Objectives
The aim of this study was to evaluate a possible relationship between DRD2/ANKK1 (rs1800497) and SLC6A3/DAT1 (rs28363170) gene polymorphisms with the response to levodopa (L‐DOPA)‐therapy in patients with Parkinson's disease (PD).
Methods
One hundred and ninety‐five patients with idiopathic PD were investigated. Patients were genotyped for rs1800497 and rs28363170 polymorphisms using PCR‐RFLP. Logistic regression was performed to assess the association of polymorphisms with the occurrence of the chronic complications of L‐DOPA therapy.
Key findings
Our results showed association between the occurrence of dyskinesia with an increased greater disease severity (P = 0.007), higher L‐DOPA dose (P = 0.007) and use of dopamine agonist (P = 0.020). Moreover, there were significant protective effects for age (P = 0.004) and male subjects (P = 0.006).
Conclusions
Clinical and demographic characteristics of Brazilian PD patients and differences in DRD2 and DAT1 genes may to determine individual variations in the therapeutic response to L‐DOPA in the Brazilian PD patients.
Rheumatoid arthritis (RA) is a progressive, autoimmune disease for which the previous studies have shown that some functional polymorphisms can influence its etiology. Knowing this, the aim of this study was to investigate the association of +2199 A/C IL-23R (rs10889677), -197 G/A IL-17A (rs2275913), and +7488 A/G IL-17F (rs763780) gene polymorphisms with RA susceptibility and clinical features in a Brazilian population. A total of 127 RA patients and 134 healthy controls were recruited for the analyses of polymorphic variants. Genotyping was performed using RFLP-PCR. Logistic regression was used to analyze the genotype distribution of the polymorphisms. Individuals carrying the homozygous CC genotype for the IL-23R polymorphism seem to be at lower risk for RA development (OR 0.22; p = 0.004), as well as those carrying the variant C allele (OR 0.56; p = 0.002). For the -197 G/A IL-17A polymorphism, the wild-type genotype (GG) was significantly associated with a 3.18-fold (OR 3.18; p = 0.033) increased risk for RA. In relation to the +7488 A/G IL-17F polymorphism, no significant difference was found between RA cases and control subjects (p > 0.05). Moreover, when investigating the relationship between polymorphisms and clinical features, no evidence of an association was found. Our findings suggest that the variants +2199 A/C IL-23R and -197 G/A IL-17A could contribute to RA development in the studied population. However, larger studies are needed to fully understand this genetic predisposition.
Objective: To evaluate agreement between 3 methods for screening anal intraepithelial lesions: anal cytology, anoscopy and human papillomavirus (HPV) detection by PCR. Study Design: This prospective, cross-sectional study screened 324 women with cervical neoplasia for anal neoplasia. Agreement between methods was calculated using the ĸ coefficient. Results: Of 324 anal cytologies performed, 31.5% (n = 102) were found to be abnormal: low-grade anal lesions were detected in 19.1% (n = 62) of cases, high-grade lesions in 3.1% (n = 10) and atypical squamous cells of undetermined significance in 9.3% (n = 30). With respect to the biopsies, 25.7% (n = 20) were positive, consisting of 7 cases of HPV infection, 5 anal intraepithelial neoplasia (AIN) grade 1, 6 AIN grade 2, and 2 AIN grade 3. Twenty-one samples (6.5%) were inadequate for HPV analysis. Of the 303 adequate samples, 84.2% (n = 255) tested positive for HPV. Agreement between cytology and anoscopy was fair (ĸ = 0.31). Agreement between PCR for HPV and cytology was slight (ĸ = 0.08) and no agreement was found between PCR for HPV and anoscopy (ĸ = 0.00). Conclusion: Agreement between the different methods of diagnosing HPV-induced anal lesions is slight to fair; however, anal cytology permits identification of cases in which lesions are present, allowing them to be referred for anoscopy and biopsy.
The prevalence of anal intraepithelial neoplasia was high among patients with cervical neoplasia who did not have HIV, particularly patients older than 35 years.
Enterococcus faecium is a lactic acid bacterium with applications in food engineering and nutrigenomics, including as starter cultures in fermented foods. To differentiate the E. faecium probiotic from pathogenic bacteria, physiological analyses are often used but they do not guarantee that a bacterial strain is not pathogenic. We report here new findings and an approach based on comparison of the genetic mobility of (1) probiotic, (2) pathogenic, and (3) nonpathogenic and non-probiotic strains, so as to differentiate probiotics, and inform their safe use. The region of the 16S ribosomal DNA (rDNA) genes of different E. faecium strains native to Pernambuco-Brazil was used with the GenBank query sequence. Complete genomes were selected and divided into three groups as noted above to identify the mobile genetic elements (MGEs) (transposase, integrase, conjugative transposon protein and phage) and antibiotic resistance genes (ARGs), and to undertake pangenome analysis and multiple genome alignment. Differences in the number of MGEs were found in ARGs, in the presence and absence of the genes that differentiate E. faecium probiotics and pathogenic bacteria genetically. Our data suggest that genetic mobility appears to be informative in differentiating between probiotic and pathogenic strains. While the present findings are not necessarily applicable to all probiotics, they offer novel molecular insights to guide future research in nutrigenomics, clinical medicine, and food engineering on new ways to differentiate pathogenic from probiotic bacteria.
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