232 research outputs found

    Production of annual ryegrass with different doses of nitrogen fertilization in topdressing.

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    Made available in DSpace on 2019-12-30T18:10:48Z (GMT). No. of bitstreams: 1 SeminaCiAgMittelmannProduction.pdf: 363245 bytes, checksum: 39152185b5b3d0a8133d04e3c3e2af64 (MD5) Previous issue date: 2019bitstream/item/207926/1/SeminaCiAg-Mittelmann-Production.pd

    Acral necrosis by Stenotrophomonas maltophilia

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    Keywords:necrosis;skin and soft tissue infection;Stenotrophomonas maltophilia Abstract Background Stenotrophomonas maltophilia (SM) has been considered a nosocomial pathogen. Nevertheless, community acquired infection may occur more frequently than usually recognized. Case We describe distal necrosis of the fingers by SM in a farmer, contracted in the community and successfully treated with a combination of cotrimoxazole and ciprofloxacin. The patient was diagnosed with chronic lymphocytic leukaemia 6 months later. Conclusions This unusual presentation shows that infection with SM should be included in the differential diagnosis of the skin and soft tissue infection, even in apparently healthy patients

    Good practices for a literature survey are not followed by authors while preparing scientific manuscripts

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    The number of citations received by authors in scientific journals has become a major parameter to assess individual researchers and the journals themselves through the impact factor. A fair assessment therefore requires that the criteria for selecting references in a given manuscript should be unbiased with respect to the authors or the journals cited. In this paper, we advocate that authors should follow two mandatory principles to select papers (later reflected in the list of references) while studying the literature for a given research: i) consider similarity of content with the topics investigated, lest very related work should be reproduced or ignored; ii) perform a systematic search over the network of citations including seminal or very related papers. We use formalisms of complex networks for two datasets of papers from the arXiv repository to show that neither of these two criteria is fulfilled in practice

    Functional Characterization of MODY2 Mutations Highlights the Importance of the Fine-Tuning of Glucokinase and Its Role in Glucose Sensing

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    Glucokinase (GK) acts as a glucose sensor in the pancreatic beta-cell and regulates insulin secretion. Heterozygous mutations in the human GK-encoding GCK gene that reduce the activity index increase the glucose-stimulated insulin secretion threshold and cause familial, mild fasting hyperglycaemia, also known as Maturity Onset Diabetes of the Young type 2 (MODY2). Here we describe the biochemical characterization of five missense GK mutations: p.Ile130Thr, p.Asp205His, p.Gly223Ser, p.His416Arg and p.Ala449Thr. The enzymatic analysis of the corresponding bacterially expressed GST-GK mutant proteins show that all of them impair the kinetic characteristics of the enzyme. In keeping with their position within the protein, mutations p.Ile130Thr, p.Asp205His, p.Gly223Ser, and p.His416Arg strongly decrease the activity index of GK, affecting to one or more kinetic parameters. In contrast, the p.Ala449Thr mutation, which is located in the allosteric activator site, does not affect significantly the activity index of GK, but dramatically modifies the main kinetic parameters responsible for the function of this enzyme as a glucose sensor. The reduced Kcat of the mutant (3.21±0.28 s−1 vs 47.86±2.78 s−1) is balanced by an increased glucose affinity (S0.5 = 1.33±0.08 mM vs 7.86±0.09 mM) and loss of cooperativity for this substrate. We further studied the mechanism by which this mutation impaired GK kinetics by measuring the differential effects of several competitive inhibitors and one allosteric activator on the mutant protein. Our results suggest that this mutation alters the equilibrium between the conformational states of glucokinase and highlights the importance of the fine-tuning of GK and its role in glucose sensing

    Highly frequent PIK3CA amplification is associated with poor prognosis in gastric cancer

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    <p>Abstract</p> <p>Background</p> <p>The phosphoinositide 3-kinase (PI3K)/Akt pathway plays a fundamental role in cell proliferation and survival in human tumorigenesis, including gastric cancer. <it>PIK3CA </it>mutations and amplification are two major causes of overactivation of this pathway in human cancers. However, until this work, there was no sound investigation on the association of <it>PIK3CA </it>mutations and amplification with clinical outcome in gastric cancer, particularly the latter.</p> <p>Methods</p> <p>Using direct sequencing and real-time quantitative PCR, we examined <it>PIK3CA </it>mutations and amplification, and their association with clinicopathological characteristics and clinical outcome of gastric cancer patients.</p> <p>Results</p> <p><it>PIK3CA </it>mutations and amplification were found in 8/113 (7.1%) and 88/131 (67%) gastric cancer patients, respectively. <it>PIK3CA </it>amplification was closely associated with increased phosphorylated Akt (p-Akt) level. No relationship was found between <it>PIK3CA </it>mutations and clinicopathological characteristics and clinical outcome in gastric cancer. <it>PIK3CA </it>amplification was significantly positively associated with cancer-related death. Importantly, Kaplan-Meier survival curves revealed that the patients with <it>PIK3CA </it>amplification had significantly shorter survival times than the patients without <it>PIK3CA </it>amplification.</p> <p>Conclusions</p> <p>Our data showed that <it>PIK3CA </it>mutations were not common, but its amplification was very common in gastric cancer and may be a major mechanism in activating the PI3K/Akt pathway in gastric cancer. Importantly, Kaplan-Meier survival curves revealed that <it>PIK3CA </it>amplification was significantly positively associated with poor survival of gastric cancer patients. Collectively, the PI3K/Akt signaling pathway may be an effective therapeutic target in gastric cancer.</p
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