2,783 research outputs found

    Mastectomy is an over-treatment in patients with occult breast cancer

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    FINAL FAST FLUX TEST FACILITY BACKUP DESIGN DEVELOPMENT REQUIREMENT REPORT.

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    FINAL FAST FLUX TEST FACILITY BACKUP DESIGN SUMMARY REPORT.

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    Two Track effects at ALICE

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    Ferritin and transferrin saturation cannot be used to diagnose iron-deficiency anemia in critically ill patients

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    Abstract Introduction: Iron-deficiency anaemia (IDA) is the most common anaemia globally. The frequency of IDA among critically ill patients is not known. The aim of our study was to analyse performance of standard iron metabolism parameters in diagnosis of IDA in the critically ill. Material and methods: We performed a retrospective analysis of consecutive anaemic patients admitted to the intensive care unit. Based on various cut-off values for ferritin and/or transferrin saturation (TfS), we determined the incidence of IDA. Results: The population consisted of 27 (53%) men and 24 (47%) women. The median haemoglobin concentration was well 96 [interquartile range (IQR 87–109)] g/L. The studied population had markedly increased concentration of C-reactive protein [119 (IQR 44–196) mg/L], ferritin [686 (385–1114) ”g/L], whereas iron concentration and TfS were below reference value. Depending on cut-off value chosen, IDA could be diagnosed in between 7.8 (ferritin < 100 ”g/L +TfS < 20%) and 56.9 % (TfS < 20%) of patients. Conclusions: Ferritin and transferrin saturation cannot be used for precise diagnosis of IDA caused by absolute or functional iron deficiency in the critically ill

    Thrombocytopenia in critically ill patients: single center data analysis

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    Introduction: Thrombocytopenia (TP) is one of the most frequent abnormalities of hemostasis found in laboratory tests in critically ill patients. The aim of this study was to determine the frequency and most probable causes of TP in patients hospitalized in the Intensive Care Unit (ICU). Material and methods: The documentation of all patients hospitalized in 2019 was analyzed retrospectively in the ICU of the university hospital. Patients diagnosed with TP at admission to the ward or during hospitalization were identified. Potential factors influencing the platelet count were analyzed. Results: During the analyzed period, 291 patients were hospitalized. In 93 patients (32%), TP was diagnosed, including 61 patients at admission (21%), and the remaining 32 patients (11%) during hospitalization. Patients with TP had higher SAPS II, APACHE II and SOFA scores than patients without TP (p <0.001 for all). Mortality in patients with TP was twice as high as in patients without TP (58% vs. 29%, p <0.001). In 18 patients (6%), only one cause of TP was potentially identified, while in 39 patients (13%), four or more factors that could potentially cause TP were identified. Conclusions: Thrombocytopenia is a relatively common problem in the critically ill population, but due to the challenges in differential diagnosis, a reliable assessment of the causes of its occurrence is difficult

    DNA content of a functioning chicken kinetochore

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    © The Author(s) 2014. In order to understand the three-dimensional structure of the functional kinetochore in vertebrates, we require a complete list and stoichiometry for the protein components of the kinetochore, which can be provided by genetic and proteomic experiments. We also need to know how the chromatin-containing CENP-A, which makes up the structural foundation for the kinetochore, is folded, and how much of that DNA is involved in assembling the kinetochore. In this MS, we demonstrate that functioning metaphase kinetochores in chicken DT40 cells contain roughly 50 kb of DNA, an amount that corresponds extremely closely to the length of chromosomal DNA associated with CENP-A in ChIP-seq experiments. Thus, during kinetochore assembly, CENP-A chromatin is compacted into the inner kinetochore plate without including significant amounts of flanking pericentromeric heterochromatin. © 2014 The Author(s).Wellcome Trust [grant number 073915]; Wellcome Trust Centre for Cell Biology (core grant numbers 077707 and 092076); Darwin Trust of Edinburg
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