Origen de la casiterita detrítica en los aluviones recientes de Tirados de la Vega-Golpejas (Salamanca)

9 páginas, 6 figuras, 5 tablas.[ES] En el sector Tirados de la Vega-Golpejas han sido detectadas dos anomalías de casiterita en los aluviones del Regato de los Lentiscos y en otros existentes al sur de Tirados de la Vega. El estudio granométrico y morfométrico de éstas casiteritas. contrastado con el de la casiterita procedente del granito de Golpejas. permite asegurar que la anomalía del Regato de los Lentiscos se debe a la dispersión de la casiterita de aquel granito. mientras que la de Tirados de la Vega procede de filones estanníferos. La aplicación del análisis factoral corrobora este hecho y permite diferenciar las casiteritas que proceden de rocas graníticas de aquellas que vienen de filones estanníferos. Según esto se puede indicar que la capacidad de migración de la casiterita desde el yacimiento estannífero de Golpejas es de unos 3 Kms.[EN] Two cassiterite anomalies have been detected in the Regato de los Lentisco and Tirados de la Vega alluviums, in the Golpejas area (Salamanca). The granometric and morphometric parameters of these cassiterites have been compared with those shown by the cassiterite crystal ocurrying in the Golpejas granite. The comparison between the two groups of data allow us to conclude that the anomaly observed in the Regato de los Lentistos has been originated by the disperssion of the cassiterite from the primary deposit of Golpejas. On the contrary, the anomaly ocurring in the alloviums to the south of Tirados de la Vega shows a different origin, and is coming from stanniferous veins. The factor anylisis corroborates the differentiation mentionated above, and indicates a migration capacite of about 3 kms. from the stannifeous deposits of Golpejas for the alluvial cassiterite.Peer reviewe

Cosmology as a search for overall equilibrium

9 pages, 1 figure.-- The original publication is available at www.springerlink.com.In this letter we will revise the steps followed by A. Einstein when he first wrote on cosmology from the point of view of the general theory of relativity. We will argue that his insightful line of thought leading to the introduction of the cosmological constant in the equations of motion has only one weakness: The constancy of the cosmological term, or what is the same, its independence of the matter content of the universe. Eliminating this feature, I will propose what I see as a simple and reasonable modification of the cosmological equations of motion. The solutions of the new cosmological equations give place to a cosmological model that tries to approach the Einstein static solution. This model shows very appealing features in terms of fitting current observations.Peer reviewe

Differential Role of gp130-Dependent STAT and Ras Signalling for Haematopoiesis Following Bone-Marrow Transplantation

INTRODUCTION: Bone marrow transplantation (BMT) is a complex process regulated by different cytokines and growth factors. The pleiotropic cytokine IL-6 (Interleukin-6) and related cytokines of the same family acting on the common signal transducer gp130 are known to play a key role in bone marrow (BM) engraftment. In contrast, the exact signalling events that control IL-6/gp130-driven haematopoietic stem cell development during BMT remain unresolved. METHODS: Conditional gp130 knockout and knockin mice were used to delete gp130 expression (gp130(ΔMx)), or to selectively disrupt gp130-dependent Ras (gp130(ΔMxRas)) or STAT signalling (gp130(ΔMxSTAT)) in BM cells. BM derived from the respective strains was transplanted into irradiated wildtype hosts and repopulation of various haematopoietic lineages was monitored by flow cytometry. RESULTS: BM derived from gp130 deficient donor mice (gp130(ΔMx)) displayed a delayed engraftment, as evidenced by reduced total white blood cells (WBC), marked thrombocytopenia and anaemia in the early phase after BMT. Lineage analysis unravelled a restricted development of CD4(+) and CD8(+) T-cells, CD19(+) B-cells and CD11b(+) myeloid cells after transplantation of gp130-deficient BM grafts. To further delineate the two major gp130-induced signalling cascades, Ras-MAPK and STAT1/3-signalling respectively, we used gp130(ΔMxRas) and gp130(ΔMxSTAT) donor BM. BMT of gp130(ΔMxSTAT) cells significantly impaired engraftment of CD4(+), CD8(+), CD19(+) and CD11b(+) cells, whereas gp130(ΔMxRas) BM displayed a selective impairment in early thrombopoiesis. Importantly, gp130-STAT1/3 signalling deficiency in BM grafts severely impaired survival of transplanted mice, thus demonstrating a pivotal role for this pathway in BM graft survival and function. CONCLUSION: Our data unravel a vital function of IL-6/gp130-STAT1/3 signals for BM engraftment and haematopoiesis, as well as for host survival after transplantation. STAT1/3 and ras-dependent pathways thereby exert distinct functions on individual bone-marrow-lineages

The analysis of structural features of humic acids fractions after mechanochemical modifications

Впервые изучено влияние модифицирующего агента тиомочевины в процессе механоактивации на структурный состав и кислотно-основные свойства основных фракций гуминовых кислот -гиматомелановые и протогуминовые кислоты

Concanavalin A—induced liver cell damage: Activation of intracellular pathways triggered by tumor necrosis factor in mice☆☆☆

AbstractBackground & Aims: Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. Intracellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-κB translocation, or Jun kinase (JNK) activation. The aim of this study was to study TNF-dependent pathways after con A injection in vivo. Methods: Con A, con A plus anti-TNF, and control buffer were injected into BALB/c mice. Immunofluorescence, Western blot, Northern blot, gel shift, Erk, and JNK activity and DNA fragmentation experiments were performed at different time points after injection. Results: DNA fragmentation in hepatocytes was increased 4–24 hours after con A injection. JNK was activated maximally (>20-fold) directly after con A injection, whereas binding and nuclear translocation of NF-κB was maximal after 4 hours. All pathways were blocked by anti-TNF. JNK activation was specific because related ERK 1 + 2 were not activated after con A. High nuclear expression of c-Jun was already evident 1 hour after con A injection; however, in contrast to JNK, anti-TNF treatment did not block c-Jun nuclear expression and DNA binding. Conclusions: In the con A model, activation of TNF-dependent pathways is associated with apoptosis of hepatocytes. Their modulation in vivo may have implications to develop new therapeutic strategies to prevent apoptosis.GASTROENTEROLOGY 1998;114:1035-104

Hepatocytes Sensitized to Tumor Necrosis Factor-α Cytotoxicity Undergo Apoptosis through Caspase-dependent and Caspase-independent Pathways

Hepatocytes can be sensitized to tumor necrosis factor (TNF)-alpha toxicity by repression of NF-kappaB activation or inhibition of RNA synthesis. To determine whether both forms of sensitization lead to TNF-alpha cytotoxicity by similar mechanisms, TNF-alpha-induced cell death in RALA255-10G hepatocytes was examined following infection with an adenovirus, Ad5IkappaB, that blocks NF-kappaB activation or following cotreatment with actinomycin D (ActD). TNF-alpha treatment of Ad5IkappaB-infected cells resulted in 44% cell death within 6 h. ActD/TNF-alpha induced no death within 6 h but did lead to 37% cell death by 24 h. In both instances, cell death occurred by apoptosis and was associated with caspase activation, although caspase activation in ActD-sensitized cells was delayed. CrmA and chemical caspase inhibitors blocked Ad5IkappaB/TNF-alpha-induced cell death but did not inhibit ActD/TNF-alpha-induced apoptosis. A Fas-associated protein with death domain (FADD) dominant negative decreased Ad5IkappaB/TNF-alpha- and ActD/TNF-alpha-induced cell death by 81 and 47%, respectively. However, downstream events differed, since Ad5IkappaB/TNF-alpha but not ActD/TNF-alpha treatment caused mitochondrial cytochrome c release. These results suggest that NF-kappaB inactivation and inhibition of RNA synthesis sensitize RALA255-10G hepatocytes to TNF-alpha toxicity through distinct cell death pathways that diverge below the level of FADD. ActD-induced hepatocyte sensitization to TNF-alpha cytotoxicity occurs through a FADD-dependent, caspase-independent pathway of apoptosis