184 research outputs found

    New constrains on the thickness of the Semail Ophiolite in the Northern Emirates

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    Near-critical angle and refraction studies were performed at IFP as piggyback studies during a wider programme of crustal imagery operated by WesternGeco on behalf of the Ministry of Energy of the United Arab Emirates. The main objective is to illuminate the base of the Semail Ophiolite along part of a regional transect (D1) crossing the Northern Emirates from the Gulf of Oman in the east up to the Arabian Gulf in the west. Results confirm that the sole thrust of the ophiolite has been folded during the Miocene stacking of the underlying Arabian Platform. The thickness of the ophiolite grades from zero in the core of the Masafi tectonic window, up to a maximum of 1.7 km below the axial part of a successor basin which has been preserved on top of the serpentinite west of the current exposure of the main ultramafic bodies. Apatite grains extracted from plagiogranites of the Semail ophiolite also provide evidences for an early unroofing of the gabbros and plagiogranites during the Late Cretaceous, with cooling ages of 72-76 Ma at the top of the ophiolite in the east (not far from the Fujairah coast line), which are coeval and also consistent with the occurrence of Late Cretaceous paleo-soils, rudists and paleo-reef deposits on top of serpentinized ultramafics in the west. Younger cooling ages of 20 Ma have been also found at the base of the ophiolite near Masafi, in the core of the nappe anticline, thus providing a Neogene age for the refolding of the allochthon and stacking of underlying parautochthonous platform carbonate units. These results, together with the occurrence of a thick sedimentary pile illuminated below the metamorphic sole along the north-trending, strike-profile D2 running parallel to the axis of the Masafi window, should stimulate a renewal of the exploration in the central part of the Emirate foothills, where the ophiolite thickness is currently limited, and was already drastically reduced by the end of its Late Cretaceous obduction. © 2010 Saudi Society for Geosciences

    Nonclassic lipoid congenital adrenal hyperplasia masquerading as familial glucocorticoid deficiency

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    Context: Familial glucocorticoid deficiency (FGD) is an autosomal recessive disorder resulting from resistance to the action of ACTH on the adrenal cortex. Affected individuals are deficient in cortisol and, if untreated, are likely to succumb to hypoglycemia and/or overwhelming infection. Mutations of the ACTH receptor (MC2R) and the melanocortin 2 receptor accessory protein (MRAP), FGD types 1 and 2 respectively, account for approximately 45% of cases. Objective: A locus on chromosome 8 has previously been linked to the disease in three families, but no underlying gene defect has to date been identified. Design: The study design comprised single-nucleotide polymorphism genotyping and mutation detection. Setting: The study was conducted at secondary and tertiary referral centers. Patients: Eighty probands from families referred for investigation of the genetic cause of FGD participated in the study. Interventions: There were no interventions. Results: Analysis by single-nucleotide polymorphism array of the genotype of one individual with FGD previously linked to chromosome 8 revealed a large region of homozygosity encompassing the steroidogenic acute regulatory protein gene, STAR. We identified homozygous STAR mutations in this patient and his affected siblings. Screening of our total FGD patient cohort revealed homozygous STAR mutations in a further nine individuals from four other families. Conclusions: Mutations in STAR usually cause lipoid congenital adrenal hyperplasia, a disorder characterized by both gonadal and adrenal steroid deficiency. Our results demonstrate that certain mutations in STAR (R192C and the previously reported R188C) can present with a phenotype indistinguishable from that seen in FGD

    Relacion Entre La Densidad Óptima Agronomica Y El Número De Granos Por Planta En Maíz (Zea Maysl.)

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    The density of sowing (D) is one of the main management practices that influences the yield (Y) of corn. There exists a density value in which the yield is maximum (OPD), depending on the environment, the genotype and its interaction. The objectives of this project were: i-To determine the OPD for two corn genotypes in different productive environments; ii- Analyze the relationship between the number of kernel fixed per plant (KNP) and its plant growing rate (PGR) to different environments and genotypes iii- Determine the KNP that is related to the OPD for two corn genotypes. Three experiments were carried out in different locations (L) of Córdoba (Argentina) during 2013/14, comparing 2 genotypes (G) in 2 management zones (MZ). The statistical design was random blocks, with a factorial arrangement of subdivided plots, with L, MZ and G being the primary, secondary and tertiary factors, respectively. In addition, 5 D were planted to obtain the relationships that estimate OPD, PGR, KNP and Y. The results indicate that OPD was affected by L; the relationship between PGR and KNP was not modified by the environment, but by G. The PGR coincident with the OPD was modified by the G interaction: L. The OPD the PGR was between 2.74 to 4.81 g d -1 , which were associated with the NGP that varied only between 509 and 603 grains p-1

    Characterization and genomic analyses of two newly isolated Morganella phages define distant members among Tevenvirinae and Autographivirinae subfamilies

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    Morganella morganii is a common but frequent neglected environmental opportunistic pathogen which can cause deadly nosocomial infections. The increased number of multidrug-resistant M. morganii isolates motivates the search for alternative and effective antibacterials. We have isolated two novel obligatorily lytic M. morganii bacteriophages (vB_MmoM_MP1, vB_MmoP_MP2) and characterized them with respect to specificity, morphology, genome organization and phylogenetic relationships. MP1s dsDNA genome consists of 163,095bp and encodes 271 proteins, exhibiting low DNA (10kb chromosomal inversion that encompass the baseplate assembly and head outer capsid synthesis genes when compared to other T-even bacteriophages. MP2 has a dsDNA molecule with 39,394bp and encodes 55 proteins, presenting significant genomic (70%) and proteomic identity (86%) but only to Morganella bacteriophage MmP1. MP1 and MP2 are then novel members of Tevenvirinae and Autographivirinae, respectively, but differ significantly from other tailed bacteriophages of these subfamilies to warrant proposing new genera. Both bacteriophages together could propagate in 23 of 27M. morganii clinical isolates of different origin and antibiotic resistance profiles, making them suitable for further studies on a development of bacteriophage cocktail for potential therapeutic applications.This study was supported by the Portuguese Foundation for Science and Technology (FCT) under the scope of the strategic funding of UID/BIO/04469/2013 unit, COMPETE 2020 (POCI-01-0145-FEDER-006684) and the Project PTDC/BBB-BSS/6471/2014 (POCI-01-0145-FEDER-016678). RL contributed to the genome sequencing analysis, supported by the KU Leuven GOA Grant ‘Phage Biosystems’. JP acknowledges the project R-3986 of the Herculesstichting.info:eu-repo/semantics/publishedVersio

    Chronic Consumption of Farmed Salmon Containing Persistent Organic Pollutants Causes Insulin Resistance and Obesity in Mice

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    Background: Dietary interventions are critical in the prevention of metabolic diseases. Yet, the effects of fatty fish consumption on type 2 diabetes remain unclear. The aim of this study was to investigate whether a diet containing farmed salmon prevents or contributes to insulin resistance in mice. Methodology/Principal Findings: Adult male C57BL/6J mice were fed control diet (C), a very high-fat diet without or with farmed Atlantic salmon fillet (VHF and VHF/S, respectively), and Western diet without or with farmed Atlantic salmon fillet (WD and WD/S, respectively). Other mice were fed VHF containing farmed salmon fillet with reduced concentrations of persistent organic pollutants (VHF/S-POPs). We assessed body weight gain, fat mass, insulin sensitivity, glucose tolerance, ex vivo muscle glucose uptake, performed histology and immunohistochemistry analysis, and investigated gene and protein expression. In comparison with animals fed VHF and WD, consumption of both VHF/S and WD/S exaggerated insulin resistance, visceral obesity, and glucose intolerance. In addition, the ability of insulin to stimulate Akt phosphorylation and muscle glucose uptake was impaired in mice fed farmed salmon. Relative to VHF/S-fed mice, animals fed VHF/S-POPs had less body burdens of POPs, accumulated less visceral fat, and had reduced mRNA levels of TNFa as well as macrophage infiltration in adipose tissue. VHF/S-POPs-fed mice further exhibited better insulin sensitivity and glucose tolerance than mice fed VHF/S. Conclusions/Significance: Our data indicate that intake of farmed salmon fillet contributes to several metabolic disorders linked to type 2 diabetes and obesity, and suggest a role of POPs in these deleterious effects. Overall, these findings may participate to improve nutritional strategies for the prevention and therapy of insulin resistance

    Intronic L1 Retrotransposons and Nested Genes Cause Transcriptional Interference by Inducing Intron Retention, Exonization and Cryptic Polyadenylation

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    Transcriptional interference has been recently recognized as an unexpectedly complex and mostly negative regulation of genes. Despite a relatively few studies that emerged in recent years, it has been demonstrated that a readthrough transcription derived from one gene can influence the transcription of another overlapping or nested gene. However, the molecular effects resulting from this interaction are largely unknown.Using in silico chromosome walking, we searched for prematurely terminated transcripts bearing signatures of intron retention or exonization of intronic sequence at their 3' ends upstream to human L1 retrotransposons, protein-coding and noncoding nested genes. We demonstrate that transcriptional interference induced by intronic L1s (or other repeated DNAs) and nested genes could be characterized by intron retention, forced exonization and cryptic polyadenylation. These molecular effects were revealed from the analysis of endogenous transcripts derived from different cell lines and tissues and confirmed by the expression of three minigenes in cell culture. While intron retention and exonization were comparably observed in introns upstream to L1s, forced exonization was preferentially detected in nested genes. Transcriptional interference induced by L1 or nested genes was dependent on the presence or absence of cryptic splice sites, affected the inclusion or exclusion of the upstream exon and the use of cryptic polyadenylation signals.Our results suggest that transcriptional interference induced by intronic L1s and nested genes could influence the transcription of the large number of genes in normal as well as in tumor tissues. Therefore, this type of interference could have a major impact on the regulation of the host gene expression
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