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  • 1
    Publication Date: 2018-05-15
    Description: Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials, Published online: 15 May 2018; doi:10.1038/s41598-018-25978-5 Author Correction: Magnetism and high magnetic-field-induced stability of alloy carbides in Fe-based materials
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
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  • 2
    Publication Date: 2018-05-07
    Description: Objectives Develop predictive models for a paediatric population that provide information for paediatricians and health authorities to identify children at risk of hospitalisation for conditions that may be impacted through improved patient care. Design Retrospective healthcare utilisation analysis with multivariable logistic regression models. Data Demographic information linked with utilisation of health services in the years 2006–2014 was used to predict risk of hospitalisation or death in 2015 using a longitudinal administrative database of 527 458 children aged 1–13 years residing in the Regione Emilia-Romagna (RER), Italy, in 2014. Outcome measures Models designed to predict risk of hospitalisation or death in 2015 for problems that are potentially avoidable were developed and evaluated using the C-statistic, for calibration to assess performance across levels of predicted risk, and in terms of their sensitivity, specificity and positive predictive value. Results Of the 527 458 children residing in RER in 2014, 6391 children (1.21%) were hospitalised for selected conditions or died in 2015. 49 486 children (9.4%) of the population were classified in the ‘At Higher Risk’ group using a threshold of predicted risk 〉2.5%. The observed risk of hospitalisation (5%) for the ‘At Higher Risk’ group was more than four times higher than the overall population. We observed a C-statistic of 0.78 indicating good model performance. The model was well calibrated across categories of predicted risk. Conclusions It is feasible to develop a population-based model using a longitudinal administrative database that identifies the risk of hospitalisation for a paediatric population. The results of this model, along with profiles of children identified as high risk, are being provided to the paediatricians and other healthcare professionals providing care to this population to aid in planning for care management and interventions that may reduce their patients’ likelihood of a preventable, high-cost hospitalisation.
    Keywords: Open access, Health services research
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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  • 3
    Publication Date: 2018-01-28
    Description: Objectives Workplace violence is relatively frequent among medical professionals who work in otorhinolaryngology units. This phenomenon reduces the quality of provided medical care and increases the incidence of depressive symptoms among physicians and nurses, seriously affecting their job satisfaction and work efficiency with a negative attitude towards providing treatment. Few existing studies have assessed workplace-violence-related factors associated with depressive symptoms among otorhinolaryngology physicians and nurses. Methods We conducted a cross-sectional study in grade A tertiary hospitals of Heilongjiang province in Northern China, to evaluate the occurrence and level of depressive symptoms among otorhinolaryngology physicians and nurses and to analyse the relationship between them and workplace-violence-related risk factors and demographic variables. Results Of all our participating professionals, (379 otorhinolaryngologists and 273 nurses), 57.2% were found to have depressive symptoms, whereas, of the respondents who had suffered from physical violence, 71.25% had depressive symptoms. Professionals with less than 1 year of experience, as well as professionals who more frequently worked alone, were more likely to suffer from depressive symptoms than their colleagues. Conclusions This research addresses an emerging issue of clinical practice, and its results differ from those of previous studies; specifically, it indicates that the frequency of depressive symptoms among otorhinolaryngology physicians and nurses may be influenced by physical violence, the number of coworkers they have for more than half of their working hours and other workplace-violence-related factors. To reduce the depressive symptoms caused by workplace violence and improve the quality of medical services, medical institutions should implement effective measures to prevent the occurrence of physical violence, strengthen team cooperation ability and increase peer support.
    Keywords: Open access, Public health
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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  • 4
    ISSN: 0014-5793
    Keywords: Dissimilatory ammonia-forming pathway ; EPR ; Hexaheme ; Nitric oxide intermediate ; Nitrite reductase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0003-9861
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 6
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; proliferation ; GENE ; MOUSE ; MICRORNA ; SUPPRESSES
    Abstract: Insulin-like growth factor 2 (IGF2), a developmentally regulated and maternally imprinted gene, is frequently overexpressed in pediatric cancers. Although loss of imprinting (LOI) at fetal promoters contributes to increased IGF2 in tumors, the magnitude of IGF2 expression suggests the involvement of additional regulatory mechanisms. A microRNA (miRNA) screen of primary Wilms' tumors identified specific overexpression of miR-483-5p, which is embedded within the IGF2 gene. Unexpectedly, the IGF2 mRNA itself is transcriptionally up-regulated by miR-483-5p. A nuclear pool of miR-483-5p binds directly to the 5' untranslated region (UTR) of fetal IGF2 mRNA, enhancing the association of the RNA helicase DHX9 to the IGF2 transcript and promoting IGF2 transcription. Ectopic expression of miR-483-5p in IGF2-dependent sarcoma cells is correlated with increased tumorigenesis in vivo. Together, these observations suggest a functional positive feedback loop of an intronic miRNA on transcription of its host gene.
    Type of Publication: Journal article published
    PubMed ID: 24298054
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  • 7
    Abstract: Exposure to aristolochic acid (AA) causes aristolochic acid nephropathy (AAN) and Balkan endemic nephropathy (BEN). Conflicting results have been found for the role of human sulfotransferase 1A1 (SULT1A1) contributing to the metabolic activation of aristolochic acid I (AAI) in vitro. We evaluated the role of human SULT1A1 in AA bioactivation in vivo after treatment of transgenic mice carrying a functional human SULT1A1-SULT1A2 gene cluster (i.e. hSULT1A1/2 mice) and Sult1a1(-/-) mice with AAI and aristolochic acid II (AAII). Both compounds formed characteristic DNA adducts in the intact mouse and in cytosolic incubations in vitro. However, we did not find differences in AAI-/AAII-DNA adduct levels between hSULT1A1/2 and wild-type (WT) mice in all tissues analysed including kidney and liver despite strong enhancement of sulfotransferase activity in both kidney and liver of hSULT1A1/2 mice relative to WT, kidney and liver being major organs involved in AA metabolism. In contrast, DNA adduct formation was strongly increased in hSULT1A1/2 mice compared to WT after treatment with 3-nitrobenzanthrone (3-NBA), another carcinogenic aromatic nitro compound where human SULT1A1/2 is known to contribute to genotoxicity. We found no differences in AAI-/AAII-DNA adduct formation in Sult1a1(-/-) and WT mice in vivo. Using renal and hepatic cytosolic fractions of hSULT1A1/2, Sult1a1(-/-) and WT mice, we investigated AAI-DNA adduct formation in vitro but failed to find a contribution of human SULT1A1/2 or murine Sult1a1 to AAI bioactivation. Our results indicate that sulfo-conjugation catalysed by human SULT1A1 does not play a role in the activation pathways of AAI and AAII in vivo, but is important in 3-NBA bioactivation.
    Type of Publication: Journal article published
    PubMed ID: 27557898
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  • 8
    Keywords: THERAPY ; RISK ; METABOLITES ; BREAST-CANCER ; PERFORMANCE ; WOMEN ; MASS-SPECTROMETRY ; ENDOMETRIAL CANCER ; HORMONES ; PERSPECTIVES ; PREMENOPAUSAL ; ENDOGENOUS ESTROGENS ; nested case-control study ; 16 alpha-hydroxyestrone,post-menopause ; 2-hydroxyestrone ; oestrogen metabolites
    Abstract: Background:It has been suggested that the relative importance of oestrogen-metabolising pathways may affect the risk of oestrogen-dependent tumours including endometrial cancer. One hypothesis is that the 2-hydroxy pathway is protective, whereas the 16alpha-hydroxy pathway is harmful.Methods:We conducted a case-control study nested within three prospective cohorts to assess whether the circulating 2-hydroxyestrone : 16alpha-hydroxyestrone (2-OHE1 : 16alpha-OHE1) ratio is inversely associated with endometrial cancer risk in postmenopausal women. A total of 179 cases and 336 controls, matching cases on cohort, age and date of blood donation, were included. Levels of 2-OHE1 and 16alpha-OHE1 were measured using a monoclonal antibody-based enzyme assay.Results:Endometrial cancer risk increased with increasing levels of both metabolites, with odds ratios in the top tertiles of 2.4 (95% CI=1.3, 4.6; P(trend)=0.007) for 2-OHE1 and 1.9 (95% CI=1.1, 3.5; P(trend)=0.03) for 16alpha-OHE1 in analyses adjusting for endometrial cancer risk factors. These associations were attenuated and no longer statistically significant after further adjustment for oestrone or oestradiol levels. No significant association was observed for the 2-OHE1 : 16alpha-OHE1 ratio.Conclusion:Our results do not support the hypothesis that greater metabolism of oestrogen via the 2-OH pathway, relative to the 16alpha-OH pathway, protects against endometrial cancer.
    Type of Publication: Journal article published
    PubMed ID: 21952628
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  • 9
    Keywords: EXPRESSION ; MICE ; DOWN-REGULATION ; METHYLATION ; METHYLTRANSFERASE ; NEPHROGENIC DIABETES-INSIPIDUS ; AQUAPORIN-2 TRAFFICKING ; WATER CHANNELS ; ENAC-ALPHA ; SET DOMAIN
    Abstract: Dot1l encodes histone H3 K79 methyltransferase Dot1a. Mice with Dot1l deficiency in renal Aqp2-expressing cells (Dot1l(AC)) develop polyuria by unknown mechanisms. Here, we report that Aqp5 links Dot1l deletion to polyuria through Aqp2. cDNA array analysis revealed and real-time RT-qPCR validated Aqp5 as the most upregulated gene in Dot1l(AC) vs. control mice. Aqp5 protein is barely detectable in controls, but robustly expressed in the Dot1l(AC) kidneys, where it colocalizes with Aqp2. The upregulation of Aqp5 is coupled with reduced association of Dot1a and H3 dimethyl K79 with specific subregions in Aqp5 5' flanking region in Dot1l(AC) vs. control mice. In vitro studies in IMCD3, MLE-15 and 293Tcells using multiple approaches including real-time RT-qPCR, luciferase reporter assay, cell surface biotinylation assay, colocalization, and co-immunoprecipitation uncovered that Dot1a represses Aqp5. Human AQP5 interacts with AQP2 and impairs its cell surface localization. The AQP5/AQP2 complex partially resides in the ER/Golgi. Consistently, AQP5 is expressed in none of 15 normal controls, but in all of 17 kidney biopsies from patients with diabetic nephropathy. In the patients with diabetic nephropathy, AQP5 colocalizes with AQP2 in the perinuclear region and AQP5 expression is associated with impaired cellular H3 dimethyl K79. Taken together, these data for the first time identify Aqp5 as a Dot1a potential transcriptional target, and an Aqp2 binding partner and regulator, and suggest that the upregulated Aqp5 may contribute to polyuria, possibly by impairing Aqp2 membrane localization, in Dot1l(AC) mice and in patients with diabetic nephropathy.
    Type of Publication: Journal article published
    PubMed ID: 23326416
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  • 10
    Keywords: HISTORY ; REPRODUCIBILITY ; POSTMENOPAUSAL WOMEN ; REPRODUCTIVE FACTORS ; FAMILIAL BREAST-CANCER ; PREMENOPAUSAL WOMEN ; HORMONE-BINDING GLOBULIN ; PROMOTES TUMOR-GROWTH ; SERUM PROLACTIN ; PROGESTERONE LEVELS
    Abstract: PURPOSE: Indirect evidence from experimental and epidemiological studies suggests that prolactin may be involved in ovarian cancer development. However, the relationship between circulating prolactin levels and risk of ovarian cancer is unknown. METHODS: We conducted a nested case-control study of 230 cases and 432 individually matched controls within three prospective cohorts to evaluate whether pre-diagnostic circulating prolactin is associated with subsequent risk of ovarian cancer. We also assessed whether lifestyle and reproductive factors are associated with circulating prolactin among controls. RESULTS: Prolactin levels were significantly lower among post- versus pre-menopausal women, parous versus nulliparous women, and past versus never users of oral contraceptives in our cross-sectional analysis of controls. In our nested case-control study, we observed a non-significant positive association between circulating prolactin and ovarian cancer risk (ORQ4vsQ1 1.56, 95 % CI 0.94, 2.63, p trend 0.15). Our findings were similar in multivariate-adjusted models and in the subgroup of women who donated blood 〉/=5 years prior to diagnosis. We observed a significant positive association between prolactin and risk for the subgroup of women with BMI 〉/=25 kg/m(2) (ORQ4vsQ1 3.10, 95 % CI 1.39, 6.90), but not for women with BMI 〈25 kg/m(2) (ORQ4vsQ1 0.81, 95 % CI 0.40, 1.64). CONCLUSIONS: Our findings suggest that prolactin may be associated with increased risk of ovarian cancer, particularly in overweight/obese women. Factors associated with reduced risk of ovarian cancer, such as parity and use of oral contraceptives, were associated with lower prolactin levels, which suggests that modulation of prolactin may be a mechanism underlying their association with risk.
    Type of Publication: Journal article published
    PubMed ID: 23378139
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