Enhancing the prebiotic effect of cellulose biopolymer in the gut by physical structuring via particle size manipulation.

Cellulose is generally recognised as dietary fibre with no limit of permissible quantity in food, and its consumption may modulate digesta content and impact positively on the gastrointestinal physiology and gut microflora. However, cellulose in its native form possessed inherent undesirable physical properties, making it unattractive for food applications. Here, we postulate that by changing cellulose size to nanometric scale, its prebiotic effect would be altered and fermented differently in contrast with micro size cellulose by the gut microbiome and promote the yield of metabolites such as short chain fatty acids (SCFAs). Using faecal matter from three healthy human donors as microbial source, in vitro fermentation of variable size fractions of cellulose from the same were fermented under anaerobic conditions, and SCFAs as well Bifidobacterium selectively isolated and analysed. The increase in production of acetate (194%), butyrate (224%) and propionate (211%) after 24 h of fermentation was significantly promoted by the size reduction and revealed size-dependent relationship as exemplified R2 values >0.83. Consequently, gavaging rats with nanometric size cellulose (125 nm) significantly (p < 0.05) increased these SCFAs yields as well Bifidobacterium counts in contrast with both control and the micro scale size cellulose. Therefore, engineered nanocellulose might have beneficial physiological impact on the gut with improved prebiotic effect.

The expression and prognostic value of SOX2, ß-catenin and survivin in esophageal squamous cell carcinoma.

Aim: We mainly explored the effect of SOX2, ß-catenin and survivin on prognosis in esophageal squamous cell carcinoma. Materials & methods: Immunohistochemistry was used to examine the expression of SOX2, ß-catenin and survivin. χ2 test was used to analyze the relationship between proteins and clinicopathological parameters. Survival analysis was used to investigate the effect of three proteins on prognosis. Results: SOX2 was related to lymph node metastasis (p = 0.004) and vascular invasion (p = 0.041). ß-catenin was associated with depth of invasion (p = 0.014), lymph node metastasis (p = 0.032) and postoperative chemoradiotherapy (p < 0.001). Survivin was related to gender (p = 0.022) and nerve invasion (p = 0.014). There was a positive correlation between SOX2 and ß-catenin. Patients with SOX2 and ß-catenin overexpression had poor prognosis. Survivin-positive patients who received postoperative chemoradiotherapy had a short time. Conclusion: SOX2, ß-catenin and survivin can be used as prognostic markers of esophageal squamous cell carcinoma.

The Silencing of SFRP2 Expression in ESCC Is Due to Methylation of the Gene Promoter.

OBJECTIVE: Our aim of the study was to investigate the expression level and methylation status of the secreted frizzled-related protein 2 in esophageal squamous cell carcinoma and to evaluate the clinical utility of the marker. MATERIAL AND METHODS: We first used Immunohistochemistry (ICH) to explore the expression level of secreted frizzled-related protein 2 protein in esophageal squamous cell carcinoma tissues and adjacent normal tissues and then used methylation-specific polymerase chain reaction and bisulfite sequencing polymerase chain reaction to detect methylation status of secreted frizzled-related protein 2. RESULTS: Secreted frizzled-related protein 2 expression was notably reduced in patients with esophageal squamous cell carcinoma, whereas methylation of secreted frizzled-related protein 2 was increased in the majority of esophageal squamous cell carcinoma specimens. CONCLUSION: Sum up, we have demonstrated the abnormal DNA hypermethylation, causing reduced or absent gene expression. Methylation testing of secreted frizzled-related protein 2 using epigenetic marker may be a significative screening method for patients with esophageal squamous cell carcinoma.

The effect of Glut1 and c-myc on prognosis in esophageal squamous cell carcinoma of Kazakh and Han patients.

AIM: Glucose transporter type 1 (Glut1) plays a crucial role in cancer-specific metabolism. We explored the expression of Glut1 and c-myc, the relationship between them and the effect of Glut1, c-myc on prognosis in esophageal squamous cell carcinoma. MATERIALS & METHODS: Immunohistochemistry was used to examine the expression of Glut1 and c-myc. χ2 test analyzes the relationship between c-myc, Glut1 and pathological parameters. Spearman correlation analyzes the relationship between c-myc and Glut1. Survival analysis was used to investigate the effect of Glut1 and c-myc on prognosis. RESULTS: Glut1 positivity was associated with tumor size (p < 0.01), depth of invasion (p = 0.021), Tumor, Node, Metastasis stage (IA+IB,II+IIB,IIIA+IIIB,IVA+IVB; p = 0.004), lymph node metastasis (p = 0.002) and nerve invasion (p = 0.050). C-myc positivity was associated with tumor location (p = 0.015), depth of invasion (p = 0.022) and lymph node metastasis (p = 0.035). There was a positive correlation between c-myc and Glut1 (r = 0.321). Patients with Glut1 c-myc co-expression had poorer prognosis. CONCLUSION: Inhibiting Glut1 c-myc co-expression may improve the prognosis of esophageal squamous cell carcinoma.

The Impact of Gene Polymorphisms on Anticoagulation Control With Warfarin.

Differences in warfarin maintenance dosages based on the presence of polymorphisms in VKORC1, CYP2C9, CYP4F2, and ORM1 can be determined through dosage adjustment according to routine guidelines. Little is known about whether routine therapy could provide consensus anticoagulation control for patients with different genotypes. This study was carried out to compare anticoagulant control in patients with different genotypes. Six hundred seventy patients using warfarin according to Chinese guidelines were enrolled. Warfarin dosages and monitored international normalized ratios (INRs) were recorded. Genotypes of VKORC1 rs9923231, CYP4F2 rs2108622, CYP2C9 rs1057910, and ORM1 rs17650 polymorphisms were determined. Warfarin dosages and INR were compared between genotypes. Patients with the AGCC*F*F*1*1 polymorphism took longer than patients with the AACC*F*F*1*1 polymorphism (20 vs 5 days, P < .001) to achieve the targeted INR range. The INR values of patients with AACC*F*F*1*3 were unstable and did not enter the stable state control phase until after 35 days. The peak INR of patients with the AACC*F*F*1*3 polymorphism was exceedingly high, with some values exceeding the control range limit of 3.0. Patients with the AACC*F*S*1*1 or AACT*F*F*1*1 polymorphisms exhibited similar INR values as the patients with the AACC*F*F*1*1 polymorphism. This study found that routine medication with warfarin provides significantly different levels of anticoagulant control between patients with wild-type genotypes and patients with heterozygous polymorphism genotypes of VKORC1 rs9923231 or CYP2C9 rs1057910. Patients with heterozygous polymorphism genotypes of VKORC1 or CYP2C9 require genotype-directed therapy with warfarin to increase efficacy and safety in anticoagulant treatment.