Mesh and simulation results of multicycle dynamics of the southern San Andreas and the northern San Jacinto faults

The dataset contains the simulation results by the finite element software EQdyna and the finite element mesh of the models presented in the article Observation-constrained multicycle dynamic models of the southern San Andreas and the northern San Jacinto Faults: addressing complexity in paleoearthquake extents and recurrences with realistic 2D fault geometry by Dunyu Liu, Benchun Duan, Katherine Scharer and Doug Yule. The compressed file mesh_simulation_result.zip contains four directories. First, the directory ./mesh/ contains the finite element mesh of the models. Second, three directories ./work_vis7_fs0.5/, ./work_vis4.2_fs0.3/, and ./work_vis12_fs0.7/ contain simulation results of Models A, B, and C, respectively, in the article. The simulations are done on TERRA at Texas A&M University High Performance Research Center (https://hprc.tamu.edu/) in 2020. The simulation data are collected to reproduce the results presented in the article. The software EQdyna that is used for numerical simulations and MATLAB scripts that are used to post-process the data and to reproduce the figures in the article are provided in the GitHub repository https://zenodo.org/badge/latestdoi/416427264. In the directory ./mesh/, FE*.txt files contain general information used to generate the finite element mesh. fac.txt and vert.txt are node-element topography and coordinates of the nodes in the finite element mesh. nsmp* files are master-slave node relation by the split-node method to simulate fault discontinuity; x(1,2,3)_1.txt files are locations of controlling points for the San Jacinto fault Claremont and Clark strands, and the southern San Andreas fault geometry derived from the SCEC Community Fault Model version 5.2 (https://doi.org/10.5281/zenodo.4651667). The controlling points are used by EQdyna to generate the mesh that comply with the complex fault geometry in the models. Rate_direction.txt contains on-fault loading strain rates derived from the geodetic dataset by Smith-Konter and Sandwell (2009, doi:10.1029/2009gl037235). Plot_Normal_Vector.m and Show_Mesh.m are MATLAB scripts used to visualize the normal vectors to the fault strikes and the whole mesh, respectively. For each directory of model results, ./0figs/ contain figures to show dynamics of all rupture scenarios in that model. cyclelog.txt(No.) contain the starting and ending earthquake cycle numbers for the corresponding totalop.txt(No.), which contain results of slips and stresses on the fault after each earthquake. interval.txt(No.) contain the intervals in years between earthquakes defined in cyclelog.txt(No.)

3-Dimensional Neuroanatomy of the Human Fetal Pelvis: Anatomical Support for Partial Urogenital Mobilization in the Treatment of Urogenital Sinus

Purpose: Retrospective reviews suggest that the functional outcomes of surgery of the urogenital sinus have often been unsatisfactory and to our knowledge the long-term results of newer surgical techniques have yet to be evaluated. A precise understanding of pelvic fetal neuroanatomy is germane for optimizing surgical correction of the urogenital sinus. Materials and Methods: The pelves of 10 human female fetuses were serially sectioned. Masson\u27s trichrome staining and immunochemistry for the neuronal marker S100 (Dako Corp., Carpinteria, California) along with anatomical computer reconstruction allowed 3-dimensional analysis of the nerves in relation to the pelvic structures as an animated motion picture. Results: Two types of neuronal structures were identified. 1) A dense perivisceral foil of branching nerves closely surrounded the pelvic organs. The localization of most nerves was on the external faces of the viscera with a limited fraction in the rectovaginal and urethrovaginal septa. This innervation was from the anterior cephalad periurethral area to the posterior caudal perirectal area. 2) A significant amount of nerves surrounded the cephalad urethra on its anterior and posterior faces. Conclusions: Based on these anatomical data during surgical repair of a urogenital sinus we would advocate minimal mobilization of the lateral faces of the vagina, avoiding dissection of the proximal urethra above the pubic bone and electing a vaginal flap in severe cases. © 2008 American Urological Association

In Utero Exposure to Benzophenone-2 Causes Hypospadias Through an Estrogen Receptor Dependent Mechanism

Purpose: Additives such as benzophenone-2 are commonly used in cosmetic products and food container plastics to filter out ultraviolet light. In pregnant women exposure may result in transplacental transfer of benzophenone-2 to fetuses. Benzophenone-2 is estrogenic in vitro and in the rat uterotropic assay. Estradiol causes hypospadias in mice and estrogen-like compounds are also postulated to cause hypospadias. We determined whether hypospadias would develop in male mice exposed to benzophenone-2 in utero and whether this outcome depended on estrogen receptor pathways. Materials and Methods: Timed pregnant C57BL/6 mice were administered benzophenone-2 (6.25 mg) or control vehicle by oral gavage from gestational days 12 through 17 and they were sacrificed on day 18. Fetuses were weighed and sexed, anogenital distance was measured and genital tubercles were harvested for paraffin sections or quantitative reverse transcriptase-polymerase chain reaction analysis of genes purportedly involved in genital tubercle development. Results: Eight of 57 benzophenone-2 treated male fetuses (14%) whose genital tubercles were examined histologically had hypospadias (p = 0.0064). Co-administration of benzophenone-2 with the estrogen receptor antagonist EM-800 resulted in normal genital tubercles, ie no hypospadias, in 26 of 26 mice. Likewise no EM-800 or control treated male genital tubercles showed hypospadias. Benzophenone-2 treated male mice had no changes in body mass adjusted anogenital distance relative to controls. Reverse transcriptase-polymerase chain reaction revealed that genital tubercles of benzophenone-2 treated male mice expressed higher levels of estrogen receptor-β relative to male controls (p = 0.04). Conclusions: These findings suggest that benzophenone-2 may cause hypospadias via signaling through the estrogen receptor. Further study of human benzophenone-2 exposure and its effects is needed to support this hypothesis. © 2007 American Urological Association

Urothelial sonic hedgehog signaling plays an important role in bladder smooth muscle formation

During bladder development, primitive mesenchyme differentiates into smooth muscle (SM) under the influence of urothelium. The gene(s) responsible for this process have not been elucidated. We propose that the Sonic hedgehog (Shh) signaling pathway is critical in bladder SM formation. Herein, we examine the role of the Shh-signaling pathway during SM differentiation in the embryonic mouse bladder. Genes in the Shh pathway and SM expression in mouse embryonic (E) bladders (E12.5, 13.5, and 14.5) were examined by immunohistochemistry (IHC), in situ hybridization, and reverse transcription polymerase chain reaction (RT-PCR). To examine the effects of disrupting Shh signaling, bladder tissues were isolated at E12.5 and E14.5, that is, before and after bladder SM induction. The embryonic bladders were cultured on membranes floating on medium with and without 10 μM of cyclopamine, an Shh inhibitor. After 3 days, SM expression was examined by assessing the following: SM α-actin (SMAA), SM γ-actin (SMGA), SM-myosin heavy chain (SM-MHC), Patched, GLI1, bone morphogenic protein 4 (BMP4), and proliferating cell nuclear antigen (PCNA) by IHC and RT-PCR. SM-related genes and proteins were not expressed in E12.5 mouse embryonic bladder before SM differentiation, but were expressed by E13.5 when SM differentiation was initiated. Shh was expressed in the urothelium in E12.5 bladders. Shh-related gene expression at E12.5 was significantly higher than at E14.5. In cyclopamine-exposed cultures of E12.5 tissue, SMAA, SMGA, GLI1, and BMP4 gene expression was significantly decreased compared with controls, but PCNA gene expression did not change. In cyclopamine-exposed E14.5 cultures, SMGA and SM-MHC gene expression did not change compared with controls. Using an in vitro embryonic bladder culture model, we were able to define the kinetics of SM- and Shh-related gene expression. Cyclopamine inhibited detrusor SM actin induction, but did not inhibit SM-MHC induction. SMAA and SMGA genes appear to be induced by Shh-signaling pathways, but the SM-MHC gene is not. Based on Shh expression by urothelium and the effects of Shh inhibition on bladder SM induction, we hypothesize that urothelial-derived Shh orchestrates induction of SM in the fetal mouse bladder. © 2007, Copyright the Authors

Flow chart of study selection in the meta-analysis.

<p>Flow chart of study selection in the meta-analysis.</p

The CXCL12 G801A Polymorphism Is Associated with Cancer Risk: A Meta-Analysis

<div><p>Background</p><p>CXCL12 is a small chemotactic cytokine belonging to the CXC chemokine family expressed in various organs. It contributes to the migration, invasion and angiogenesis of cancer cells. Recently, the CXCL12 G801A polymorphism was shown to be associated with an increased risk of various kinds of cancers, but the results were too inconsistent to be conclusive.</p><p>Methods</p><p>To solve the problem of inadequate statistical power and conflicting results, a meta-analysis of published case-control studies was performed, including 4,435 cancer cases and 6,898 controls. Odds ratios (ORs) and their 95% confidence intervals (CIs) were used to determine the strength of association between CXCL12 G801A polymorphism and cancer risk.</p><p>Results</p><p>A significant association between CXCL12 G801A polymorphism and cancer risk was found under all genetic models. Further, subgroup analysis stratified by ethnicity suggested a significant association between CXCL12 G801A polymorphism and cancer risk in the Asian subgroup under all genetic models. However, in the Caucasian subgroup, a significant association was only found under an additive genetic model and a dominant genetic model. The analysis stratified by cancer type found that CXCL12 G801A polymorphism may increase the risk of breast cancer, lung cancer, and “other” cancers. Based on subgroup stratified by source of controls, a significant association was observed in hospital-based studies under all genetic models.</p><p>Conclusions</p><p>The CXCL12 G801A polymorphism is associated with an increased risk of cancer based on current published data. In the future, large-scale well-designed studies with more information are needed to better estimate possible gene-gene or gene-environment interactions.</p></div

Funnel plot for studies of the association of CXCL12 G801A polymorphism and cancer risk under a dominant genetic model (GA+AA vs. GG).

<p>Funnel plot for studies of the association of CXCL12 G801A polymorphism and cancer risk under a dominant genetic model (GA+AA vs. GG).</p