548 research outputs found

    <i>Acarinina multicamerata</i> n. sp. (Foraminifera): a new marker for the Paleocene-Eocene thermal maximum

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    During the Paleocene–Eocene thermal maximum (PETM), low to mid-latitude planktic foraminiferal assemblages were characterized by blooms of the surface-dwelling Acarinina. Among this group a new ‘excursion taxon’ is identified, Acarinina multicamerata n. sp. Previously, this taxon was lumped together with Acarinina sibaiyaensis El-Naggar. Considering that A. sibaiyaensis already occurred prior to the hyperthermal event, both in open ocean and ocean margin deposits, it is proposed that these taxa are differentiated in order to avoid taxonomic and biostratigraphic ambiguities. Acarinina multicamerata n. sp. occurred exclusively during the PETM, hence this taxon represents an excellent biostratigraphic marker of the PETM, while its common occurrence in various marine settings makes it an excellent marker of Subzone P5b or its new equivalent zone E1

    Reassessing the biostratigraphy and the paleobathymetry of the Gonfolite Lombarda Group in the Como area (northern Italy)

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    Calcareous nannofossil and foraminiferal analyses have been carried out on outcrops from the type-area of the Gonfolite Lombarda Group (Como, northern Italy). In these marine fine- to coarse-grained clastics, rapidly accumulating at the southern front of the uprising Alpine range during the Oligo-Miocene, a scarce, but reliable, sequence of calcareous nannofossil events has been observed, allowing to refine the previous age assignments. Planktonic foraminifera were found to be extremely rare and provided limited biostratigraphic information. The Villa Olmo Conglomerate and the Chiasso Formation contain the Last Occurrence (LO) of Sphenolithus distentus and the First Occurrence (FO) of Triquetrorhabdulus carinatus, which are characteristic of the nannofossil zones NP24 and NP25 (Chattian), respectively. The lower part of the Como Conglomerate was deposited during the zone NP25, whilst the upper part of the Como Conglomerate straddles the Chattian/Aquitanian boundary in zone NN1. The deposition of the Prestino Mudstones also occurred during zone NN1. However, the upper part of this formation has been dated as Burdigalian during nannofossil zone NN2. The deposition of the upper part of the Val Grande Sandstone has been assigned to the NN3 zone owing to the presence of the taxon Sphenolithus belemnos, which is restricted to NN3. The upper part of the investigated section is characterized by the deposition of the Lucino Conglomerate and its fine-grained members (Lucinasco and Lurate Caccivio Mudstones). The Lucinasco Mudstones have been dated as late Burdigalian corresponding to zone NN4, whilst the overlying Lurate Caccivio Mudstones were deposited during the Langhian part of the zone NN5, based on the presence of S. heteromorphus and the absence of H. ampliaperta. On the whole, the base and the top of the outcropping Gonfolite Lombarda Group result from our study to be younger than hitherto proposed, allowing to resolve certain previous conflicts with the few radiometric dates available for clasts from the Gonfolite Lombarda Group. The depth of deposition was upper bathyal during the Chattian and the Aquitanian and shallowed to neritic during the deposition of the Langhian Lurate Caccivio Mudstones

    Statins, fibrates, and venous thromboembolism: a meta-analysis.

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    Aims The aim is to make a systematic review of the literature to assess the effect of lipid-lowering drugs on venous thromboembolism (VTE) occurrence. Methods and results MEDLINE and EMBASE databases were searched to identify studies that evaluated the effect of lipid-lowering drugs, in particular statins and fibrates, on VTE risk until April 2009. A scoring system was used to divide studies into two quality categories. Odds ratios (ORs) and 95% confidence intervals (CIs) were then calculated and pooled using a fixed and a random-effects model. Statistical heterogeneity was evaluated through the use of I2 statistics. Three randomized controlled trials (RCTs), three cohort, and eight case\u2013control studies were included in our systematic review, for a total of 863 805 patients. Statins use significantly reduced VTE risk [OR, 0.81; 95% CI, 0.66\u20130.99, random-effect model)]. There was a very high heterogeneity among the studies (I2 > 80%). The use of fibrates was associated with a significant increase in the risk of VTE (OR, 1.58; 95% CI, 1.23\u20132.02), without heterogeneity (I2 = 0%). Data on other lipid-lowering drugs were lacking. Conclusion This meta-analysis of available literature suggests that statins may lower the risk of VTE, whereas fibrates may increase this risk. Due to several methodological limitations, this conclusion should be considered with caution, and additional, specifically designed RCTs are warranted

    Generalized Hamiltonian structures for Ermakov systems

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    We construct Poisson structures for Ermakov systems, using the Ermakov invariant as the Hamiltonian. Two classes of Poisson structures are obtained, one of them degenerate, in which case we derive the Casimir functions. In some situations, the existence of Casimir functions can give rise to superintegrable Ermakov systems. Finally, we characterize the cases where linearization of the equations of motion is possible

    Herg1 gene and HERG1 protein are overespressed in colorectal cancers and regulate cell invasion of tumor cells

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    The acquisition of the capacity to invade surrounding tissues confers a more malignant phenotype to tumor cells and is necessary for the establishment of metastases. The understanding of the molecular mechanisms underlying cell invasion in human solid tumors such as colorectal cancers could provide not only more sensitive prognostic analyses but also novel molecular targets for cancer therapy.We report in this article that K+ ion channels belonging to the HERG family are important determinants for the acquisition of an invasive phenotype in colorectal cancers. The herg1 gene and HERG1 protein are expressed in many colon cancer cell lines, and the activity of HERG channels modulates colon cancer cell invasiveness. Moreover, the amount of HERG1 protein expressed on the plasma membrane is directly related to the invasive phenotype of colon cancer cells.Finally, both the herg1 gene and HERG1 protein were expressed in a high percentage of primary human colorectal cancers, with the highest incidence occurring in metastatic cancers, whereas no expression could be detected either in normal colonic mucosa or in adenomas

    HERG potassium channels are constitutively expressed in primary human acute myeloid leukemias and regulate cell proliferation of normal and leukemic hemopoietic progenitors

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    An important target in the understanding of the pathogenesis of acute myeloid leukemias (AML) relies on deciphering the molecular features of normal and leukemic hemopoietic progenitors. In particular, the analysis of the mechanisms involved in the regulation of cell proliferation is decisive for the establishment of new targeted therapies. To gain further insight into this topic we report herein a novel approach by analyzing the role of HERG K+ channels in the regulation of hemopoietic cell proliferation. These channels, encoded by the human ether-a-go-go-related gene (herg), belong to a family of K, channels, whose role in oncogenesis has been recently demonstrated. We report here that herg is switched off in normal peripheral blood mononuclear cells (PBMNC) as well as in circulating CD34(+) cells, however, it is rapidly turned on in the latter upon induction of the mitotic cycle. Moreover, herg appears to be constitutively activated in leukemic cell lines as well as in the majority of circulating blasts from primary AML. Evidence is also provided that HERG channel activity regulates cell proliferation in stimulated CD34(+) as well as in blast cells from AML patients. These results open new perspectives on the pathogenetic role of HERG K+ channels in leukemias

    Mutations in NNT encoding nicotinamide nucleotide transhydrogenase cause familial glucocorticoid deficiency

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    This work has been supported by the Medical Research Council UK (New Investigator Research Grant G0801265 to L.A.M., Clinical Research Training Fellowship Grant G0901980 to C.R.H. and Project Grant G0700767 to P.J.K.)
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