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Anisotropy of Magnetic Susceptibility (AMS) is a valid tool to investigate magma flow direction within dikes. However, geometrically inverse magnetic fabric characterized by maximum magnetic susceptibility axis (kmax) perpendicular to the dike wall may complicate the interpretation of flow trajectories. To better understand the nature of this fabric, we present a multiscale study on 19 dikes (383 samples) in the Miocene Alftafjordur volcanic system (Iceland), where 80% of the samples show a geometrically inverse magnetic fabric. We carried out (1) AMS measurements at different magnetic fields and temperatures, along with Anisotropy of Anhysteretic Remanent Magnetization (AARM) analysis; (2) hysteresis loops and FORC diagrams; (3) thin section analysis; (4) structural fieldwork. A variable Ti‐content (0.1 < x < 0.6, Fe3‐xTixO4) titanomagnetite is the main magnetic carrier, and the contribution of the paramagnetic elongated crystals to the magnetic fabric is negligible. Single domain is not the prevailing domain state of the magnetic particles, suggesting that its occurrence cannot be the main cause for the inverse fabric. AMS analysis at different fields and temperatures along with AARM allow us to exclude any mineral phase change of the titanomagnetite across the dike. Nevertheless, kmax is parallel to a diffuse horizontal column‐like fracture pattern perpendicularly oriented with respect to the dike strike. This suggests that the Ti‐magnetite mineral orientation during dike cooling was affected by the fracture network progressively developing columnar basalts. This study demonstrates that the interpretation of AMS data on old and deep volcanic bodies is not straightforward and observations at different scales are required. Key Points: Our analyses about the magnetic fabric of the Alftafjordur dike swarm revealed that most of the samples show an inverse magnetic fabricThe origin of the inverse magnetic fabric is associated with the development of horizontal fractures during the cooling stage of dikesIt is not straightforward to infer the magma flow direction on deep and old exhumed dikes by using standard low‐field AMS measurements only [ABSTRACT FROM AUTHOR]

Understanding the mechanisms of shallow magma storage (less than ~10‐km depth) is crucial to defining volcanic plumbing systems and their effect on volcano unrest. Sills are common structures to emplace shallow magma. Many factors may control sill emplacement, but their relative importance has not been evaluated so far. To define a hierarchy among a selection of the proposed factors, we performed analogue models by injecting water at constant flux (magma analogue) within gelatin (crust analogue), investigating the effects of: interface strength and rigidity contrast between layers, density layering, ratio of layer thickness, compressive stresses, magma flow rate, and buoyancy pressure. Our results show that a strong rigidity contrast (i.e., a stiff layer overlying a weak one) and a higher buoyancy pressure are necessary and sufficient conditions for sill emplacement. Low rigidity contrasts require other contributions (weak interface and compressive stress) to develop sills; however, without rigidity contrast sill formation is always inhibited. These experiments suggest that sill emplacement is primarily controlled by rigidity contrasts and magma buoyancy pressure; the second‐order parameters are lateral compression and weak interfaces; the third‐order parameters are the ratio of layer thicknesses, magma flow rate, and density layering. These results are in agreement with field observations in Iceland, Tenerife, Utah, and La Réunion, supporting our proposed hierarchy. Key Points: Understanding what controls a dike to sill rotation is important to improve our knowledge on magma storage in the upper crustWe have defined a hierarchy among selected parameters controlling sill emplacement to understanding shallow magma transferAnalogue models show that high rigidity contrast and magma buoyancy pressure are necessary and sufficient conditions for sill emplacement [ABSTRACT FROM AUTHOR]

Abstract: Volcanic eruptions are usually fed by dikes. Understanding how crustal inhomogeneities and topographic loads control the direction (lateral/vertical) and extent (propagation/arrest) of dikes is crucial to forecast the opening of a vent. Many factors, including buoyancy, crustal layering, and topography, may control the vertical or lateral propagation of a dike. To define a hierarchy between these factors, we have conducted analogue models, injecting water (magma analogue) within gelatin (crust analogue). We investigate the effect of crustal layering (both rigidity and density layering), topography, magma inflow rate, and the density ratio between host rock and magma. Based on the experimental observations and scaling considerations, we suggest that rigidity layering (a stiffer layer overlying a weaker one) and topographic gradient favor predominantly lateral dike propagation; inflow rate, density layering, and density ratio play a subordinate role. Conversely, a softer layer overlying a stiffer one favors vertical propagation. Our results highlight the higher efficiency of a stiff layer in driving lateral dike propagation and/or inhibiting vertical propagation with respect to the Level of Neutral Buoyancy proposed by previous studies. [ABSTRACT FROM AUTHOR]

The low-density lipoprotein receptor-related protein 1 ( LRP1) is an ubiquitously expressed endocytic receptor that, among its several functions, is involved in the catabolism of coagulation factor VIII ( FVIII) and in the regulation of its plasma concentrations. Although LRP1/ CD91 polymorphisms have been associated with increased FVIII levels and a consequent thrombotic risk, no data are available on LRP1/ CD91 expression in patients with inherited FVIII deficiency. With the aim of elucidating this issue, 45 consecutive patients with haemophilia A ( HA) (18 severe, 5 moderate and 22 mild HA) were enrolled in this cross-sectional, single-centre survey. The LRP1/ CD91 mean fluorescence intensity ( MFI) in monocytes from HA patients was significantly higher than that detected in 90 healthy blood donors (105 vs. 67, P < 0.001). This over-expression was independent of hepatitis C virus infection status and varied according to the severity of the haemophilia, being higher in patients with more severe FVIII deficiency. In conclusion, our study documents for the first time that LRP1/ CD91 is over-expressed on monocytes from HA patients, with the intensity of expression varying according to the severity of the FVIII deficiency. Further studies are needed to assess the clinical implications of these findings. [ABSTRACT FROM AUTHOR]

The author examines the role of reactive oxygen species (ROS)-producing enzyme, Nox4, in tumor progression and angiogenesis. The author explains the process of angiogenesis, the process in which tumors become hypoxic and the composition of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complexes and how they affect tumor progression of slow-growing tumors.

OBJECTIVE: Systemic sclerosis (SSc) is a disorder characterized by vascular damage and fibrosis of the skin and internal organs. Despite marked tissue hypoxia, there is no evidence of compensatory angiogenesis. The ability of mesenchymal stem cells (MSCs) to differentiate into endothelial cells was recently demonstrated. The aim of this study was to determine whether impaired differentiation of MSCs into endothelial cells in SSc might contribute to disease pathogenesis by decreasing endothelial repair. METHODS: MSCs obtained from 7 SSc patients and 15 healthy controls were characterized. The number of colony-forming unit-fibroblastoid colonies was determined. After culture in endothelial-specific medium, the endothelial-like MSC (EL-MSC) phenotype was assessed according to the surface expression of vascular endothelial growth factor receptors (VEGFRs). Senescence, chemoinvasion, and capillary morphogenesis studies were also performed. RESULTS: MSCs from SSc patients displayed the same phenotype and clonogenic activity as those from controls. In SSc MSCs, a decreased percentage of VEGFR-2+, CXCR4+, VEGFR-2+/CXCR4+ cells and early senescence was detected. After culturing, SSc EL-MSCs showed increased expression of VEGFR-1, VEGFR-2, and CXCR4, did not express CD31 or annexin V, and showed significantly decreased migration after specific stimuli. Moreover, the addition of VEGF and stromal cell-derived factor 1 to cultured SSc EL-MSCs increased their angiogenic potential less than that in controls. CONCLUSION: Our data strongly suggest that endothelial repair may be affected in SSc. The possibility that endothelial progenitor cells could be used to increase vessel growth in chronic ischemic tissues may open up new avenues in the treatment of vascular damage caused by SSc. [ABSTRACT FROM AUTHOR]