Introduction
The influence of aligners on the activity of the masticatory muscles is still controversial, especially regarding the behaviour associated with awake bruxism (AB).
Objective
To compare ...the frequency of AB behaviours between patients treated with aligners and fixed appliances.
Methods
The sample comprised 38 Class I patients (mean age 22.08 years), divided by simple randomisation into two groups: OA group; orthodontic aligners (n 19) and FA group; fixed appliance (n 19). The frequency of AB was investigated by the ecological momentary assessment using an online device (mentimeter), during 7 following days at different timepoints, before and after appliance placement and in the 2nd, 3rd, 4th and 6th months of orthodontic treatment. These variables were also evaluated: level of anxiety by the State‐Trait Anxiety Inventory, stress by the Perceived Stress Scale, catastrophising related to pain and degree of hypervigilance by the Pain Vigilance and Awareness Questionnaire, and the presence of facial pain evaluated by the DC/TMD.
Results
There was no difference between groups in the frequency of AB behaviours, with mean of 53.5% for group OA and 51.3% for FA. The most frequent behaviour was slightly touching the teeth, and in FA group, there was a significant reduction in this behaviour soon after appliance placement. The groups did not differ concerning the degree of anxiety, stress, catastrophising, hypervigilance and facial pain.
Conclusion
The orthodontic treatment performed with aligners or fixed appliances did not influence the frequency of AB during the 6 months of treatment.
Registry of Clinical Trials
(REBEC): RBR‐9zytwf.
Genome-wide association study-identified prostate cancer risk variants explain only a relatively small fraction of its familial relative risk, and the genes responsible for many of these identified ...associations remain unknown. To discover novel prostate cancer genetic loci and possible causal genes at previously identified risk loci, we performed a transcriptome-wide association study in 79,194 cases and 61,112 controls of European ancestry. Using data from the Genotype-Tissue Expression Project, we established genetic models to predict gene expression across the transcriptome for both prostate models and cross-tissue models and evaluated model performance using two independent datasets. We identified significant associations for 137 genes at
< 2.61 × 10
, a Bonferroni-corrected threshold, including nine genes that remained significant at
< 2.61 × 10
after adjusting for all known prostate cancer risk variants in nearby regions. Of the 128 remaining associated genes, 94 have not yet been reported as potential target genes at known loci. We silenced 14 genes and many showed a consistent effect on viability and colony-forming efficiency in three cell lines. Our study provides substantial new information to advance our understanding of prostate cancer genetics and biology. SIGNIFICANCE: This study identifies novel prostate cancer genetic loci and possible causal genes, advancing our understanding of the molecular mechanisms that drive prostate cancer.
The association of fitness with cancer risk is not clear.
We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for risk of lung, colorectal, ...endometrial, breast, and prostate cancer in a subset of UK Biobank participants who completed a submaximal fitness test in 2009-12 (N = 72,572). We also investigated relationships using two-sample Mendelian randomisation (MR), odds ratios (ORs) were estimated using the inverse-variance weighted method.
After a median of 11 years of follow-up, 4290 cancers of interest were diagnosed. A 3.5 ml O
⋅min
⋅kg
total-body mass increase in fitness (equivalent to 1 metabolic equivalent of task (MET), approximately 0.5 standard deviation (SD)) was associated with lower risks of endometrial (HR = 0.81, 95% CI: 0.73-0.89), colorectal (0.94, 0.90-0.99), and breast cancer (0.96, 0.92-0.99). In MR analyses, a 0.5 SD increase in genetically predicted O
⋅min
⋅kg
fat-free mass was associated with a lower risk of breast cancer (OR = 0.92, 95% CI: 0.86-0.98). After adjusting for adiposity, both the observational and genetic associations were attenuated.
Higher fitness levels may reduce risks of endometrial, colorectal, and breast cancer, though relationships with adiposity are complex and may mediate these relationships. Increasing fitness, including via changes in body composition, may be an effective strategy for cancer prevention.
Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and ...52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10
), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62-4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification.
The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This ...has now been corrected in both the PDF and HTML versions of the Article. Furthermore, In the original HTML version of this Article, the order of authors within the author list was incorrect. The consortium PRACTICAL consortium was incorrectly listed after Bogdan Pasaniuc and should have been listed after Kathryn L. Penney. This error has been corrected in the HTML version of the Article; the PDF version was correct at the time of publication.
Background
Testicular germ cell tumour (TGCT) is highly heritable but > 50% of the genetic risk remains unexplained. Epidemiological observation of greater relative risk to brothers of men with TGCT ...compared to sons has long alluded to recessively acting TGCT genetic susceptibility factors, but to date none have been reported. Runs of homozygosity (RoH) are a signature indicating underlying recessively acting alleles and have been associated with increased risk of other cancer types.
Objective
To examine whether RoH are associated with TGCT risk.
Methods
We performed a genome‐wide RoH analysis using GWAS data from 3206 TGCT cases and 7422 controls uniformly genotyped using the OncoArray platform.
Results
Global measures of homozygosity were not significantly different between cases and controls, and the frequency of individual consensus RoH was not significantly different between cases and controls, after correction for multiple testing. RoH at three regions, 11p13‐11p14.3, 5q14.1‐5q22.3 and 13q14.11‐13q.14.13, were, however, nominally statistically significant at p < 0.01. Intriguingly, RoH200 at 11p13‐11p14.3 encompasses Wilms tumour 1 (WT1), a recognized cancer susceptibility gene with roles in sex determination and developmental transcriptional regulation, processes repeatedly implicated in TGCT aetiology.
Discussion and conclusion
Overall, our data do not support a major role in the risk of TGCT for recessively acting alleles acting through homozygosity, as measured by RoH in outbred populations of cases and controls.
Reference values are necessary for classifying children, for health screening, and for early prevention as many non-communicable diseases aggravate during growth and development. While physical ...fitness reference standards are available in children aged 6 and older, such information is lacking in preschool children. Therefore, the purposes of this study were (1) to provide sex-and age-specific physical fitness reference standards for Spanish preschool children; and (2) to study sex differences across this age period and to characterise fitness performance throughout the preschool period.
Cross-sectional.
A total of 3179 preschool children (1678 boys) aged 2.8–6.4 years old from Spain were included in the present study. Physical fitness was measured using the PREFIT battery.
Age- and sex-specific percentiles for the physical fitness components are provided. Boys performed better than girls in the cardiorespiratory fitness, muscular strength, and speed-agility tests over the whole preschool period studied and for the different percentiles. In contrast, girls performed slightly better than boys in the balance test. Older children had better performance in all fitness tests than their younger counterparts.
Our study provides age- and sex-specific physical fitness reference standards in preschool children allowing interpretation of fitness assessment. Sexual dimorphism in fitness tests exists already at preschool age, and these differences become larger with age. These findings will help health, sport, and school professionals to identify preschool children with a high/very low fitness level, to examine changes in fitness over time, and to analyse those changes obtained due to intervention effects.
Although genome-wide association studies (GWAS) for prostate cancer (PrCa) have identified more than 100 risk regions, most of the risk genes at these regions remain largely unknown. Here we ...integrate the largest PrCa GWAS (N = 142,392) with gene expression measured in 45 tissues (N = 4458), including normal and tumor prostate, to perform a multi-tissue transcriptome-wide association study (TWAS) for PrCa. We identify 217 genes at 84 independent 1 Mb regions associated with PrCa risk, 9 of which are regions with no genome-wide significant SNP within 2 Mb. 23 genes are significant in TWAS only for alternative splicing models in prostate tumor thus supporting the hypothesis of splicing driving risk for continued oncogenesis. Finally, we use a Bayesian probabilistic approach to estimate credible sets of genes containing the causal gene at a pre-defined level; this reduced the list of 217 associations to 109 genes in the 90% credible set. Overall, our findings highlight the power of integrating expression with PrCa GWAS to identify novel risk loci and prioritize putative causal genes at known risk loci.
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