This meta-analysis suggests 25 G needle systems are more sensitive than 22 G needles for diagnosing pancreatic malignancy.

The aim of this study was to investigate factors contributing to poor bowel preparation in patients undergoing colonoscopy procedures. We used a reproducible search strategy to identify studies, searching 10 medical databases, including PubMed, Ovid, Medline, and Cochrane Library Database for reports published between 2000 and 2016. Fully published studies, evaluating risk factors for inadequate bowel preparation, were included. Two reviewers independently scored the identified studies for methodology and abstracted pertinent data. Pooling was conducted with both fixed-effects and random-effects models; results were presented from the random effects model when heterogeneity was significant. Odds ratios (OR) estimates with 95% confidence interval were calculated. Heterogeneity was assessed by I statistics. Twenty-four studies with a total of 49 868 patients met the inclusion criteria. Age (OR: -1.20), male sex (OR: 0.85), inpatient status (OR: 0.57), diabetes mellitus (OR: 0.58), hypertension (OR: 0.58), cirrhosis (OR: 0.49), narcotic use (OR: 0.59), constipation (OR: 0.61), stroke (OR; 0.51), and tricyclic antidepressant (TCA) use (0.51), were associated with inadequate bowel preparation. In our sensitivity analysis comparing Western and Asian countries, we found that diabetes, cirrhosis, male sex, history of stroke and TCA use were stronger risk factors for inadequate bowel preparation in Western countries than in Asian countries. We also found that history of stroke, TCA use, and race were risk factors for inadequate bowel preparation in patients receiving conventional bowel preparation compared with those receiving split-dose bowel preparation. Multiple risk factors affect the quality of bowel preparation and specific risk factors can be intervened upon, in different populations, to optimize preparation.

Our data show a strong association between clinically active IBD and poor sleep quality and demonstrate that patients in clinical remission with abnormal sleep have a high likelihood of subclinical disease activity.

Tumor stem cell marker Doublecortin-like kinase1 (DCLK1) is upregulated in several solid tumors. The role of DCLK1 in hepatocellular carcinoma (HCC) is unclear. We immunostained tissues from human livers with HCC, cirrhosis controls (CC), and non-cirrhosis controls (NCC) for DCLK1. Western blot and ELISA analyses for DCLK1 were performed with stored plasma samples. We observed increased immunoreactive DCLK1 in epithelia and stroma in HCC and CCs compared with NCCs, and observed a marked increase in plasma DCLK1 from patients with HCC compared with CC and NCC. Analysis of the Cancer Genome Atlas’ HCC dataset revealed that DCLK1 is overexpressed in HCC tumors relative to adjacent normal tissues. High DCLK1-expressing cells had more epithelial-mesenchymal transition (EMT). Various tumor suppressor miRNAs were also downregulated in HCC tumors. We evaluated the effects of DCLK1 knockdown on Huh7.5-derived tumor xenograft growth. This was associated with growth arrest and a marked downregulation of cMYC, and EMT transcription factors ZEB1, ZEB2, SNAIL, and SLUG via let-7a and miR-200 miRNA-dependent mechanisms. Furthermore, upregulation of miR-143/145, a corresponding decrease in pluripotency factors OCT4, NANOG, KLF4, and LIN28, and a reduction of let-7a, miR-143/145, and miR-200-specific luciferase activity was observed. These findings suggest that the detection of elevated plasma DCLK1 may provide a cost-effective, less invasive tool for confirmation of clinical signs of cirrhosis, and a potential companion diagnostic marker for patients with cirrhosis and HCC. Our results support evaluating DCLK1 as a biomarker for detection and as a therapeutic target for eradicating HCC.

Doublecortin-like kinase 1 (Dclk1), a microtubule-associated kinase, marks the fifth lineage of intestinal epithelial cells called tuft cells that function as tumor stem cells in Apc mutant models of colon cancer. In order to determine the role of Dclk1 in dextran sulfate sodium (DSS) induced colonic inflammation both intestinal epithelial specific Dclk1 deficient (VillinCre;Dclk1f/f) and control (Dclk1f/f) mice were fed 3% DSS in drinking water for 9 days, allowed to recover for 2 days, and killed. The clinical and histological features of DSS-induced colitis were scored and immunohistochemical, gene expression, pro-inflammatory cytokines/chemokines, and immunoblotting analyses were used to examine epithelial barrier integrity, inflammation, and stem and tuft cell features. In DSS-induced colitis, VillinCre;Dclk1f/f mice demonstrated exacerbated injury including higher clinical colitis scores, increased epithelial barrier permeability, higher levels of pro-inflammatory cytokines and chemokines, decreased levels of Lgr5, and dysregulated Wnt/b-Catenin pathway genes. These results suggest that Dclk1 plays an important role in regulating colonic inflammatory response and colonic epithelial integrity.

No abstract

There is a high rate of unnecessary PEG placement when done prophylactically in patients with head and neck cancer.

Background In Barrett’s esophagus (BE), the normal esophageal squamous epithelium is replaced by specialized metaplastic columnar epithelium. BE is a premalignant lesion which can progress to esophageal adenocarcinoma (EAC). Currently there are no early molecular indicators that would predict progression from BE to EAC. As the only permanent residents of the epithelium, stem cells have been implicated in this metaplastic progression. Aim To determine the expression of DCAMKL-1 and other putative gastrointestinal stem cell markers in normal esophageal mucosa (NEM), BE and EAC. Methods Human NEM, BE, EAC and multi-tissue microarrays were analyzed for DCAMKL-1 and immunohistochemically scored based on staining intensity and tissue involvement, with epithelia and stroma scored separately. Total RNA isolated from BE and paired NEM was subjected to real-time RT-PCR analysis for DCAMKL-1, LGR5 and Musashi-1 mRNA expression. Results DCAMKL-1 is minimally expressed in squamous NEM, but increased in BE (with and without dysplasia) and EAC tissues. In EAC, we found increased stromal DCAMKL-1 staining compared to adjacent epithelia. Within the sub-mucosa of dysplastic BE tissues, an increase in endothelial cell expression of DCAMKL-1 was observed. Finally, an upregulation of DCAMKL-1, LGR5 and Musashi-1 mRNA was seen in BE compared to squamous NEM. Conclusions Here we report progressive increase of DCAMKL-1 expression in BE from dysplasia to EAC. Furthermore, there was an increase in putative stem cell markers DCAMKL-1, LGR5 and Msi-1 mRNA. These data taken together suggest that regulation of resident stem cells may play an important role in progression of BE to EAC.