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cirrhosis, with 50% of providers seeing more than 10 patients per year. Most providers (90%) were board certified in Internal Medicine or Family Practice and 63% were full-time clinical faculty. 52% of PCPs reported using ultrasound and alpha-fetoprotein (AFP) for surveillance in patients with cirrhosis, and 96% reported this combination was effective at reducing HCC-related mortality. However, a high proportion of providers believed clinical exam (45%), liver enzyme testing (59%), and AFP alone (89%) were also effective at reducing HCC-related mortality. Providers were more likely to use ultrasound if they believed ultrasound and AFP were effective at reducing mortality in cirrhosis (p=0.003), did not overuse surveillance in those without cirrhosis (p=0.002), reported their practice patterns were influenced by published literature (p=0.04) or patient preference (p=0.04), and were interested in CME activities about HCC surveillance (p=0.04). Although 83% of providers would perform ultrasound-based surveillance in a 50-year old patient with compensated cirrhosis, rates were only 68% in those with ascites, 63% in those with morbid obesity, and 50% in elderly patients. The only predictor of surveillance underutilization in clinical vignettes was lack of belief that ultrasound and AFP were effective at reducing HCC-related mortality (p=0.04). Conclusions: Primary care providers have misconceptions about appropriate HCC surveillance test choice, likely contributing to ineffective HCC surveillance in clinical practice.

Background & Aims: Little is known about how bacteria establish chronic infections of mucosal surfaces. Helicobacter pylori (H pylori), a chronic pathogen that lives in the gastric mucosa of humans, interacts with the trefoil factor family (TFF) protein TFF1, which is found in gastric mucus. We aimed to characterize the interaction of H pylori with TFF1 and to assess the role of this interaction in mediating colonization. Methods: Subcellular fractions of H pylori were immobilized and then probed with TFF1, TFF2, or TFF3. The effect of glycosidases and preincubation with monosaccharides on the interaction and binding of TFF1 to a H pylori adhesin was assessed. The interaction between H pylori adhesin and TFF1 was characterized using surface plasmon resonance, flow cytometry, nondenaturing polyacrylamide gel electrophoresis, coimmunofluoresence, and incubation with tissue sections. Results: The H pylori core oligosaccharide portion (rough form) of lipopolysaccharide (RF-LPS) bound to TFF1 and to a lesser extent TFF3; this interaction was inhibited by incubation of RF-LPS with mannosidase, glucosidase, or mixed monosaccharides. TFF1 also bound to human serum albumin‐conjugated mannose and glucose. The optimum pH for binding was 5.0‐6.0 for TFF1 and 7.0 for TFF3. H pylori bound TFF1 in gastric mucus ex vivo; binding of LPS-coated latex beads to human antral gastric tissue was inhibited by TFF1. Conclusions: TFF1 interacts specifically with H pylori RF-LPS. The pH dependence of this interaction indicates that binding of H pylori to TFF1 in the stomach could promote colonization of the mucus layer adjacent to the gastric epithelial surface.