Teacher enthusiasm: a potential cure of academic cheating

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The role of pargasitic amphibole in the formation of major geophysical discontinuities in the shallow upper mantle

Several explanations have been proposed for variation in geophysical properties and depths to the lithosphere-asthenosphere boundary (LAB) and mid-lithospheric discontinuities (MLD). Here we investigate the proposal that the dehydration solidus of pargasitic amphibole-bearing upper mantle with very low bulk water (hundreds ppm) may be one of the main reasons for the observed geophysical anomalies. The pargasite dehydration solidus may be associated with a very small degree of partial melting in the upper mantle at temperatures and pressures in excess of 1050 °C (for geochemically more depleted) or 1100 °C (for geochemically more fertile upper mantle) and from 1 to 3 GPa (~ 30 to 90 km) respectively. This small amount of partial melt may be responsible for changes in geophysical properties (e.g. lower seismic velocity, higher attenuation of seismic waves, higher electrical conductivity) in association with the LAB and MLD. This simple petrologic model is tested on the abundant geophysical data of the Carpathian-Pannonian region (CPR), central Europe. The high resolution heat flow data available in the CPR allows us to estimate the depths to intersection of area specific depth-temperature curves with the dehydration solidus temperatures (1050 and 1100 °C isotherms). There is relatively small mismatch (< 5 km) between the position of these intersections and the geophysically determined LAB in the central area of the CPR. These observations lend support for the proposition that the dehydration solidus may be largely responsible for depth variation of the LAB in young continental rift areas. Towards the margins of the CPR, however, where the heat flow is lower (< ~ 70 mW/m2), the predictive capability of the dehydration solidus model deteriorates. This is because, for lower geothermal gradients, pargasitic amphibole breaks down at ~90 km (or ~ 3 GPa) before temperature exceeds the dehydration solidus temperatures. Consequently we should expect changes in geophysical properties attributable to hydrous silicate melt at ~90 km depth in areas where surface heat flow is lower (i.e. Precambrian cratonic shields, Phanerozoic continental lithospheres or, possibly older oceanic plates). Alternatively, in these areas, the intersection of the geotherm with pargasite breakdown may correlate with the MLD rather than the LAB, which is at deeper levels. A global review is also included to assess whether: 1) the position of the dehydration solidus temperatures in the upper mantle (~1050 and 1100 °C isotherms) could explain the origin of the LAB under younger oceanic plates with higher surface heat flow; 2) there is indeed global anomalies at ~90 km depth, which are often interpreted as MLDs, in older continental areas, older oceanic crust and cratons with lower surface heat flow

Investigation of RasGRP3 expression and function in human breast cancers and breast-derived ductal adenocarcinoma cell lines

RasGRP3 is a member of the Ras guanine nucleotide releasing protein (RasGRP) family of the Ras-specific guanine nucleotide exchange factors. These proteins play role in the regulation of the activity of Ras signaling pathway which constitutive activation is demonstrated in many cancer types. The RasGRP3 protein has potential oncogenic effect, the amplification of the gen of the protein is observed in many malignant cancer types. Recent investigations have highlighted that RasGRP3 plays a role in tumorigenesis, hence it exerts effect on the proliferation, migration, survival and tumorigenecity of prostate adenocarcinoma-derived and melanoma cells. In light of this potential oncogenic effect we have examined the change of expression and potencial function of RasGRP3 in breast-derived ductal adenocarcinoma. The RasGRP3 and phosphoRasGRP3 expressions were examined in human ductal adenocarcinoma-derived samples from different grades and in 1 primary ductal adenocarcinoma-derived cell line called BT-474 and 5 different metastatic: JIMT-1, MCF7, SK-BR-3, MDA-MB-453 és T-47D cell lines both in mRNA (Q-PCR) and protein levels (Western blot; immunhisto-and cytochemistry). To explore the biological function of the protein RasGRP3 knockdown cultures were created on MCF7 and T-47D cell lines. To examine the role of RasGRP3 in the viability of cells annexin-V/PI staining was performed. To clarify the function of the protein in cell proliferation and in the developement of resistance against chemotherapeutic drugs Tamoxifen and Herceptin CyQuant assay was performed. To observe the RasGRP3 function in tumor formation and maintance SCID mouse model was used. According to our results the expression of RasGRP3 and the active phosphoRasGRP3 were elevated at protein level on the human ductal adenocarcinoma samples. This expression was increased in the tumor samples compared to the normal. RasGRP3 was found typically in the cytoplasm of the cells, while the phosphoRasGRP3 showed strong nuclear reaction. The RasGRP3 expression of the BT-474 cell line was lower then in the metastatics. The downregulation of RasGRP3 induced apoptosis, inhibited cell proliferation and sensitizied the T-47D cells to killing by Tamoxifen and Herceptin. In vivo tumor growth in mouse xenografts of both cell lines were decreased. Suppression of RasGRP3 expression inhibited downstream RasGRP3 responses AKT and ERK1/2 phosphorylation were reduced. Our results suggest the RasGRP3 may have an importante role in the regulation of cell growth, chemotherapeutic resistance, and tumor formation in breast cancer.1 page(s

A new ELISA method for the measurement of total α2-plasmin inhibitor level in human body fluids

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Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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