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1.  A Real-Time Localization System for an Endoscopic Capsule Using Magnetic Sensors † 
Sensors (Basel, Switzerland)  2014;14(11):20910-20929.
Magnetic sensing technology offers an attractive alternative for in vivo tracking with much better performance than RF and ultrasound technologies. In this paper, an efficient in vivo magnetic tracking system is presented. The proposed system is intended to localize an endoscopic capsule which delivers biomarkers around specific locations of the gastrointestinal (GI) tract. For efficiently localizing a magnetic marker inside the capsule, a mathematical model has been developed for the magnetic field around a cylindrical magnet and used with a localization algorithm that provides minimum error and fast computation. The proposed tracking system has much reduced complexity compared to the ones reported in the literature to date. Laboratory tests and in vivo animal trials have demonstrated the suitability of the proposed system for tracking a magnetic marker with expected accuracy.
PMCID: PMC4279517  PMID: 25379813
in vivo tracking; magnetic localization system; real-time tracking; gastrointestinal tract; endoscopic capsule
2.  Dietary supplementation with soy isoflavones or replacement with soy proteins prevents hepatic lipid droplet accumulation and alters expression of genes involved in lipid metabolism in rats 
Genes & Nutrition  2013;9(1):373.
Accumulation of hepatic lipid droplet (HLD) is the hallmark pathology of non-alcoholic fatty liver disease (NAFLD). This study examined the effects of soy isoflavones (ISF) and different amounts of soy proteins on the accumulation of HLD, lipid metabolism and related gene expression in rats. Weanling Sprague–Dawley rats were fed diets containing either 20 % casein protein without (D1) or with (D2) supplemental ISF (50 mg/kg diet) or substitution of casein with increasing amounts of alcohol-washed soy protein isolate (SPI, 5, 10, and 20 %; D3, D4, D5) for 90 days. Dietary casein (20 %) induced accumulation of HLD in female, but not in male rats. Both soy proteins and ISF remarkably prevented the formation of HLD. Soy proteins lowered hepatic total cholesterol and triglyceride in a dose-dependent manner. Interestingly, soy proteins but not ISF significantly increased free fatty acids in the liver of the female rats compared to D1. Proteomic analysis showed that at least 3 enzymes involved in lipogenesis were down-regulated and 7 proteins related to fatty acid β-oxidation or lipolysis were up-regulated by soy protein over D1. Additionally, 9 differentially expressed proteins identified were related to amino acid metabolism, 5 to glycolysis and 2 to cholesterol metabolism. Dietary ISF and SPI markedly reduced hepatic-peroxisome-proliferator-activated receptor γ2 (PPARγ2) and fat-specific protein 27 (FSP27) in female rats. Overall, this study has shown that partial or full replacement of dietary casein by soy protein or supplementation with soy ISF can effectively prevent the accumulation of HLD. The potential molecular mechanism(s) involved might be due to suppression of lipogenesis and stimulation of lipolysis and down-regulation of PPARγ2 and FSP27. This suggests that consumption of soy foods or supplements might be a useful strategy for the prevention or treatment of fatty liver diseases.
Electronic supplementary material
The online version of this article (doi:10.1007/s12263-013-0373-3) contains supplementary material, which is available to authorized users.
PMCID: PMC3896634  PMID: 24292949
Soy proteins; Isoflavones; Fatty liver; Lipid metabolism; Gene expression
3.  Correction: Negligible Colon Cancer Risk from Food-Borne Acrylamide Exposure in Male F344 Rats and Nude (nu/nu) Mice-Bearing Human Colon Tumor Xenografts 
PLoS ONE  2013;8(9):10.1371/annotation/f040499f-8485-4f7f-88bd-6720379064e9.
PMCID: PMC3770789
4.  Negligible Colon Cancer Risk from Food-Borne Acrylamide Exposure in Male F344 Rats and Nude (nu/nu) Mice-Bearing Human Colon Tumor Xenografts 
PLoS ONE  2013;8(9):e73916.
Acrylamide, a possible human carcinogen, is formed in certain carbohydrate-rich foods processed at high temperature. We evaluated if dietary acrylamide, at doses (0.5, 1.0 or 2.0 mg/kg diet) reflecting upper levels found in human foods, modulated colon tumorigenesis in two rodent models. Male F344 rats were randomized to receive diets without (control) or with acrylamide. 2-weeks later, rats in each group received two weekly subcutaneous injections of either azoxymethane (AOM) or saline, and were killed 20 weeks post-injections; colons were assessed for tumors. Male athymic nude (nu/nu) mice bearing HT-29 human colon adenocarcinoma cells-derived tumor xenografts received diets without (control) or with acrylamide; tumor growth was monitored and mice were killed 4 weeks later. In the F344 rat study, no tumors were found in the colons of the saline-injected rats. However, the colon tumor incidence was 54.2% and 66.7% in the control and the 2 mg/kg acrylamide-treated AOM-injected groups, respectively. While tumor multiplicity was similar across all diet groups, tumor size and burden were higher in the 2 mg/kg acrylamide group compared to the AOM control. These results suggest that acrylamide by itself is not a “complete carcinogen”, but acts as a “co-carcinogen” by exacerbating the effects of AOM. The nude mouse study indicated no differences in the growth of human colon tumor xenografts between acrylamide-treated and control mice, suggesting that acrylamide does not aid in the progression of established tumors. Hence, food-borne acrylamide at levels comparable to those found in human foods is neither an independent carcinogen nor a tumor promoter in the colon. However, our results characterize a potential hazard of acrylamide as a colon co-carcinogen in association with known and possibly other environmental tumor initiators/promoters.
PMCID: PMC3764052  PMID: 24040114
5.  Gastric precancerous lesions are associated with gene variants in Helicobacter pylori-susceptible ethnic Malays 
AIM: To identify genes associated with gastric precancerous lesions in Helicobacter pylori (H. pylori)-susceptible ethnic Malays.
METHODS: Twenty-three Malay subjects with H. pylori infection and gastric precancerous lesions identified during endoscopy were included as “cases”. Thirty-seven Malay subjects who were H. pylori negative and had no precancerous lesions were included as “controls”. Venous blood was collected for genotyping with Affymetrix 50K Xba1 kit. Genotypes with call rates < 90% for autosomal single nucleotide polymorphisms (SNPs) were excluded. For each precancerous lesion, associated SNPs were identified from Manhattan plots, and only SNPs with a χ2 P value < 0.05 and Hardy Weinberg Equilibrium P value > 0.5 was considered as significant markers.
RESULTS: Of the 23 H. pylori-positive subjects recruited, one sample was excluded from further analysis due to a low genotyping call rate. Of the 22 H. pylori-positive samples, atrophic gastritis only was present in 50.0%, complete intestinal metaplasia was present in 18.25%, both incomplete intestinal metaplasia and dysplasia was present in 22.7%, and dysplasia only was present in 9.1%. SNPs rs9315542 (UFM1 gene), rs6878265 (THBS4 gene), rs1042194 (CYP2C19 gene) and rs10505799 (MGST1 gene) were significantly associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia with foci of dysplasia and dysplasia, respectively. Allele frequencies in “cases” vs “controls” for rs9315542, rs6878265, rs1042194 and rs10505799 were 0.4 vs 0.06, 0.6 vs 0.01, 0.6 vs 0.01 and 0.5 vs 0.02, respectively.
CONCLUSION: Genetic variants possibly related to gastric precancerous lesions in ethnic Malays susceptible to H. pylori infection were identified for testing in subsequent trials.
PMCID: PMC3691040  PMID: 23801863
Gastric precancerous lesions; Gene polymorphisms; Genome-wide association; Helicobacter pylori; Malays
6.  Barrett's Esophagus in an Area with an Exceptionally Low Prevalence of Helicobacter pylori Infection 
ISRN Gastroenterology  2011;2011:394734.
Objective. This study was undertaken to gain an insight into the relationship between Helicobacter pylori (H. pylori) infection, Barrett's esophagus and reflux esophagitis in an area of exceptionally low prevalence of H. pylori infection. Methods. A total of 1895 consecutive upper endoscopies performed between January 2005 and July 2007 were reviewed. 120 cases of columnar-lined esophagus and endoscopic esophagitis were evaluated. H. pylori infection was determined using the urease test and/or histology. Results. The rate of endoscopic esophagitis was 5.49% (80 Malays, 24 non-Malays) while histological reflux esophagitis was found in 3.75% (56 Malays, 15 non-Malays). Barrett's esophagus was present in 0.79% (11 Malays, 4 non-Malays). H. pylori infection was present in 8/120 or 6.67% subjects. Conclusion. The low rate of Barrett's esophagus in this population does not support the hypothesis that the absence of H. pylori infection is more than a minor risk factor for Barrett's esophagus.
PMCID: PMC3168394  PMID: 21991505

Results 1-6 (6)