High intracranial pressure variability (ICPV) is associated with favorable outcome in traumatic brain injury, by mechanisms likely involving better cerebral blood flow regulation. However, less is known about ICPV in aneurysmal subarachnoid hemorrhage (aSAH). In this study, we investigated the explanatory variables for ICPV in aSAH and its association with delayed cerebral ischemia (DCI) and clinical outcome. In this retrospective study, 242 aSAH patients, treated at the neurointensive care, Uppsala, Sweden, 2008-2018, with ICP monitoring the first ten days post-ictus were included. ICPV was evaluated on three time scales (1) ICPV-1m-ICP slow wave amplitude of wavelengths between 55 and 15s, (2) ICPV-30m-the deviation from the mean ICP averaged over 30min, and (3) ICPV-4h-the deviation from the mean ICP averaged over 4h. The ICPV measures were analyzed in the early phase (day 1-3), in the early vasospasm phase (day 4-6.5), and the late vasospasm phase (day 6.5-10). High ICPV was associated with younger age, reduced intracranial pressure/volume reserve (high RAP), and high blood pressure variability in multiple linear regression analyses for all ICPV measures. DCI was associated with reduced ICPV in both vasospasm phases. High ICPV-1m in the post-ictalearly phase and theearly vasospasm phase predicted favorable outcome in multiple logistic regressions, whereas ICPV-30m and ICPV-4h in the late vasospasm phase had a similar association. Higher ICPV may reflect more optimal cerebral vessel activity, as reduced values are associated with an increased risk of DCI and unfavorable outcome after aSAH.Higher ICPV may reflect more optimal cerebral vessel activity, as reduced values are associated with an increased risk of DCI and unfavorable outcome after aSAH.Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. Long intergenic non-protein coding RNA 520 (LINC00520) was one of the newly discovered lncRNA which has been demonstrated to be dysregulated in several cancers. So far, the function and mechanism of LINC00520 in non-small cell lung cancer (NSCLC) are unclear. In this paper, our group first showed that LINC00520 level was elevated in non-small cell lung cancer (NSCLC) tissue and cells. In addition, SP1 could bind directly to the promoter region of LINC00520 and thus promote its transcription. Increased LINC00520 was distinctly correlated with advanced tumor stage and shorter survival time in NSCLC patients. Further functional investigations provided evidences that forced down regulation of LINC00520 inhibited NSCLC cell proliferation, invasion, metastasis and EMT, while contributing to cells apoptosis. Mechanistically, we found that LINC00520 serving as a competing endogenous RNA to be involved in the modulation of miR-577 expressions, and thus affected the expression of CCNE2 which was a target gene of miR-577. Moreover, in NSCLC cells with si-LINC00520, up regulation of CCNE2 led to an increase of cell growth and invasion. Taken together, LINC00520 displayed its tumor-promotive roles through modulating the miR-577/CCNE2 axis, highlighting a potential therapeutic strategy for NSCLC patients. Multiple myeloma (MM) is the second most frequent hematologic malignancy after lymphoma, contributing to approximately 10% of all hematologic malignancies. The prognosis of patients with MM is impacted by the heterogeneity of the disease, with worse outcomes reported in patients classified as International Staging System stage III, those with high-risk cytogenetics and elevated serum lactate dehydrogenase, and among patients who are elderly and have comorbidities. Previous studies have demonstrated an association between the presence of lung disease and worse outcomes; however, this impact in a real-world setting is not well understood. This retrospective, observational, cohort study included data from the nationwide US Optum® de-identified electronic health record (EHR) database from January 1, 2006, to December 31, 2019. MM patients with asthma or chronic obstructive pulmonary disease (COPD) were compared with MM patients without asthma or COPD for time to next treatment and overall survival using one-sn these patients.These real-world data suggest that patients with asthma or COPD do not experience a shorter time interval to next treatment, but have significantly worse overall survival from start of first-line therapy and numerically worse survival from the start of later lines. Future investigations with larger datasets may improve the understanding of the influence of individual treatments on outcomes in these patients. Atopic dermatitis (AD) severity was measured in two phase3 US studies of crisaborole ointment, 2%, in patients aged ≥ 2years using the Investigator's Static Global Assessment (ISGA), an FDA-recommended scale. Eczema Area and Severity Index (EASI) is a validated scale used globally to assess AD severity in clinical trials. The objective of this study is to aid interpretability of ISGA by translating ISGA scores to EASI scores. ISGA was mapped to EASI using published EASI severity strata by Chopra etal. and Leshem etal. and pooled data from phase3 trials CrisADe CORE 1 and CORE 2, which evaluated crisaborole in patients aged ≥ 2years with mild-to-moderate AD (crisaborole, n = 1016; vehicle, n = 506). Least squares mean (LSM) percentage change from baseline (%CFB) in EASI and proportion of patients with 50%, 75%, and 90% improvement (EASI-50, EASI-75, and EASI-90, respectively) on day 29 were computed for mapped EASI. this website The relationship between changes in ISGA and changes in EASI was assessed using data from three abrocitinib trials. ISGA was mapped to EASI using 70,000 random simulations. LSM (standard error) for %CFB in mapped EASI at day 29 (crisaborole versus vehicle) was -26.3% (17) versus 45.2% (35) (P = 0.0671) using Chopra strata and -43.1% (4.6) versus -5.2% (8.4) (P < 0.0001) using Leshem strata. EASI-50, EASI-75, and EASI-90 rates were 72.1% versus 57.6%, 63.0% versus 47.8%, and 55.0% versus 40.1%, respectively, using Chopra strata (P < 0.0001 for each difference). These rates were 68.8% versus 54.0%, 54.8% versus 40.5%, and 38.9% versus 27.2%, respectively (P < 0.0001 for each difference) using Leshem strata. Mean two-point improvement in ISGA was comparable to EASI-90. Mapped EASI results were consistent with ISGA results in crisaborole phase3 trials. Simulation methodologies yielded consistent results and may aid in interpretability of ISGA across clinical studies. ClinicalTrials.gov identifier NCT02118766, NCT02118792.ClinicalTrials.gov identifier NCT02118766, NCT02118792.