126 research outputs found

    Inhaled dry salt micro particles in the treatment of bronchopulmonary dysplasia: a five case series report

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    Background. Despite current medical advances, to this day there is no single medical intervention to effectively prevent or treat bronchopulmonary dysplasia (BPD) in both preterm and term infants. Along with protective ventilation strategies, various drugs are being used or are being researched at this very moment, with the sole purpose of improving the general outcome for these patients. Inhaled dry salt micro particles therapy is now one of them. Materials and methods. This report presents five patients, diagnosed with severe BPD. All of them received, complementary to classical BPD management and respiratory support, continuous inhaled dry salt micro particles, via SaltMed cartridges, for a period of 12 to 30 days. After only 24 hours of administration, we were able to observe a significant improvement in respiratory function and dynamics. It was possible to use a lower fraction of inspired oxygen (FiO2), mean airway pressure (MAP) and peak inspiratory pressure (PIP) in all mechanically ventilated patients. Higher tidal volumes were recorded and we observed improvement in oxygenation indexes. Conclusion. Continuously inhaled dry salt micro particles, administered complementary to classic BPD management, could improve respiratory and overall morbidity and mortality in infants with any form of BPD. Further study of these possible effects is needed, as there is no data published on this matter so far

    Towards Critical Occidentalism Studies: Re-inventing the 'West' and 'Japan' in Mangaesque Popular Cultures

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    This paper investigates the reproduction of the imagined geography of the ‘West’ in contemporary Japan by employing a relational, intersectional and positional approach in order to examine Occidentalism and its hegemonic identification and othering process. Particular attention will be paid to emerging Japanese subcultures enacting a parodic and sexualised re-invention of Westernness and Japaneseness within a globalising mangaesque media mix

    CDKN1B mutation and copy number variation are associated with tumor aggressiveness in luminal breast cancer

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    The CDKN1B gene, encoding for the CDK inhibitor p27kip1, is mutated in defined human cancer subtypes, including breast, prostate carcinomas and small intestine neuroendocrine tumors. Lessons learned from small intestine neuroendocrine tumors suggest that CDKN1B mutations could be subclonal, raising the question of whether a deeper sequencing approach could lead to the identification of higher numbers of patients with mutations. Here, we addressed this question and analyzed human cancer biopsies from breast (n = 396), ovarian (n = 110) and head and neck squamous carcinoma (n = 202) patients, using an ultra-deep sequencing approach. Notwithstanding this effort, the mutation rate of CDKN1B remained substantially aligned with values from the literature, showing that essentially only hormone receptor-positive breast cancer displayed CDKN1B mutations in a relevant number of cases (3%). However, the analysis of copy number variation showed that another fraction of luminal breast cancer displayed loss (8%) or gain (6%) of the CDKN1B gene, further reinforcing the idea that the function of p27kip1 is important in this type of tumor. Intriguingly, an enrichment for CDKN1B alterations was found in samples from premenopausal luminal breast cancer patients (n = 227, 4%) and in circulating cell-free DNA from metastatic luminal breast cancer patients (n = 59, 8.5%), suggesting that CDKN1B alterations could correlate with tumor aggressiveness and/or occur later during disease progression. Notably, many of the identified somatic mutations resulted in p27kip1 protein truncation, leading to loss of most of the protein or of its C-terminal domain. Using a gene-editing approach in a luminal breast cancer cell line, MCF-7, we observed that the expression of p27kip1 truncating mutants that lose the C-terminal domains failed to rescue most of the phenotypes induced by CDKN1B gene knockout, indicating that the functions retained by the C-terminal portion are critical for its role as an oncosuppressor, at least in luminal breast cancer. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland
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