This cross-sectional research aims to study the effect of yoga practice on the illness perception, and wellbeing of healthy adults during 4–10 weeks of lockdown due to COVID19 outbreak. A total of 668 adults (64.7% males, M = 28.12 years, SD = 9.09 years) participated in the online survey. The participants were grouped as; yoga practitioners, other spiritual practitioners, and non-practitioners based on their responses to daily practices that they follow. Yoga practitioners were further examined based on the duration of practice as; long-term, mid-term and beginners. Multivariate analysis indicates that yoga practitioners had significantly lower depression, anxiety, & stress (DASS), and higher general wellbeing (SWGB) as well as higher peace of mind (POMS) than the other two groups. The results further revealed that the yoga practitioners significantly differed in the perception of personal control, illness concern and emotional impact of COVID19. However, there was no significant difference found for the measure of resilience (BRS) in this study. Yoga practitioners also significantly differed in the cognitive reappraisal strategy for regulating their emotions than the other two groups. Interestingly, it was found that beginners -those who had started practicing yoga only during the lockdown period reported no significant difference for general wellbeing and peace of mind when compared to the mid- term practitioner. Evidence supports that yoga was found as an effective self- management strategy to cope with stress, anxiety and depression, and maintain wellbeing during COVID19 lockdown.

The complicated, evolving landscape of cancer mutations poses a formidable challenge to identify cancer genes among the large lists of mutations typically generated in NGS experiments. The ability to prioritize these variants is therefore of paramount importance. To address this issue we developed OncoScore, a text-mining tool that ranks genes according to their association with cancer, based on available biomedical literature. Receiver operating characteristic curve and the area under the curve (AUC) metrics on manually curated datasets confirmed the excellent discriminating capability of OncoScore (OncoScore cut-off threshold = 21.09; AUC = 90.3%, 95% CI: 88.1–92.5%), indicating that OncoScore provides useful results in cases where an efficient prioritization of cancer-associated genes is needed.

BackgroundChronic Myeloid Leukaemia (CML) is caused by the BCR/ABL1 fusion gene. Both the presence and the levels of BCR/ABL1 expression seem to be critical for CML progression from chronic phase (CP) to blast crisis (BC). After the oncogenic translocation, the BCR/ABL1 gene is under the transcriptional control of BCR promoter but the molecular mechanisms involved in the regulation of oncogene expression are mostly unknown.MethodsA region of 1443bp of the functional BCR promoter was studied for transcription factor binding sites through in-silico analysis and Chromatin Immunoprecipitation experiments. BCR and BCR/ABL1 expression levels were analysed in CML cell lines after over-expression or silencing of MYC transcription factor. A luciferase reporter assay was used to confirm its activity on BCR promoter.ResultsIn the present study we demonstrate that MYC and its partner MAX bind to the BCR promoter, leading to up-regulation of BCR and BCR/ABL1 at both transcriptional and protein levels. Accordingly, silencing of MYC expression in various BCR/ABL1 positive cell lines causes significant downregulation of BCR and BCR/ABL1, which consequently leads to decreased proliferation and induction of cell death.ConclusionsHere we describe a regulatory pathway modulating BCR and BCR/ABL1 expression, showing that the BCR promoter is under the transcriptional control of the MYC/MAX heterodimer. Since MYC is frequently over-expressed in BC, this phenomenon could play a critical role in BCR/ABL1 up-regulation and blast aggressiveness acquired during CML evolution.

In this article, we perform sentiment analyses of Twitter location data. We use two case studies: US presidential elections of 2016 and UK general elections of 2017. For US elections, we plot state-wise user sentiment towards Hillary Clinton and Donald Trump. For UK elections, we download two disparate datasets, using keywords and location coordinates, looking for similar tendencies in sentiment towards political candidates and parties. The overall objective of the two case studies is to evaluate similarity between sentiment of location-based tweets and on-ground public opinion reflected in election results. We discover Twitter location sentiment does indeed corroborate with the election result in both cases. We also discover similar tendencies in Twitter sentiment towards political candidates and parties regardless of the methodology adopted for data collection.

Despite the advent of tyrosine kinase inhibitors, a proportion of chronic myeloid leukemia patients in chronic phase fail to respond to imatinib or to second-generation inhibitors and progress to blast crisis. Until now, improvements in the understanding of the molecular mechanisms responsible for chronic myeloid leukemia transformation from chronic phase to the aggressive blast crisis remain limited. Here we present a large parallel sequencing analysis of 10 blast crisis samples and of the corresponding autologous chronic phase controls that reveals, for the first time, recurrent mutations affecting the ubiquitin-conjugating enzyme E2A gene ( UBE2A , formerly RAD6A ). Additional analyses on a cohort of 24 blast crisis, 41 chronic phase as well as 40 acute myeloid leukemia and 38 atypical chronic myeloid leukemia patients at onset confirmed that UBE2A mutations are specifically acquired during chronic myeloid leukemia progression, with a frequency of 16.7% in advanced phases. In vitro studies show that the mutations here described cause a decrease in UBE2A activity, leading to an impairment of myeloid differentiation in chronic myeloid leukemia cells.

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For children and young adults with T-lineage acute lymphoblastic leukemia (T-ALL), event free survival following relapse is < 10%. We recently showed that rearrangements of the mixed lineage leukemia gene (KMT2A-R) are associated with induction failure and an inferior survival in T-ALL. Because there are currently no molecular features that inform treatment strategies in T-ALL, we hypothesized that transcriptional alterations related to KMT2A-R and MLLT10-R T-ALL could identify biologically relevant genes and signaling pathways for the development of targeted therapies for these groups of patients. We analyzed microarray data from a retrospective cohort of 100 T-ALL patients to identify novel targets for KMT2A (n = 12) or MLLT10 (n = 9) chimeras. We identified 330 probe sets that could discriminate between these groups, including novel targets, like RUNX2, TCF4 or MYO6. The results were further validated in two independent data sets and the functional networks were analyzed to identify pathways that may be of pathogenic or therapeutic relevance.Electronic supplementary materialThe online version of this article (10.1186/s40364-018-0141-z) contains supplementary material, which is available to authorized users.