[Biological characteristics and functions of NG2-glia].

NG2-glia are a major type of glial cells that are widely distributed in the central nervous system (CNS). Under physiological conditions, they mainly differentiate into oligodendrocytes and contribute to the myelination of axons, so they are generally called oligodendrocyte progenitor cells. Emerging evidence suggests that NG2-glia not only act as the precursors of oligodendrocytes but also possess many other biological properties and functions. For example, NG2-glia can form synapse with neurons and participate in energy metabolism and immune regulation. Under pathological conditions, NG2-glia can also differentiate into astrocytes, Schwann cells and even neurons, which are involved in CNS injury and repair. Therefore, a deeper understanding of the biological characteristics and functions of NG2-glia under physiological and pathological conditions will be helpful for the treatment of CNS injury and disease. This article reviews the recent advances in the biological characteristics and functions of NG2-glia.

[Structural, mechanistic and functional insights into topoisomerase II].

Topoisomerases are nuclear enzymes that regulate the overwinding or underwinding of DNA helix during replication, transcription, recombination, repair, and chromatin remodeling. These enzymes perform topological transformations by providing a transient DNA break, through which the unique problems of DNA entanglement that occur owing to unwinding and rewinding of the DNA helix can be resolved. In mammals, topoisomerases are classified into two types, type I topoisomerase (Top1) and type II topoisomerase (Top2), depending on the number of strands cut in one round of action. Top1 induces single-strand breaks in DNA, and Top2 induces double-strand breaks. In cells from vertebrate species, there are two forms of Top2, designated alpha and beta. Top2α is involved in the cellular proliferation and pluripotency, while Top2ß plays key roles in neurodevelopment. In this review, we cover recent advances in structural, mechanistic and functional insights into Top2.

Foveal pit morphological changes in asymptomatic carriers of the G11778A mutation with Leber's hereditary optic neuropathy.

AIM: To investigate the foveal pit morphology changes in unaffected carriers and affected Leber's hereditary optic neuropathy (LHON) patients with the G11778A mutation from one family. METHODS: This study was a prospective cross-sectional study. Both eyes from 16 family members (age from 9 to 47y) with the G11778A mutation were analyzed and compared with 1 eye from 20 normal control subjects. Eleven family members with the G11778A mutation but without optic neuropathy were classified as unaffected carriers (n=22 eyes). Five family members (n=10 eyes) expressed the LHON phenotype and were classified as affected patients. Retinal images of all the subjects were taken by optical coherence tomography (OCT), and an automatic algorithm was used to segment the retina to eight layers. Horizontal and vertical OCT images centered on the fovea were used to measure intra-retinal layer thicknesses and foveal morphometry. RESULTS: Thicker foveal thickness, thinner foveal pit depth, and flatter foveal slopes were observed in unaffected carriers and affected LHON patients (all P<0.001). Further, the slopes of all four sectors in the LHON were flatter than those in the unaffected carriers (all P<0.001). Compared with the control group, affected LHON patients had a thinner retinal nerve fiber layer (RNFL), ganglion cell layer and inner plexiform layer (GCL+IPL), and total retina (all P<0.01). The retinal nerve fiber layer (RNFL) of affected patients was 38.0% thinner than that of controls while the GCL+IPL was 40.1% thinner. CONCLUSION: The foveal pit morphology shows changes in both unaffected carriers and affects patients. RNFL and GCL+IPL are thinner in affected LHON patients but not in unaffected carriers.

Expanding the Phenotypic and Genotypic Landscape of Nonsyndromic High Myopia: A Cross-Sectional Study in 731 Chinese Patients.

Purpose: High myopia (HM) is defined as a refractive error worse than -6.00 diopter (D). This study aims to update the phenotypic and genotypic landscape of nonsyndromic HM and to establish a biological link between the phenotypic traits and genetic deficiencies. Methods: A cross-sectional study involving 731 participants varying in refractive error, axial length (AL), age, myopic retinopathy, and visual impairment. The phenotypic traits were analyzed by four ophthalmologists while mutational screening was performed in eight autosomal causative genes. Finally, we assessed the clinical relevance of identified mutations under the guidance of the American College of Medical Genetics and Genomics. Results: The relationship between refractive error and AL varied in four different age groups ranging from 3- to 85-years old. In adult groups older than 21 years, 1-mm increase in AL conferred 10.84% higher risk of pathologic retinopathy (Category ≥2) as well as 7.35% higher risk of low vision (best-corrected visual acuities <0.3) with P values < 0.001. The prevalence rates of pathologic retinopathy and low vision both showed a nonlinear positive correlation with age. Forty-five patients were confirmed to harbor pathogenic mutations, including 20 novel mutations. These mutations enriched the mutational pool of nonsyndromic HM to 1.5 times its previous size and enabled a statistically significant analysis of the genotype-phenotype correlation. Finally, SLC39A5, CCDC111, BSG, and P4HA2 were more relevant to eye elongation, while ZNF644, SCO2, and LEPREL1 appeared more relevant to refracting media. Conclusions: Our findings shed light on how multiple HM-related phenotypes are associated with each other and their link with gene variants.

[Myopic proptosis and the associated changes in axial components of the eye].

OBJECTIVE: To investigate the correlation between proptosis and changes of axial components in myopic eyes. METHODS: One hundred and eighty-nine myopic and emmetropic eyes were included. There are one hundred and eighty-three right eyes and six left eyes. Based on axial length (AL), subjects were divided into three groups: low-myopia & emmetropia group, moderate myopia group, high myopia group. Refraction of the eye (SE, spherical equivalent) was measured by retinoscopy examination under mydriasis. Proptosis was measured by Exophthalmometer (K-0161 Hertel-Type). Axial components including axial length and corneal curvature and were measured by partial coherence laser interferometry (IOL-master). The correlation in results among proptosis, axial components, and refraction was evaluated. RESULTS: The proptosis in high myopia group was bigger than in the other groups (P < 0.01). The proptosis in moderate myopia group was bigger than in low-myopia and emmetropia group (P < 0.01). The axial length was shorter than 25 mm in low-myopia and emmetropia group, from 25.00 to 27.00 mm in moderate myopia group and equal or longer than 27 mm in high myopia group. There was an increasing trend in proptosis [ranging from (14.66 +/- 1.94) mm, (16.16 +/- 1.40) mm to (18.30 +/- 1.63) mm] and axial length [ranging from (23.54 +/- 0.73) mm, (25.77 +/- 0.53) mm to (30.08 +/- 2.09) mm] among the three groups, the order of groups in the ranging was from low-myopia and emmetropia group, moderate myopia group to high myopia group. There was a highly significant correlation between proptosis and AL (R(2) = 0.990, F = 18 450.30, P < 0.01). Refraction results in low-myopia and emmetropia group, moderate myopia group and high myopia group were (-0.76 +/- 1.29) diopters (D), (-5.33 +/- 2.37) diopters (D) and (-15.92 +/- 5.12) diopters (D) respectively. There was a moderate correlation between proptosis and SE (R(2) = 0.500, F = 187.05, P < 0.01). There was a highly significant correlation between axial length and refraction (R(2) = 0.892, F = 1537.83, P < 0.01). CONCLUSION: Myopic proptosis increases with the increasing AL and SE of the eye. The eyeball tends to expand backward and proptosis forward with the increasing AL and the proptosis forward appears to be more obvious.

The glial scar in spinal cord injury and repair.

Glial scarring following severe tissue damage and inflammation after spinal cord injury (SCI) is due to an extreme, uncontrolled form of reactive astrogliosis that typically occurs around the injury site. The scarring process includes the misalignment of activated astrocytes and the deposition of inhibitory chondroitin sulfate proteoglycans. Here, we first discuss recent developments in the molecular and cellular features of glial scar formation, with special focus on the potential cellular origin of scar-forming cells and the molecular mechanisms underlying glial scar formation after SCI. Second, we discuss the role of glial scar formation in the regulation of axonal regeneration and the cascades of neuro-inflammation. Last, we summarize the physical and pharmacological approaches targeting the modulation of glial scarring to better understand the role of glial scar formation in the repair of SCI.