Sugar-(fructose, xylose, glucose, lactose, maltose, sucrose) glycine solutions of water activity adjusted to 0.90 (by adding NaCI) were heated at 45-6X.The behavior of fructose-glycine solutions was well described by a zero-order reaction model, but for the other sugars a fractional-order (-0.5) kinetic model was necessary. Activation energies for glucose, fructose and sucrose systems were 25.7, 29.3 and 36.6 kcahmole, respectively. At pH 6 the descending order for color development was xylose > glucose > fructose > lactose > maltose > sucrose; at pH lower than 6 fructose browned faster than glucose. The role of hydrolysis of sucrose as related to Maillard's browning of heated sucrose-glycine solutions was studied. Caramelization browning seemed to contribute noticeably to total color development only in fructose-glycine solutions.

In adolescent patients with GERD, esomeprazole 20 or 40 mg daily for 8 weeks was well tolerated, and GERD-related symptoms were significantly reduced from baseline values in both groups.

A 13-year-old girl presented with epigastric pain, nausea, and heartburn. The patient had normal physical examination and blood tests. Upper endoscopy revealed bile reflux, cobblestone mucosa, and small nodule with whitish cap at the fundus (Figs 1 and 2). Gastric biopsies showed foveolar hyperplasia and foamy macrophages in the lamina propria, consistent with Helicobacter pylori gastritis and xanthelasma (Fig. 3). The patient was treated for H pylori, but her parents refused a second upper endoscopy to determine whether the lesion disappeared.Xanthelasma, a benign lesion, is a rare finding in the adult population with only 1 case reported in a child. In adults, it is mainly found in the gastric mucosa and occasionally in the esophagus or duodenum (1). The lesion appears as a yellowish-whitish nodule or plaque, single or multiple, from 0.5 to 10.0 mm (2,3). Etiology is unknown, but gastric xanthelasmas are seen when there are other pathological changes, such as chronic and atrophic gastritis, intestinal metaplasia, and bile reflux. Studies in adults show that these lesions are highly associated with H pylori infection (4). Although these lesions are not at increased risk for gastric cancer, biopsies are recommended to differentiate them from gastric tumors (3). Follow-up should include upper endoscopy to better understand the behavior of these lesions.

Objectives: To analyze the IBD5 locus in a homogenous cohort of Ashkenazi Jewish (AJ) children with Crohn disease (CD). Patients and Methods: A total of 83 AJ children with CD and 73 AJ healthy controls were studied. Genotyping for single nucleotide polymorphisms (SNPs) including OCTN1 (SLC22A4; 1672C!T), OCTN2 (SLC22A5; 207G!C), IGR2096, IGR2198, and IGR2230 genes was performed using the TaqMan system. NOD2/CARD15 variants also were typed using established methods. Results: All IBD5 SNPs tested were in linkage disequilibrium (D 0 >0.8), and showed significant association with CD in our cohort of AJ children. The IGR2096 SNP, which is not located within the same linkage disequilibrium block as the OCTN1 and 2 SNPs, showed an even stronger association with CD (P ¼ 0.017; odds ratio ¼ 1.7). Patients with CD who had the OCTN1 susceptibility allele were more likely to carry 1 of the 3 NOD2/CARD15 SNPs tested (P ¼ 0.01; odds ratio ¼ 4.8). Conclusions: We have demonstrated a significant association between the IBD5 locus and CD in a homogenous cohort of pediatric AJ patients. Due to the tight linkage disequilibrium in the region, it is not possible to identify the causative IBD5 variant. Future functional studies will ultimately reveal the causative gene variant at this locus. JPGN 48:531-537, 2009.