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This article aims to verify the relationship between the composition and diversity of oral microbiota with overweight and obese children and adolescents. This systematic review was registered in PROSPERO, followed PRISMA 2020, and included an electronic search until March 2022, in PubMed/MEDLINE, Web of Science, Scopus, and The Cochrane Library databases. Studies were eligible if they compared the oral microbiota according to nutrition status among children and adolescents. Independent peers using JBI Critical Appraisal Checklists assessed the quality of studies. Eleven studies were eligible to be included in this review, with a total of 1,695 children and adolescents, 224 were obese, 190 were overweight, 1,154 were eutrophics and 127 were underweight. The most frequent phyla in overweight and obese children and adolescents, in comparison to their counterparts were Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria and Fusobacteria. It was identified that nine of the eleven articles selected showed an association between oral microbiota and overweight and obesity in children and adolescents. We observed that there is an important association between oral bacterial composition diversity and overweight and obesity. This finding indicates the relevance of the evaluation and surveillance in oral health to control cases of overweight and obesity in children and adolescents. [ABSTRACT FROM AUTHOR]

Background: The objective of this study is to evaluate the diagnostic accuracy of plasma‐based liquid biopsy for the detection of the BRAF V600E mutation in circulating cell‐free DNA from patients with ameloblastoma. Methods: This is a prospective diagnostic accuracy study conducted based on the Standards for Reporting Diagnostic Accuracy recommendations. The index test was the plasma‐based liquid biopsy, whereas the reference standard was the conventional tissue biopsy. The target condition was the detection of BRAF V600E mutation. The study population consisted of individuals with ameloblastoma recruited from three tertiary hospitals from Brazil. A negative control group composed of three individuals with confirmed wild‐type BRAF lesions were included. The participants underwent plasma circulating cell‐free DNA and tumor tissue DNA isolation, and both were submitted to using competitive allele‐specific TaqMan™ real‐time polymerase chain reaction technology mutation detection assays. Sensitivity and specificity measures and positive and negative predictive values were calculated. Results: Twelve patients with conventional ameloblastoma were included. BRAF V600E mutation was detected in 11/12 (91.66%) ameloblastoma tissue samples. However, the mutation was not detected in any of the plasma‐based liquid biopsy circulating cell‐free DNA samples in both ameloblastomas and negative control group. The sensitivity and specificity of plasma‐based liquid biopsy for the detection of the BRAF V600E mutation in circulating cell‐free DNA was 0.0 and 1.0, respectively. The agreement between index test and reference standard results was 26.66%. Conclusion: Plasma‐based liquid biopsy does not seem to be an accurate method for the detection of the BRAF V600E mutation in circulating circulating cell‐free DNA from patients with ameloblastoma, regardless of tumor size, anatomic location, recurrence status, and other clinicopathological features. [ABSTRACT FROM AUTHOR]

Aim: To verify the association of the TNF‐α, IL‐6, and IL‐10 polymorphisms with chronic temporomandibular disorder pain development in female elderly patients. Methods: Participants were evaluated according to Diagnostic Criteria for Temporomandibular Disorders. The genomic DNA was extracted from blood according to the Salting Out method followed by a quantification using the NanoDrop spectrophotometer. The –308G/A TNF‐α polymorphism analysis was performed by the polymerase chain reaction‐restriction fragment length polymorphism technique, the determination of –174G/C IL‐6 polymorphism was performed by polymerase chain reaction, and the evaluation of the –1082A/G IL‐10 polymorphism was carried out by polymerase chain reaction‐ allele‐specific amplification. Data were analyzed using the BioEstat 5.3 software. Results: The –308G/A TNF‐α polymorphism showed a significant difference when genotypes of cases with chronic temporomandibular disorder pain and controls were compared (p =.025). There was a lack of association regarding the –174G/C IL‐6 polymorphism (p =.286) however, a positive association between the –1082A/G IL‐10 polymorphism with chronic temporomandibular disorder was observed (p =.020). Conclusion: The analyzed data of elderly subjects support the possible involvement of the GA genotype of the –308G/A TNF‐α and the AA genotype of the –1082A/G IL‐10 polymorphisms in the pathogenesis of chronic temporomandibular disorder pain. [ABSTRACT FROM AUTHOR]

This study evaluated IL-6 salivary levels as well as the +3954 polymorphism of IL-1β in patients with burning mouth syndrome and healthy individuals, through case-control studies. This systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We conducted this research in PubMed/MEDLINE, Cochrane Library and Web of Science databases. The risk of bias was measured based in the Newcastle-Ottawa Scale. Researches with a group of patients with burning mouth syndrome and a control group in which the presence of the +3954 polymorphism of IL-1β and/ or IL-6 salivary levels through non-stimulated saliva were evaluated to detect if this interleukin concentrations are increased in patients and if the polymorphism is a risk factor for this syndrome. We identified seven studies with total of 440 participants, 229 patients with burning mouth syndrome and 211 healthy controls, ages 24-84 years old. The female gender was predominant. Patients in the majority of studies did not present increased levels of IL-6 and the +3954 polymorphism of IL-1β is not a risk factor for this syndrome. A few studies researched biomarkers in this pathology and more investigations are required not only to identify salivary levels and the polymorphism evaluated, but also other interleukins and polymorphisms in order to clarify the etiopathogenesis of this syndrome as well as for propose new diagnostic methods and treatments. [ABSTRACT FROM AUTHOR]

Hepatitis C virus (HCV) is the major cause of hepatocellular carcinoma (HCC). The risk to develop HCC increases with the severity of liver inflammation and hepatic fibrosis. It is believed that a balance between the releases of pro- and anti-inflammatory cytokines will determine the clinical course of HCV and the risk to develop HCC. The inteleukin-10 (IL-10) and the tumor necrosis factor alpha (TNF-α) play key roles in the Th1 and Th2 balance during the inflammatory response against HCV. The aim of the present study was to investigate the association between polymorphisms in TNF-α -308 G>A (rs1800629), IL-10 -1082 G>A (rs1800896) and -819/-592 (rs1800871/rs1800872) with HCC risk in individuals with HCV. The present study evaluated 388 chronic HCV patients. Polymorphisms were determined by real-time PCR. Diplotypes associated with low IL-10 production and the TNF-α GG genotype were significantly associated with HCC occurrence after multivariate logistic regression analysis ( P = 0.027 and P = 0.029, respectively). Additionally, the IL-10 -819 (-592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging ( P = 0.044 and P = 0.025, respectively). Patients carrying low production haplotypes of IL-10 and the TNF-α GG genotype have higher risk to develop HCC. J. Med. Virol. 88:1587-1595, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Folate metabolism dysfunction can lead to DNA hypomethylation and abnormal chromosomal segregation. Previous investigations of this association have produced controversial results. Here we performed a case-control study in patients with Turner syndrome (TS) to determine the effects of genetic polymorphisms of folate pathway genes as potential risk factors for somatic chromosomal nondisjunction. TS is a useful model for this investigation because patients with TS show a high frequency of chromosome mosaicism. Here we investigated the possible association of polymorphisms of the MTHFR gene with TS risk, which has been previously investigated with controversial results. We also examined the effects of MTR, RFC1, and TYMS gene polymorphisms in TS for the first time. The risk was evaluated according to allelic and genotype (independent and combined) frequencies among 70 patients with TS and 144 age-matched healthy control subjects. Polymorphism genotyping was performed by PCR, PCR-RFLP, and PCR-ASA. The polymorphisms MTHFR 677C>T and 1298A>C, MTR 2756A>G, RFC1 80G>A, and TYMS 2R/3R-alone or in combinations-were not associated with the risk of chromosomal aneuploidy in TS. In conclusion, our present findings did not support a link between impaired folate metabolism and abnormal chromosome segregation leading to somatic nondisjunction in TS patients. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Epidemiological and experimental studies indicate that the altered fetal and neonatal environment influences physiological functions and may increase the risk of developing chronic diseases in adulthood. Because homocysteine (Hcy) metabolic imbalance is considered a risk factor for neurodegenerative diseases, we investigated whether maternal Vitamin B deficiency during early development alters the offspring's methionine-homocysteine metabolism in their brain. To this end, the dams were submitted to experimental diet one month before and during pregnancy or pregnancy/lactation. After birth, the offspring were organized into the following groups: control (CT), deficient diet during pregnancy and lactation (DPL) and deficient diet during pregnancy (DP). The mice were euthanized at various stages of development. Hcy, cysteine, glutathione (GSH), S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), folate and cobalamin concentrations were measured in the plasma and/or brain. At postnatal day (PND) 0, total brain of female and male offspring exhibited decreased SAM/SAH ratios. Moreover, at PND 28, we observed decreased GSH/GSSG ratios in both females and males in the DPL group. Exposure to a Vitamin B-deficient diet during the ontogenic plasticity period had a negative impact on plasma folate and brain cortex SAM concentrations in aged DPL males. We also observed decreased plasma GSH concentrations in both DP and DPL males (PND 210). Additionally, this manipulation seemed to affect the female and male offspring differently. The decreased plasma GSH concentration may reflect redox changes in tissues and the decreased brain cortex SAM may be involved in changes of gene expression, which could contribute to neurodegenerative diseases over the long term. [ABSTRACT FROM AUTHOR]

Objetives: to describe the clinical and laboratory characteristics, determine rates of response to treatment and pinpoint risk factors that influence the survival of pediatric patients with acute lymphoblastic leukemia (ALL). Methods: this is a retrospective series of case studies involving 108 patients aged 18 years or under hospitalized for ALL treatment at the Fundaçao de Hematologia e Hemoterapia de Pernambuco (HEMOPE), Brazil, between January 1993 and December 2001. The following variables were analyzed: gender age, main symptoms and signs, white blood-cell count, immunophenotype and risk group on diagnosis; rates of remission and relapse, death and overall survival;place of relapse and risk factors for survival. Descriptive measurements were used for the statistical analysis. The patient survival time was estimated using the Kaplan-Meier survival function and Log Rank. The effect of risk factors on survival time was evaluated using the Cox Regression Model. Results: the results showed a male:female ratio of 1.7:1, a median age of eight years on diagnosis, the frequency of musculoskeletal complaints was 51%, of infiltration of the central nervous system 8%, of ALL- Precursor B 81% and ALL-T 19%. The distribution of the groups corresponded to True Basic Risk (12%), Basic Risk (21%) and High Risk (67%). The rates of remission, relapse and overall survival were 86%, 24% and 62.5%, respectively. Conclusions: the variable having an impact on overall survival was the white blood-cell count. The overall survival rate in the study was influenced by the high frequency of high-risk patients. [ABSTRACT FROM AUTHOR]

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Interleukin 12 plays an important role in immunoregulation between the T helper 1/T helper 2 lymphocytes and in the antiviral and antitumor immune response. The aim of this study was to investigate the possible association between the interleukin 12B polymorphism rs3212227 and the risk to develop Hodgkin's lymphoma in childhood and adolescents. A total of 100 patients with Hodgkin's lymphoma and a group of 181 healthy controls were selected at random from a forensic laboratory of the University of Pernambuco. The AA genotype was detected in the controls (53.04%) and the AC genotype was found in the patients (54%). The AC genotype showed an association with the development of Hodgkin's lymphoma (odds ratio = 2.091, 95% confidence interval = 1.240–3.523, p = 0.007). When AC + CC genotypes were analyzed together, an increase in risk of 1.9 times more chances for HL development could be observed (odds ratio = 1.923, 95% confidence interval = 1.166–3.170, p = 0.014). However, there was no association between the AC and CC genotypes of the interleukin 12B polymorphism with the clinical risk group (p = 0.992, p = 0.648, respectively). Our results suggest that the presence of the C allele may be contributing to the development of Hodgkin's lymphoma in children and adolescents. [ABSTRACT FROM AUTHOR]

Background: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease, which includes a spectrum of hepatic pathology such as simple steatosis, steatohepatitis, fibrosis and cirrhosis. The increased serum levels of homocysteine (Hcy) may be associated with hepatic fat accumulation. Genetic mutations in the folate route may only mildly impair Hcy metabolism. The aim of this study was to investigate the relation between liver steatosis with plasma homocysteine level and MTHFR C677T and A1298C polymorphisms in Brazilian patients with NAFLD.Methods: Thirty-five patients diagnosed with NAFLD by liver biopsy and forty-five healthy controls neither age nor sex matched were genotyped for C677T and A1298C MTHFR polymorphisms using PCR-RFLP and PCR-ASA, respectively, and Hcy was determined by HPLC. All patients were negative for markers of Wilson's, hemochromatosis and autoimmune diseases. Their daily alcohol intake was less than 100 g/week. A set of metabolic and serum lipid markers were also measured at the time of liver biopsies.Results: The plasma Hcy level was higher in NAFLD patients compared to the control group (p = 0.0341). No statistical difference for genotypes 677C/T (p = 0.110) and 1298A/C (p = 0.343) in patients with NAFLD and control subjects was observed. The genotypes distribution was in Hardy-Weinberg equilibrium (677C/T p = 0.694 and 1298 A/C p = 0.188). The group of patients and controls showed a statistically significant difference (p < 0.001) for BMI and HOMA_IR, similarly to HDL cholesterol levels (p < 0,006), AST, ALT, γGT, AP and triglycerides levels (p < 0.001). A negative correlation was observed between levels of vitamin B12 and Hcy concentration (p = 0.005).Conclusion: Our results indicate that plasma Hcy was higher in NAFLD than controls. The MTHFR C677T and A1298C polymorphisms did not differ significantly between groups, despite the 677TT homozygous frequency was higher in patients (17.14%) than in controls (677TT = 4.44%) (p > 0.05). The suggested genetic susceptibility to the MTHFR C677T and A1298C should be confirmed in large population based studies. [ABSTRACT FROM AUTHOR]

The aim of this study was to examine the prevalence and genetic variability of the capsid L1 gene of rare HPV genotypes that were found in the cervical lesions of women from North-East Brazil. A total number of 263 patients were included in this study. HPV detection was performed using PCR followed by direct sequencing of MY09/11, as well as type-specific PCR to detect the Alpha-9 species. Epitope prediction was performed to determine whether or not the genetic variants are inserted in B-cell and T-cell epitopes. The prevalence of rare HPV types in cervical lesions was found to be 9.47%. The rare HPV genotypes that were detected were HPV-53, 54, 56, 61, 62, 66, 70, and 81. The genetic variability in the L1 gene of rare HPV types involved thirty nucleotide changes, eight of which were detected for the first time in this study. Moreover, some of these variants are embedded in B-cell or T-cell epitope regions. The results of this research suggest that rare HPV types might be involved in cervical lesions and some of these variants can be found in B-cell and T-cell epitopes. Data on the prevalence and variability of rare HPV types will assist in clarifying the role of these viruses in carcinogenesis. [ABSTRACT FROM AUTHOR]

In schistosomiasis mansoni (SM), periportal fibrosis (PPF) arises due to an inflammatory response exacerbated by parasite eggs in the intrahepatic portal space, culminating in the deposition of collagen and extracellular matrix proteins. This fibrosis results from a remodeling process of the extracellular matrix, in which metalloproteinases play a significant role. The study evaluated the association between MMP-3 polymorphism (-1171 5A>6A) (rs 3025058) and sociodemographic factors with PPF in individuals with SM. This is an analytical cross-sectional study involving 242 individuals infected with S. mansoni , of these 122 were diagnosed with hepatosplenic form (HS) and 119 hepatointestinal form (HI), all from the state of Pernambuco, Brazil. Polymerase chain reaction with restriction enzyme digestion (Psyl) was used to determine the MMP-3 polymorphism (-1171 5A>6A). There was a significant association between the male gender and the HS form (OR = 1.7623 95% CI [1.0481–2.9631]; p-value = 0.0439) as well as individuals aged over 41, also had a greater chance of developing this clinical form of the disease (OR = 2.8299; 95% CI [1.5211–5.2650]; p-value = 0.0014), with greater emphasis on individuals over 61 years old (OR= 8.5541; 95% CI [3.6895–19.8326], p-value= 0.0000). There was no statistically significant association between the MMP-3 polymorphism (-1171 5A>6A) between the clinical groups (5A6A CI [0.7144–1.9879] p-value 0.5882 5A5A CI [0.0912–2.9231] p-value 0.7331 5A6A / 5A5A CI [0.6904–1.8937] p-value 0.6949). In conclusion, the results showed no association between the MMP-3 polymorphism (-1171 5A>6A) and the development of PPF. In addition, males, and age over 41 were predictive factors for the HS form of the disease in this Brazilian population. Summary: This study investigated the association between the MMP-3 (5A/6A) polymorphism and periportal fibrosis in patients with schistosomiasis mansoni in the state of Pernambuco, Northeast Brazil. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract: The polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene are associated with leukemogenesis. In order to investigate the influence of two polymorphisms in the MTHFR gene, 677C>T and 1298A>C, on the risk of acute lymphoblastic leukemia (ALL) we performed a case–control study in children from different Brazilians’ regions. Genotyping of 176 ALL and 199 unselected healthy subjects was performed using PCR-RFLP assay. There was no association between the 677C>T or 1298A>C and risk of ALL in total case–control sample. However, 677T allele was linked to a decrease risk of ALL [odds ratio (OR), 0.43; 95% confidence interval (CI), 0.22–0.86], whereas the 1298A>C polymorphism presents an elevated risk factor [OR, 2.01; 95% CI, 1.01–3.99] in non-White children. Our investigation provides interesting data concerning the opposite effect of A1298C polymorphisms, particularly in the light of relatively scarce data regarding the MTHFR role in leukemia susceptibility in different populations. [Copyright &y& Elsevier]