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The karstification process causes mineral dissolution and mechanical removal of carbonate rocks, creating multiscale secondary porosity that greatly affects the development of karst reservoirs. The carbonate rock weathering is mainly nucleated from fractures and bedding planes and spreads out for large areas, forming a ghost-rock karst system divided by different weathering intensities. Locally, where the hydrodynamic conditions are high total removal of the weathered rock lead to the rise of the cave network and eventually the collapse or subsidence of dolines and other karst landforms. This case study presents the use of 2D and 3D GPR data to map karst levels and features in depth of a karst system in the semiarid region of NE Brazil. Synthetic GPR data and direct observation on doline crack walls support the division of karst units into ghost-rock, alterite, and residual soil zones, marked by low-amplitude reflections, and fresh to slightly weathered bedrock, indicated by vertical high-amplitude GPR zones. High-resolution aerial images and digital elevation model provide the surface geometry and distribution of karst landforms, controlled by an orthogonal weathering/fracture system identified in the GPR profiles and time slices. In addition, the karst system was vertically divided into four zones and the area of occurrence of karst units in each zone was estimated. Pore space was then calculated for each zone, assuming porosities to the filling material. We analyzed the estimated pore space distribution compared with a gas-bearing karst reservoir in China. [ABSTRACT FROM AUTHOR]

The increasing population of defects in strained austenite not only increases the heterogeneous nucleation site density for pearlite transformation, but also increases the austenite free energy due to the strain. This fact leads to a reduction in the critical free energy for pearlite nucleation, which triggers pearlite formation compared with austenite transformation without straining. Besides, a significant refinement of the pearlite colony size due to hard impingement between neighboring colonies is achieved. [ABSTRACT FROM AUTHOR]

The evolution of a rifted and sheared continental margin may control the formation of marginal ridges, which are prominent morphostructural features located at the extremities of fracture zones. We investigate the Ceará Terrace, a marginal ridge located at the western limit of the Romanche Fracture Zone in the Brazilian Equatorial Margin. Our data consist of 2000 km of 2D seismic lines parallel and orthogonal to the continental equatorial margin, as well as four exploratory wells. The Ceará Terrace has an evolution similar to that of the Ivory Coast-Ghana Ridge, the corresponding conjugate end of the Romanche Fracture Zone in the western African continental margin. The Ceará Terrace surface morphology displays an asymmetric ridge; the north slope is aligned to the Romanche Fracture Zone, related to a bathymetric step at ~ 850 m. The paleo relief represents a ridge consisting of a rift sequence (Lower Cretaceous) that is similar to the Ivory Coast-Ghana Ridge. This ridge is bounded by two half-grabens to the southeast associated with the reactivation of preexisting tectonic weakness zones related to the Precambrian Transbrasiliano Lineament. This structure was buried by a drift sequence, which comprises three sedimentary units: Unit 1, shale; unit 2, limestone that interfingers with shale and sandstone; and unit 3, limestone and shale. The fossil ridge is located near a seamount associated with important Oligocene volcanic units. Both conjugate marginal ridges were formed by a Late Albian to Cenomanian transpressional event (marked by folds and tectonic uplift) and flexural uplift due to erosion and thermal exchanges with oceanic spreading centers. Differences in the amplitude of uplift are related to the thermal influences of the distinct oceanic spreading centers. Furthermore, the results indicate that the studied area is still tectonically active. [ABSTRACT FROM AUTHOR]

Background:KRAS mutation testing is required to select patients with metastatic colorectal cancer (CRC) to receive anti-epidermal growth factor receptor antibodies, but the optimal KRAS mutation test method is uncertain.Methods:We conducted a two-site comparison of two commercial KRAS mutation kits - the cobas KRAS Mutation Test and the Qiagen therascreen KRAS Kit - and Sanger sequencing. A panel of 120 CRC specimens was tested with all three methods. The agreement between the cobas test and each of the other methods was assessed. Specimens with discordant results were subjected to quantitative massively parallel pyrosequencing (MPP). DNA blends were tested to determine detection rates at 5% mutant alleles.Results:Reproducibility of the cobas test between sites was 98%. Six mutations were detected by cobas that were not detected by Sanger, and five were confirmed by MPP. The cobas test detected eight mutations which were not detected by the therascreen test, and seven were confirmed by MPP. Detection rates with 5% mutant DNA blends were 100% for the cobas and therascreen tests and 19% for Sanger.Conclusion:The cobas test was reproducible between sites, and detected several mutations that were not detected by the therascreen test or Sanger. Sanger sequencing had poor sensitivity for low levels of mutation. [ABSTRACT FROM AUTHOR]

Acquired resistance to selective FLT3 inhibitors is an emerging clinical problem in the treatment of FLT3-ITD(+) acute myeloid leukaemia (AML). The paucity of valid pre-clinical models has restricted investigations to determine the mechanism of acquired therapeutic resistance, thereby limiting the development of effective treatments. We generated selective FLT3 inhibitor-resistant cells by treating the FLT3-ITD(+) human AML cell line MOLM-13 in vitro with the FLT3-selective inhibitor MLN518, and validated the resistant phenotype in vivo and in vitro. The resistant cells, MOLM-13-RES, harboured a new D835Y tyrosine kinase domain (TKD) mutation on the FLT3-ITD(+) allele. Acquired TKD mutations, including D835Y, have recently been identified in FLT3-ITD(+) patients relapsing after treatment with the novel FLT3 inhibitor, AC220. Consistent with this clinical pattern of resistance, MOLM-13-RES cells displayed high relative resistance to AC220 and Sorafenib. Furthermore, treatment of MOLM-13-RES cells with AC220 lead to loss of the FLT3 wild-type allele and the duplication of the FLT3-ITD-D835Y allele. Our FLT3-Aurora kinase inhibitor, CCT137690, successfully inhibited growth of FLT3-ITD-D835Y cells in vitro and in vivo, suggesting that dual FLT3-Aurora inhibition may overcome selective FLT3 inhibitor resistance, in part due to inhibition of Aurora kinase, and may benefit patients with FLT3-mutated AML. [ABSTRACT FROM AUTHOR]

Acquired resistance to selective FLT3 inhibitors is an emerging clinical problem in the treatment of FLT3-ITD+ acute myeloid leukaemia (AML). The paucity of valid pre-clinical models has restricted investigations to determine the mechanism of acquired therapeutic resistance, thereby limiting the development of effective treatments. We generated selective FLT3 inhibitor-resistant cells by treating the FLT3-ITD+ human AML cell line MOLM-13 in vitro with the FLT3-selective inhibitor MLN518, and validated the resistant phenotype in vivo and in vitro. The resistant cells, MOLM-13-RES, harboured a new D835Y tyrosine kinase domain (TKD) mutation on the FLT3-ITD+ allele. Acquired TKD mutations, including D835Y, have recently been identified in FLT3-ITD+ patients relapsing after treatment with the novel FLT3 inhibitor, AC220. Consistent with this clinical pattern of resistance, MOLM-13-RES cells displayed high relative resistance to AC220 and Sorafenib. Furthermore, treatment of MOLM-13-RES cells with AC220 lead to loss of the FLT3 wild-type allele and the duplication of the FLT3-ITD-D835Y allele. Our FLT3-Aurora kinase inhibitor, CCT137690, successfully inhibited growth of FLT3-ITD-D835Y cells in vitro and in vivo, suggesting that dual FLT3-Aurora inhibition may overcome selective FLT3 inhibitor resistance, in part due to inhibition of Aurora kinase, and may benefit patients with FLT3-mutated AML. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which reports a case of reciprocal translocation, t(14;19)(q32;p13), that juxtaposes the erythropoietin receptor precursor (EPOR) at chromosomes 19p13 to the immunoglobulin heavy chain locus (IGH@) enhancer resulting in its overexpression.

A response from the author of the article "A comparison of three methods for detecting KRAS mutations in formalin-fixed colorectal cancer specimens" in the September 25, 2012 issue which analyses Kristen Reticular Activating System (KRAS) mutation is presented.