ABSTRACT
The etiological agent of Chagas disease is the protozoan Trypanosoma cruzi. According to the World Health Organization, about seven to eight million people are infected with T. cruzi worldwide. The main routes of transmission are vectorial and oral, which has assumed great epidemiological importance, since there is no legislation that requires the pasteurization of açaí pulp. The present work aimed to look T. cruzi in 35 samples of açaí ice cream sold at different points of sale, covering 11 different cities in São Paulo State. Thus, the parasitological technique of forced sieving and the molecular test of Polymerase Chain Reaction were performed. For PCR analysis were used the 121/122 primer that amplifies the kinetoplast of the T. cruzi DNA (kDNA). By the forced sieving technique, the açaí pulp aliquots were analyzed under different storage temperatures and in different periods. One positive sample (2.86%) were observed at six hours at room temperature, but without motility and negative to the PCR technique. Two other açaí samples (5.71%) were positive by PCR, but negative by forced sieving. The results indicate the need for quality control and good manufacturing practices for the safe consumption of açaí-derived products.
Subject(s)
Chagas Disease , Euterpe , Trypanosoma cruzi , Brazil , DNA, Protozoan , Humans , Polymerase Chain Reaction , Trypanosoma cruzi/geneticsABSTRACT
PURPOSE: Analyze the expression of caspase-9, Smac/DIABLO, XIAP, let-7a, and let-7b in patients with normal gastric tissue, chronic gastritis, and gastric adenocarcinoma. METHODS: The expression of caspase-9, Smac/DIABLO, XIAP, let-7a, and let-7b by qRT-PCR was analyzed in 158 samples from 53 patients with normal gastric mucosa, 86 with chronic gastritis, and 19 with gastric cancer. RESULTS: The comparison between the gastric cancer and the control group revealed a decreased expression of caspase-9 in gastric cancer tissues; considering the Helicobacter pylor presence, comparable results were revealed. Smac/DIABLO was increased in gastric cancer cells, while XIAP demonstrated no significant difference in the gene expression. The microRNA analysis revealed a decreased expression of let-7a and let-7b in samples positive to H. pylori infection and in gastric cancer group, regardless of the presence of the bacterium. CONCLUSION: Our study provided some evidence of low activity of the intrinsic apoptosis pathway, as well as the influence of H. pylori on let-7a and let-7b expression.
Subject(s)
Adenocarcinoma/genetics , Apoptosis/genetics , Biomarkers, Tumor/genetics , Carcinogenesis/genetics , Stomach Neoplasms/genetics , Adenocarcinoma/pathology , Adult , Aged , Apoptosis Regulatory Proteins/genetics , Biopsy , Caspase 9/genetics , Female , Gastric Mucosa/microbiology , Gastric Mucosa/pathology , Gastritis/genetics , Gastritis/microbiology , Gastritis/pathology , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Helicobacter Infections/genetics , Helicobacter Infections/microbiology , Helicobacter Infections/pathology , Helicobacter pylori/isolation & purification , Humans , Male , MicroRNAs/genetics , Middle Aged , Mitochondrial Proteins/genetics , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathology , X-Linked Inhibitor of Apoptosis Protein/geneticsABSTRACT
The process of combating neoplasms and mononuclear cells, and during H. pylori infection, several pro-inflammatory and anti-inflammatory cytokines are synthesized. In view of the involvement of the IL-6 law and the presence of H. pylori in the development of gastric diseases, the present study aimed to characterize the promoter-region polymorphism -597 (G/A) (rs1800797), -572 (C/G) (rs1800796), and -174 (G/C) (rs1800795) by PCR-RFLP in 375 gastric biopsy specimens from patients with peptic symptoms. A total of 375 samples were analyzed: 87 patients (without lesion without gastric tissue); 236 patients with gastritis and 52 patients with gastric cancer analyzed the PCR-RFLP techniques. All the results were normalized in relation to the presence of H. pylori. The frequencies of the three polymorphisms were compared in the Control vs Gastritis groups and a statistically significant test observed: -174 (G/C) (OR: 1.27; 95% CI: 0.84-1.93; P = 0.26), 572 (C/G) (OR: 1.42; 95% CI: 0.78-2.59; P = 0.25), and 597 (G/A) (OR: 0.98; 95% CI, 0.64-1.52; P = 0.94). Similar results were obtained when the gastric cancer group was compared to the control group: -174 (G/C) (OR: 1.27; 95% CI: 0.66-2.47; P = 0.47), -572 (C/G) (OR: 1.07; 95% CI: 0.43-2.68; P = 0.88), and -597 (G/A) (OR: 1.01; 95% CI, 0.5-0.9; P = 0.99). The haplotypes were and were not observed statistically significant differences. In conclusion, we found no correlations between any of the three polymorphisms in the IL-6 gene analyzed in this study and a higher risk of gastritis or gastric cancer.
