Aldridgedesai2819

1-0.6) and elevated C-reactive protein (CRP; p<0.001; OR 1.004; 95% CI 1.002-1.008) were associated with ICU admission.One-hundred and four patients (32.4%) died. Age >65 years (p=0.011; OR 5; 95% CI 1.6-21.9), neutrophils (p=0.047), neutrophillymphocyte ratio (NLR; p=0.028), CRP (p<0.001) and albumin (p=0.002) were associated with mortality. When analysis adjusted for age, CRP (p<0.001; OR 1.006; 95% CI 1.004-1.008) and albumin (p=0.005; OR 0.94; 95% CI 0.90-0.98) remained associated with mortality.

COVID-19 has high mortality. BAME and male patients were associated with ICU admission. ALK inhibitor cancer High CRP and low albumin (after correcting for age) were associated with mortality.

COVID-19 has high mortality. BAME and male patients were associated with ICU admission. High CRP and low albumin (after correcting for age) were associated with mortality.

We determined the impact of a system-wide multicomponent intervention to improve recognition and documentation of cognitive frailty syndromes on hospital administrative coding for delirium.

A multicomponent intervention including introduction of structured patient assessment including cognitive/delirium screen, regular audit/feedback and educational seminars was undertaken (2012-17). Sensitivity and specificity of administrative

, 10th revision (ICD-10) delirium codes for the gold standard of prospectively clinically diagnosed delirium were calculated in consecutive patients admitted to acute medicine over five 8-week cycles (2010-18).

Among 1,281 consecutive unselected admissions to acute medicine overall (mean / standard deviation age = 70.0/19.2 years; n=615 (48.0%) male), 320 had clinical delirium diagnosis (n=220 delirium only; n=100 delirium on dementia). Sensitivity of delirium coding increased from 12.8% (95% confidence interval (CI) 5.6-26.7) in 2010 to 60.2% (95% CI 50.1-69.7; p

<0.0001) in 2018 while specificity remained at >99% throughout.

A multicomponent intervention increased sensitivity of hospital administrative diagnostic coding for delirium almost six-fold without increasing the false positive diagnosis rate.

A multicomponent intervention increased sensitivity of hospital administrative diagnostic coding for delirium almost six-fold without increasing the false positive diagnosis rate.

This study investigated the clinical significance of

F-fluorodeoxyglucose positron emission tomography / computed tomography (

F-FDG PET/CT) in identifying the causes of fever of unknown origin (FUO).

Patients with a fever who received an

F-FDG PET/CT examination were retrospectively selected. The means of the two groups were compared using an independent-samples t-test.

Among the 89 included patients, 66 were diagnosed using

F-FDG PET/CT. The sensitivity, specificity and diagnostic accuracy of

F-FDG PET/CT for the diagnosis of patients with FUO were 84.5%, 25.8%, and 64.0%, respectively. The detection rates of

F-FDG PET/CT for neoplastic diseases, infectious diseases and non-infectious inflammatory diseases were 100%, 61.3%, and 75%, respectively. The difference in C-reactive protein (CRP) levels between the two groups was statistically significant.

F-FDG PET/CT has great clinical importance in diagnosing and identifying causes of FUO and improves the accuracy of FUO diagnosis when combined with serum CRP levels.

18F-FDG PET/CT has great clinical importance in diagnosing and identifying causes of FUO and improves the accuracy of FUO diagnosis when combined with serum CRP levels.The study by Benjamin and colleagues demonstrates that mutant YAP expression is sufficient to enhance tumor cell dissemination in zebrafish and mice. Moreover, the integration of approaches in biology and engineering taken here provides an important framework to link physical, physiological, and molecular properties of disseminated tumor cells (DTC). Similar integrated approaches will pave the way for future studies to generate global cancer cell dissemination maps and provide further insight into the prognostic value of DTCs for metastatic organotropisms.See related article by Benjamin et al., p. 3867.IL6 is targeted as part of treatment in adoptive cell therapy (ACT) because of its protumor effects and its role in the cytokine release syndrome. However, another major role of IL6 is to polarize naïve CD4+ T cells from Tregs to Th17 cells. While Th17 T cells are associated with autoimmunity, they are present around many different solid tumor cancers and their role in tumor microenvironments is unclear. In this issue of Cancer Research, Knochelmann and colleagues show that Th17 cells with less in vitro expansion in IL6-driven Th17 ACT provide greater solid tumor control and robust immune memory, highlighting advancement in the field of ACT application to solid tumor immunotherapy.See related article by Knochelmann et al., p. 3920.The TMPRSS2-ERG fusion is the most common genomic rearrangement in human prostate cancer. However, in established adenocarcinoma, it is unknown how the ERG oncogene promotes a cancerous phenotype and maintains downstream androgen receptor (AR) signaling pathways. In this study, we utilized a murine prostate organoid system to explore the effects of ERG on tumorigenesis and determined the mechanism underlying prostate cancer dependence on ERG. Prostate organoids lacking PTEN and overexpressing ERG (Pten-/- R26-ERG) faithfully recapitulated distinct stages of prostate cancer disease progression. In this model, deletion of ERG significantly dampened AR-dependent gene expression. While ERG was able to reprogram the AR cistrome in the process of prostate carcinogenesis, ERG knockout in established prostate cancer organoids did not drastically alter AR binding, H3K27ac enhancer, or open chromatin profiles at these reprogrammed sites. Proteomic analysis of DNA-bound AR complexes demonstrated that ERG deletion causes a loss of recruitment of critical AR coregulators and basal transcriptional machinery, including NCOA3 and RNA polymerase II, but does not alter AR binding itself. Together, these data reveal a novel mechanism of ERG oncogene addiction in prostate cancer, whereby ERG facilitates AR signaling by maintaining coregulator complexes at AR bound sites across the genome. SIGNIFICANCE These findings exploit murine organoid models to uncover the mechanism of ERG-mediated tumorigenesis and subsequent oncogenic dependencies in prostate cancer.