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BACKGROUND Progressive keratoconus can lead to severely impaired vision, but there is currently no consensus on the definition of progressive disease. Errors in the measurement of the parameters commonly used to establish progressive disease were evaluated in an attempt to determine the limits at which a true change in the values can be detected. The possible association between measurement error and disease severity was also investigated to evaluate the need for limits based on disease severity. METHODS Sixty-one eyes were studied in 61 patients with keratoconus. Four replicate measurements were made in each patient using a Scheimpflug-based tomographic system (denoted the PC) and an auto-keratometer (denoted the AK). The repeatability coefficient, i.e., the level below which differences between two measurements are found in 95% of paired observations, was calculated. Patients were further divided into three groups based on disease severity (parameter magnitude). RESULTS Increasing magnitude of all the keratsive keratoconus. Further studies are, however, required.Acknowledgements have been examined as important elements in measuring the contributions to and intellectual debts of a scientific publication. Unlike previous studies that were limited in the scope of analysis and manual examination. The present study aimed to conduct the automatic classification of acknowledgements on a large scale of data. To this end, we first created a training dataset for acknowledgements classification by sampling the acknowledgements sections from the entire PubMed Central database. Second, we adopted various supervised learning algorithms to examine which algorithm performed best in what condition. In addition, we observed the factors affecting classification performance. We investigated the effects of the following three main aspects classification algorithms, categories, and text representations. The CNN+Doc2Vec algorithm achieved the highest performance of 93.58% accuracy in the original dataset and 87.93% in the converted dataset. The experimental results indicated that the characteristics of categories and sentence patterns influenced the performance of classification. Most of the classifiers performed better on the categories of financial, peer interactive communication, and technical support compared to other classes.Interferon (IFN) stimulates a whole repertoire of cellular genes, collectively referred to as ISGs (Interferon-stimulated genes). ISG20, a 3´-5´ exonuclease enzyme, has been previously shown to bind and degrade hepatitis B Virus (HBV) transcripts. Here, we show that the N6-methyladenosine (m6A)-modified HBV transcripts are selectively recognized and processed for degradation by ISG20. Moreover, this effect of ISG20 is critically regulated by m6A reader protein, YTHDF2 (YTH-domain family 2). Previously, we identified a unique m6A site within HBV transcripts and confirmed that methylation at nucleotide A1907 regulates HBV lifecycle. In this report, we now show that the methylation at A1907 is a critical regulator of IFN-α mediated decay of HBV RNA. We observed that the HBV RNAs become less sensitive to ISG20 mediated degradation when methyltransferase enzymes or m6A reader protein YTHDF2 are silenced in HBV expressing cells. By using an enzymatically inactive form ISG20D94G, we further demonstrated that ISG20 forms a complex with m6A modified HBV RNA and YTHDF2 protein. Due to terminal redundancy, HBV genomic nucleotide A1907 position is acquired twice by pregenomic RNA (pgRNA) during transcription and therefore the sites of methylation are encoded within 5´ and 3´ epsilon stem loops. We generated HBV mutants that lack m6A site at either one (5´ or 3´) or both the termini (5´& 3´). this website Using these mutants, we demonstrated that m6A modified HBV RNAs are subjected to ISG20-mediated decay and propose sequence of events, in which ISG20 binds with YTHDF2 and recognizes m6A-modified HBV transcripts to carry out the ribonuclease activity. This is the first study, which identifies a hitherto unknown role of m6A modification of RNA in IFN-α induced viral RNA degradation and proposes a new role of YTHDF2 protein as a cofactor required for IFN-α mediated viral RNA degradation.INTRODUCTION Pneumonia in children is a common disease yet determining its aetiology remains elusive. OBJECTIVES To determine the a) aetiology, b) factors associated with bacterial pneumonia and c) association between co-infections (bacteria + virus) and severity of disease, in children admitted with severe pneumonia. METHODS A prospective cohort study involving children aged 1-month to 5-years admitted with very severe pneumonia, as per the WHO definition, over 2 years. Induced sputum and blood obtained within 24 hrs of admission were examined via PCR, immunofluorescence and culture to detect 17 bacteria/viruses. A designated radiologist read the chest radiographs. RESULTS Three hundred patients with a mean (SD) age of 14 (±15) months old were recruited. Significant pathogens were detected in 62% of patients (n = 186). Viruses alone were detected in 23.7% (n = 71) with rhinovirus (31%), human metapneumovirus (HMP) [22.5%] and respiratory syncytial virus (RSV) [16.9%] being the commonest. Bacteria alone was detected in 25% (n = 75) with Haemophilus influenzae (29.3%), Staphylococcus aureus (24%) and Streptococcus pneumoniae (22.7%) being the commonest. Co-infections were seen in 13.3% (n = 40) of patients. Male gender (AdjOR 1.84 [95% CI 1.10, 3.05]) and presence of crepitations (AdjOR 2.27 [95% CI 1.12, 4.60]) were associated with bacterial infection. C-reactive protein (CRP) [p = 0.007]) was significantly higher in patients with co-infections but duration of hospitalization (p = 0.77) and requirement for supplemental respiratory support (p = 0.26) were not associated with co-infection. CONCLUSIONS Bacteria remain an important cause of very severe pneumonia in developing countries with one in four children admitted isolating bacteria alone. Male gender and presence of crepitations were significantly associated with bacterial aetiology. Co-infection was associated with a higher CRP but no other parameters of severe clinical illness.

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