Breastfeeding and the risk of dental caries: a systematic review and meta-analysis

Aim To synthesise the current evidence for the associations between breastfeeding and dental caries, with respect to specific windows of early childhood caries risk. Methods Systematic review, meta-analyses and narrative synthesis following searches of PubMed, CINAHL and EMBASE databases. Results Sixty-three papers included. Children exposed to longer versus shorter duration of breastfeeding up to age 12 months (more versus less breastfeeding), had a reduced risk of caries (OR 0.50; 95%CI 0.25, 0.99, I2 86.8%). Children breastfed > 12 months had an increased riskof caries when compared with children breastfed 12 months, those fed nocturnally or more frequently had afurther increased caries risk (five studies, OR 7.14; 3.14, 16.23, I2 77.1%). There was a lack of studies on children aged > 12 months simultaneously assessing caries risk in breastfed, bottle-fed and children not bottle or breastfed, alongside specific breastfeeding practices, consuming sweet drinks and foods, and oral hygiene practices limiting our ability to tease out the risks attributable to each. Conclusion Breastfeeding in infancy may protect against dental caries. Further research needed to understand the increased risk of caries in children breastfed after 12 month

Scaling of divertor power footprint width in RF-heated type-III ELMy H-mode on the EAST superconducting tokamak

Dedicated experiments for the scaling of divertor power footprint width have been performed in the ITER-relevant radio-frequency (RF)-heated H-mode scheme under the lower single null, double null and upper single null divertor configurations in the Experimental Advanced Superconducting Tokamak (EAST) under lithium wall coating conditioning. A strong inverse scaling of the edge localized mode (ELM)-averaged power fall-off width with the plasma current (equivalently the poloidal field) has been demonstrated for the attached type-III ELMy H-mode as $\lambda_{q} \propto I_{{\rm p}}^{-1.05}$ by various heat flux diagnostics including the divertor Langmuir probes (LPs), infra-red (IR) thermograph and reciprocating LPs on the low-field side. The IR camera and divertor LP measurements show that \lambda_{q,{\rm IR}} \approx {\lambda_{q,{\rm div\mbox{-}LPs}}}/{1.3}=1.15B_{{\rm p,omp}}^{-1.25} , in good agreement with the multi-machine scaling trend during the inter-ELM phase between type-I ELMs or ELM-free enhanced Dα (EDA). H-mode. However, the magnitude is nearly doubled, which may be attributed to the different operation scenarios or heating schemes in EAST, i.e., dominated by electron heating. It is also shown that the type-III ELMs only broaden the power fall-off width slightly, and the ELM-averaged width is representative for the inter-ELM period. Furthermore, the inverse Ip (Bp) scaling appears to be independent of the divertor configurations in EAST. The divertor power footprint integral width, fall-off width and dissipation width derived from EAST IR camera measurements follow the relation, λint cong λq + 1.64S, yielding $\lambda_{\rm int}^{{\rm EAST}} =(1.39\pm 0.03)\lambda_{q}^{{\rm EAST}} +(0.97\pm 0.35)\,{\rm mm}$ . Detailed analysis of these three characteristic widths was carried out to shed more light on their extrapolation to ITER

Partial Loss of USP9X Function Leads to a Male Neurodevelopmental and Behavioral Disorder Converging on Transforming Growth Factor beta Signaling

BACKGROUND: The X-chromosome gene USP9X encodes a deubiquitylating enzyme that has been associated with neurodevelopmental disorders primarily in female subjects. USP9X escapes X inactivation, and in female subjects de novo heterozygous copy number loss or truncating mutations cause haploinsufficiency culminating in a recognizable syndrome with intellectual disability and signature brain and congenital abnormalities. In contrast, the involvement of USP9X in male neurodevelopmental disorders remains tentative.METHODS: We used clinically recommended guidelines to collect and interrogate the pathogenicity of 44 USP9X variants associated with neurodevelopmental disorders in males. Functional studies in patient-derived cell lines and mice were used to determine mechanisms of pathology.RESULTS: Twelve missense variants showed strong evidence of pathogenicity. We define a characteristic phenotype of the central nervous system (white matter disturbances, thin corpus callosum, and widened ventricles); global delay with significant alteration of speech, language, and behavior; hypotonia; joint hypermobility; visual system defects; and other common congenital and dysmorphic features. Comparison of in silico and phenotypical features align additional variants of unknown significance with likely pathogenicity. In support of partial loss-of-function mechanisms, using patient-derived cell lines, we show loss of only specific USP9X substrates that regulate neurodevelopmental signaling pathways and a united defect in transforming growth factor signaling. In addition, we find correlates of the male phenotype in Usp9x brain-specific knockout mice, and further resolve loss of hippocannpal-dependent learning and memory.CONCLUSIONS: Our data demonstrate the involvement of USP9X variants in a distinctive neurodevelopmental and behavioral syndrome in male subjects and identify plausible mechanisms of pathogenesis centered on disrupted transforming growth factor beta signaling and hippocampal function.Genetics of disease, diagnosis and treatmen