All groups improved their balance performance, but contrary to expectations, investigational groups did not outperform the Control group at practice or retention. Unexpectedly, the IT+SC group reported greater nervousness than the Control and IT groups, suggesting that the employed success criteria may have induced performance-related anxiety. Regression analyses revealed that self-efficacy increase from initial practice predicted performance at the end of practice and at retention. These findings highlight the potential contribution of psychological factors on motor function and rehabilitation in individuals with PD. This article is protected by copyright. All rights reserved.Due to its hemizygous inheritance and role in sex determination, the X chromosome is expected to play an important role in the evolution of sexual dimorphism, and to be enriched for sexually antagonistic genetic variation. By forcing the X chromosome to only be expressed in males over > 40 generations, we changed the selection pressures on the X to become similar to those experienced by the Y. This releases the X from any constraints arising from selection in females, and should lead to specialization for male fitness, which could occur either via direct effects of X-linked loci or trans-regulation of autosomal loci by the X. We found evidence of masculinization via upregulation of male-benefit sexually antagonistic genes, and downregulation of X-linked female benefit genes. Potential artifacts of the experimental evolution protocol are discussed and cannot be wholly discounted, leading to several caveats. Interestingly, we could detect evidence of microevolutionary changes consistent with previously documented macroevolutionary patterns, such as changes in expression consistent with previously established patterns of sexual dimorphism, an increase in the expression of metabolic genes related to mitonuclear conflict, and evidence that dosage compensation effects can be rapidly altered. These results confirm the importance of the X in the evolution of sexual dimorphism and as a source for sexually antagonistic genetic variation, and demonstrate that experimental evolution can be a fruitful method for testing theories of sex chromosome evolution. This article is protected by copyright. All rights reserved.BACKGROUND Although estrogen deficiency has been proposed as a risk factor for oral mucosal inflammatory diseases in post-menopausal women, the mechanisms involved remain unclear.  https://www.selleckchem.com/  This study aimed to investigate the effect of 17β-estradiol (E2) on the inflammatory response stimulated by interleukin-1 beta (IL-1β) in human oral mucosal epithelial cells (hOMECs) and its possible mechanism. METHODS Primary hOMECs were obtained from female infants and cultured in keratinocyte growth medium. The hOMECs at second passage were collected and stimulated by 10-7 M ICI182,780 or 10-7 M G1 for 1 h, E2 (10-7 M, 10-8 M, 10-9 M) for 36 h, 100ng/ml IL-1β for 12 h, respectively. Human beta-2 defensin (hBD-2), tumor necrosis factor-alpha (TNF)-α, IL-6, IL-8, estrogen receptor-alpha (ERα), estrogen receptor-beta (ERβ), and G protein-coupled receptor 30 (GPR30) mRNA levels and protein levels were measured by real-time quantitative polymerase chain reaction (RT-qPCR), enzyme linked immunosorbent assay (ELISA), and Western Blot (WB) respectively. RESULTS Expression of hBD-2 and inflammatory cytokines increased after IL-1β stimulation, which was down-regulated by E2 pretreatment. With ICI182,780, the suppression of E2 on hBD-2 mRNA was attenuated. With G1, the mRNA and protein expression of hBD-2 were reduced. CONCLUSION Pretreatment of hOMECs with E2 at physiological concentrations inhibited the IL-1β-induced expression of hBD-2 and inflammatory cytokines. The protective effects of E2 suggest its potential use treating oral inflammatory diseases in clinical practice. This article is protected by copyright. All rights reserved.Monocyte-derived macrophages play a role in the repair of the injured brain. We previously reported that a deficiency of the Parkinson's disease (PD)-associated gene DJ-1 delays repair of brain injury produced by stereotaxic injection of ATP, a component of damage-associated molecular patterns. Here, we show that a DJ-1 deficiency attenuates monocyte infiltration into the damaged brain owing to a decrease in C-C motif chemokine ligand 2 (CCL2) expression in astrocytes. Like DJ-1-knockout (KO) mice, CCL2 receptor (CCR2)-KO mice showed defects in monocyte infiltration and delayed recovery of brain injury, as determined by 9.4 T magnetic resonance imaging analysis and immunostaining for tyrosine hydroxylase and glial fibrillary acid protein. Notably, transcriptome analyses showed that genes related to regeneration and synapse formation were similarly downregulated in injured brains of DJ-1-KO and CCR2-KO mice compared with the injured wild-type brain. These results indicate that defective astrogliosis in DJ-1-KO mice is associated with decreased CCL2 expression and attenuated monocyte infiltration, resulting in delayed repair of brain injury. Thus, delayed repair of brain injury could contribute to the development of PD. MAIN POINTS A DJ-1 deficiency attenuates infiltration of monocytes owing to a decrease in CCL2 expression in astrocytes, which in turn led to delay in repair of brain injury. © 2020 Wiley Periodicals, Inc.BACKGROUND The Childhood Atopic Dermatits Impact Scale (CADIS) with 45 items may be burdensome to complete. We therefore aimed to develop a CADIS short-form. METHODS Parents of 300 children completed the prototype CADIS. Exploratory factor analysis was conducted on the 45-item CADIS version. The most representative items were chosen. Confirmatory factor analysis was used to confirm the a priori factor structure. Content validity was assessed in a focus group of patients, parents, clinicians, methodologists and industry delegates. Internal consistency, 48-hour test-retest reliability, construct validity and responsiveness of the newly developed short-form were assessed. RESULTS 270 families provided data at baseline, 34 after 48 hours and 228 after four weeks. Fourteen items of three different factors fulfilled the proposed eligibility criteria and were included in the draft short-form. After the content validity rating, one item relating to the child's sleep was added to further improve content validity. The confirmatory factor analyses showed good model fit and a 15-item short-form was initiated, the CADIS-SF15.