14%, p3 medications (OR 1.3 [1.1-1.4], p less then 0.01) were independent predictors of developing postoperative delirium. An episode of delirium was associated with longer hospital LOS (6 days vs. 3 days, p less then 0.01), higher odds of ICU admission (OR 2 [1.3-4.5], p less then 0.01), longer ICU LOS (2 days vs. 1 day, p less then 0.01) and higher odds of unplanned intubation (OR 1.8 [1.2-3.4], p less then 0.01). CONCLUSIONS The incidence of delirium after EGS was 26%. Frailty and polypharmacy were associated with increased risk of delirium. Delirium appears to be associated with higher rates in-hospital adverse events. BACKGROUND Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Skin barrier defects contribute to disease initiation and development, however underlying mechanisms remain elusive. OBJECTIVE To understand the underlying cause of barrier defect, we investigated aberrant expression of specific microRNAs (miRNAs) in AD. Delineating the molecular mechanism of dysregulated miRNA-network, we focused on identification of specific drugs, which can modulate miRNA expression and repair defective barrier in AD. METHODS A screen for differentially expressed miRNAs between healthy skin and AD lesional skin resulted in the identification of miR-335, as the most consistently downregulated miRNA in AD. Using in silico prediction combined with experimental validation, we characterized downstream miR-335 targets and elucidated the molecular pathways by which this microRNA maintains epidermal homeostasis in healthy skin. RESULTS miR-335 was identified as a potent inducer of keratinocyte differentiation, and exerts this effect by directly repressing SOX6. Recruiting SMARCA complex components, SOX6 suppresses epidermal differentiation and epigenetically silence critical genes involved in keratinocyte differentiation. In AD lesional skin, miR-335 expression is aberrantly lost. SOX6 is abnormally expressed throughout the epidermis, where it impairs skin barrier development. We demonstrate that miR-335 is epigenetically regulated by histone deacetylases (HDACs), and a screen for suitable HDAC inhibitors identified belinostat as a candidate drug which can restore epidermal miR-335 expression and rescue the defective skin barrier in AD. CONCLUSION Belinostat is of clinical significance not only as a candidate drug for AD treatment, but also as a potential means of stopping the atopic march and further progression of this systemic allergic disease. BACKGROUND & AIMS There is controversy over inclusion of granulocyte colony stimulating factor (G-CSF) in treatment of decompensated cirrhosis. Previous studies tested only a single cycle of G-CSF administration or were underpowered to detect changes in survival time. We performed an adequately powered study to determine whether multiple cycles of G-CSF increase survival of patients 1 year after the start of therapy. METHODS We conducted an open-label trial of 100 patients with decompensated cirrhosis without acute-on-chronic liver failure at a tertiary centre from July 2016 through June 2018. The patients were randomly assigned to a group given 5 days of G-CSF every 3 months, with standard medical therapy, in 4 cycles (group A, n=50) or standard medical therapy alone (group B, n=50). The primary outcome was survival for 12 months after treatment began. Secondary outcomes were increase in number of CD34+ cells at day 6 compared with day 0, along with reductions in Child Turcotte Pugh and model for end-stage lwas no improvement in nutrition in either group, compared with baseline. G-CSF was safe and well tolerated. CONCLUSIONS Administration of multiple cycles of G-CSF increases numbers of hematopoietic stem cells and survival of patients with decompensated cirrhosis receiving standard medical treatment. Addition of G-CSF to medical treatment might provide a bridge to liver transplantation for these patients. ClincialTrials.gov no NCT03415698. BACKGROUND & AIMS We studied incidence and mortality trends of colorectal cancer (CRC) in 39 countries according to age, sex, and anatomical location (colon vs rectum). METHODS We retrieved incidence data from registries from 36 countries. The registries included Cancer Incidence in 5 Continents (CI5) volumes I-XI; the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute; and the Nordic Cancer Registries from Europe. We obtained mortality data from 39 countries of the World Health Organization database. We evaluated average annual percent changes in CRC incidence and mortality in the past decade using joinpoint regression analysis. RESULTS From 2007 to 2016, 2006 to 2015, or 2005 to 2014, depending on the availability of the data, the incidence of colon cancer increased in 10 of 36 countries analyzed (all in Asia or Europe); India had the greatest increase, followed by Poland. All 10 of these countries have medium-high Human Development Index (HDI) scores. selleck products Six countries had a din countries with medium-high HDI and in younger populations. Preventive strategies are needed for countries with increasing CRC and rectal cancer incidence and mortality. BACKGROUND & AIMS Approximately one-third of patients with IBS-diarrhea (IBS-D) have increased bile acid (BA) synthesis or excretion. An open-label study showed benefits of colesevelam on bowel functions, consistent with luminal BA sequestration by colesevelam. We compared the effects of colesevelam vs placebo on symptoms and gene expression patterns in the sigmoid colon mucosa in patients with BA diarrhea associated with IBS-D. METHODS We performed a double-blind, parallel-group study of 30 adults with IBS-D and evidence of increased BA synthesis or fecal excretion, from December 2017 through December 2018 at a single center. Patients were randomly assigned (11) to groups given colesevelam (3 tablets, 625 mg each) or matching placebo, orally twice daily for 4 weeks. Stool diaries documented bowel functions for 8 days before and 28 days during colesevelam or placebo. Stool and fasting serum samples were collected for analyses of fecal BAs and serum levels of C4 and FGF19. We measured colonic transit by scintigraphy, mucosal permeability by in vivo excretion of saccharide probes, and mRNA levels in rectosigmoid biopsies.