Injection ◽  
Hydraulic Stimulation ◽  
Structure Interaction ◽  
Geothermal Reservoirs ◽  
Biot Coefficient ◽  
Matrix Permeability ◽  
Stress Changes ◽  
Process Structure ◽  
Stimulation Of

Hydraulic stimulation of geothermal reservoirs in low-permeability basement and crystalline igneous rock can enhance permeability by reactivation and shear dilation of existing fractures. The process is characterized by interaction between fluid flow, deformation, and the fractured structure of the formation. The flow is highly affected by the fracture network, which in turn is deformed because of hydromechanical stress changes caused by the fluid injection. This process-structure interaction is decisive for the outcome of hydraulic stimulation, and, in analysis of governing mechanisms, physics-based modeling has potential to complement field and experimental data. Here, we show how recently developed simulation technology is a valuable tool to understand governing mechanisms of hydromechanical coupled processes and the reactivation and deformation of faults. The methodology fully couples flow in faults and matrix with poroelastic matrix deformation and a contact mechanics model for the faults, including dilation because of slip. Key elements are high aspect ratios of faults and strong nonlinearities in highly coupled governing equations. Example simulations using our open-source software illustrate direct and indirect hydraulic fault reactivation and corresponding permeability enhancement. We investigate the effect of the fault and matrix permeability and the Biot coefficient. A higher matrix permeability leads to more leakage from a permeable fault and thus suppresses reactivation and slip of the fault compared to the case with a lower matrix permeability. If a fault is a barrier to flow, increase of pressure because of the fluid injection results in stabilization of the fault; the situation is opposite if the fault is highly permeable compared to the matrix. For the given setup, lowering the Biot coefficient results in more slip than the base case. While conceptually simple, the examples illustrate the strong hydromechanical couplings and the prospects of physics-based numerical models in investigating the dynamics.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

scholarly journals The Role of BMP Signaling in Osteoclast Regulation

2021 ◽  
Vol 9 (3) ◽  
pp. 24
Author(s):  
Brian Heubel ◽  
Anja Nohe
Keyword(s):  
Bone Formation ◽  
Bone Morphogenetic Proteins ◽  
Bone Diseases ◽  
Bmp Signaling ◽  
Bone Homeostasis ◽  
Direct Stimulation ◽  
Federal Drug Administration ◽  
Bmp Pathway ◽  
Stimulation Of

The osteogenic effects of Bone Morphogenetic Proteins (BMPs) were delineated in 1965 when Urist et al. showed that BMPs could induce ectopic bone formation. In subsequent decades, the effects of BMPs on bone formation and maintenance were established. BMPs induce proliferation in osteoprogenitor cells and increase mineralization activity in osteoblasts. The role of BMPs in bone homeostasis and repair led to the approval of BMP2 by the Federal Drug Administration (FDA) for anterior lumbar interbody fusion (ALIF) to increase the bone formation in the treated area. However, the use of BMP2 for treatment of degenerative bone diseases such as osteoporosis is still uncertain as patients treated with BMP2 results in the stimulation of not only osteoblast mineralization, but also osteoclast absorption, leading to early bone graft subsidence. The increase in absorption activity is the result of direct stimulation of osteoclasts by BMP2 working synergistically with the RANK signaling pathway. The dual effect of BMPs on bone resorption and mineralization highlights the essential role of BMP-signaling in bone homeostasis, making it a putative therapeutic target for diseases like osteoporosis. Before the BMP pathway can be utilized in the treatment of osteoporosis a better understanding of how BMP-signaling regulates osteoclasts must be established.

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