Home reading environment, sociometric and demographic factors associated with dyslexia in primary school students in China: A case-control study.

Background: Developmental dyslexia (DD) has been generally recognized as a multifactorial psychological disorder in recent decades. However, studies on reading and learning environment, social and demographic factors affecting Chinese developmental dyslexia (DD) are still scarce in China. This study aims to explore multidimensional home influencing factors associated with DD before and after birth. Methods: A total of 60 dyslexic and 252 normal elementary school students graded 2-5 were recruited in Shantou, China. The Least Absolute Shrinkage and Selection Operator (LASSO) regression model was used for the social and demographic variables screening. Odds ratios (ORs) with 95 % confidence intervals (CIs) for associations between DD and related factors were estimated by multivariate logistic regression models. Results: Through LASSO regression, we ultimately identified 13 key variables, including maternal education level and family monthly income, among others. The logistic regression analyses showed that the risk of DD was higher in children with lower maternal education levels. Divergent parenting styles may be a risk factor for developing DD as opposed to consistent parenting styles (OR = 4.93, 95%CI: 1.11-21.91). Children whose mothers suffered from malnutrition during pregnancy were more likely to develop DD (OR = 10.31, 95%CI: 1.84-37.86), as well as exposure to second-hand smoking at home every day (OR = 5.33, 95%CI: 1.52-18.66). Interestingly, children's active reading (OR = 0.26, 95%CI: 0.08-0.84; OR = 0.17, 95%CI: 0.04-0.76 for "sometimes" and "often" compared to none, respectively), children having extracurricular reading fairy tale books (OR = 0.37, 95%CI: 0.15-0.90), and children having extracurricular reading composition books (OR = 0.25, 95%CI: 0.09-0.69) were significant protective factors for DD. Conclusions: Home reading environment, several educational, sociometric and demographic factors may influence the development of dyslexia. We should pay attention to these factors on the development of dyslexia, so as to provide the well social and familial environment to ensure the healthy development of children.

ZNF382 controls mouse neuropathic pain via silencer-based epigenetic inhibition of Cxcl13 in DRG neurons.

Nerve injury-induced changes of gene expression in dorsal root ganglion (DRG) are critical for neuropathic pain genesis. However, how these changes occur remains elusive. Here we report the down-regulation of zinc finger protein 382 (ZNF382) in injured DRG neurons after nerve injury. Rescuing this down-regulation attenuates nociceptive hypersensitivity. Conversely, mimicking this down-regulation produces neuropathic pain symptoms, which are alleviated by C-X-C motif chemokine 13 (CXCL13) knockdown or its receptor CXCR5 knockout. Mechanistically, an identified cis-acting silencer at distal upstream of the Cxcl13 promoter suppresses Cxcl13 transcription via binding to ZNF382. Blocking this binding or genetically deleting this silencer abolishes the ZNF382 suppression on Cxcl13 transcription and impairs ZNF382-induced antinociception. Moreover, ZNF382 down-regulation disrupts the repressive epigenetic complex containing histone deacetylase 1 and SET domain bifurcated 1 at the silencer-promoter loop, resulting in Cxcl13 transcriptional activation. Thus, ZNF382 down-regulation is required for neuropathic pain likely through silencer-based epigenetic disinhibition of CXCL13, a key neuropathic pain player, in DRG neurons.

The excitatory effects of the chemokine CCL2 on DRG somata are greater after an injury of the ganglion than after an injury of the spinal or peripheral nerve.

We compared the expression of chemokine receptor CCR2 protein in the dorsal root ganglia (DRG) injured by the chronic constriction injury (CCI), the spinal nerve ligation (SNL) and a chronic compression of DRG (CCD). Each of these injuries produced the same significant increase in CCR2 protein in the DRG, as assessed by Western blot analyses. Whole-cell patch-clamp recordings revealed that CCL2, a ligand for CCR2 receptor, depolarized nociceptive DRG neurons from rats of the all three models. A greater percentage of these neurons was depolarized by CCL2 after CCD than after either of the other injuries. Furthermore, CCL2 significantly lowered current threshold only in CCD neurons but not in CCI or SNL neurons. CCL2 significantly lowered the net whole-cell potassium currents in neurons after CCD but not after CCI or SNL. Thus, the injury-induced effects of CCL2 in increasing the excitability of the cell bodies of DRG neurons depend on the site of the injury--with greater effects occurring after an injury of the ganglion than after an injury of the spinal or peripheral nerve.