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Biomedical subjects

Xinghuai Sun

Publications and source records attributed to Xinghuai Sun.

6 recordsLinked to original sources

Glaucoma and brain functional networks: a bidirectional Mendelian randomisation study.

OBJECTIVE: Glaucoma is a complex neurodegenerative ocular disorder accompanied by brain functional abnormalities that extend beyond the visual system. However, the causal association between the two remains unclear at present. This study aimed to investigate the potential causal relationships between glaucoma and brain functional networks in order to provide novel insights into the neuropathic mechanism of glaucoma. METHODS AND ANALYSIS: Based on the genome-wide association studies data of glaucoma and resting-state functional MRI (Rs-fMRI), a bidirectional Mendelian randomisation (MR) analysis was conducted between glaucoma and brain functional networks. Inverse variance weighting was applied as the primary method to estimate causality with false discovery rate correction. Additional sensitivity analyses were conducted to evaluate the robustness of the results. RESULTS: Forward MR analysis suggested that glaucoma was causally associated with two brain networks between the subcortical cerebellum and the attention or visual network (p=0.022), as well as the default mode and central executive network (p=0.008), but without significance after false discovery rate correction (q>0.1). Reverse MR analysis revealed 19 Rs-fMRI traits related to glaucoma risk, including the salience or central executive network in the frontal region (p=0.0005, q=0.08) and the motor network (p=0.0009, q=0.08) with significant causality. CONCLUSIONS: This MR study revealed potentially causal relationships between glaucoma and brain functional networks. Especially, the functional connectivity of the motor network between the postcentral or precentral areas may potentially lead to increased risk of glaucoma.

Humans↗

Muller glia induce retinal progenitor cells to differentiate into retinal ganglion cells.

Retinal progenitor cells could differentiate into various retinal cells that made cell-replacement therapy possible. Here, we investigated the role of cellular microenvironment on their regulation and differentiation and found that the percentage of proliferating cells and the percentage of retinal ganglion cells produced from them increased, when retinal progenitor cells were cocultured with Muller glia. Muller glia conditioned medium had the similar results. It is speculated that rather than traditional supportive roles, Muller glia may have an active regulatory role inducing retinal progenitor cells to proliferate and differentiate into ganglion cells by secreting some diffusible and membrane-associated factors. Identification of Muller glia-derived factors will be made to elucidate the molecular mechanisms of neurogenesis.

Animals↗

Presymptomatic genetic diagnosis for consulters from a large Chinese family with juvenile open angle glaucoma.

PURPOSE: To provide genetic counseling and presymptomatic diagnosis to family members by investigating the genetic cause of a large primary juvenile open angle glaucoma (JOAG) pedigree with an autosomal dominant pattern. METHODS: Ocular examinations were performed on all members of the pedigree in order to determine their disease status. Subjects were labeled as affected individuals, unaffected individuals, and suspects. Genomic DNA was extracted from the peripheral blood of the family members. Three exons of MYOC, 12 coding exons of OPTN, and two coding exons of CYP1B1 were amplified by polymerase chain reaction (PCR). Direct DNA sequencing was used to identify mutations in MYOC, OPTN, and CYP1B1. Presymptomatic diagnoses were made for the consulters based on the results of both clinical examination and genetic analysis. RESULTS: One heterozygous mutation in the MYOC gene was identified in all patients of the pedigree. It was a cytosine to thymine transition at nucleotide 1,109, which corresponded to an amino acid residue change from proline to leucine at codon 370. The Pro370Leu mutation correlated with a severe JOAG phenotype as previously reported. Two adolescents, who were labeled as suspects, were detected to carry the same mutation and thus had a high risk of developing glaucoma. Close follow-up at regular intervals was recommended. In addition, no pathogenic mutations of OPTN and CYP1B1 were detected. CONCLUSIONS: The Pro370Leu mutation of the MYOC gene contributed to JOAG in this pedigree. Early onset, rapid development, poor response to medicine and high penetrance are characteristics of this mutation. Genetic analysis is valuable for providing genetic counseling and presymptomatic diagnosis to members in typical autosomal inheritance pedigrees with JOAG.

Adolescent↗

Structure and function of myelinated nerve fibers in the rabbit eye following ischemia/reperfusion injury.

The rabbit eye presents a valuable model to study the effects of vascular occlusion on the function and structure of myelinated nerve fibers. The rabbit eye has a band of myelinated nerve fibers within the intraocular compartment that are supplied by a narrow band of retinal vasculature. These vessels were transiently occluded ( approximately 8 hours) using laser photocoagulation and the transmission of electrical signals along the nerve fibers was assessed by recording the visual evoked response (VER). Morphological damage was assessed by histological techniques. The ischemic insult produced no permanent change in retinal function as assessed by electroretinography, but the VER was suppressed, indicating failure of nerve fiber transmission. Histologically, the visible damage to the region supported by the retinal vasculature worsened following reperfusion, showing evidence of demyelination and necrosis followed by macrophage responses and gliosis. This rabbit model of ischemia/reperfusion of the retinal vasculature offers a rare opportunity to reliably study the response of myelinated nerve fibers to ischemia/reperfusion insults and has demonstrated the susceptibility of myelinated nerve fibers to such insults.

Animals↗

The protective role of Mecobalamin following optic nerve crush in adult rats.

PURPOSE: To evaluate the potential for Mecobalamin as a neuroprotective agent in optic nerve crush injury. METHODS: Twenty-four adult Sprague-Dawley rats were randomly divided into four groups. One group acted as normal controls, while in the other three groups the right eye was subjected to optic nerve crush injury. Of the three crush injury groups one group received no treatment, while the other two groups received intramuscular injections of VitaminB12 or Mecobalamin (10 microg) immediately after crush injury and then every two days. All the rats were sacrificed one month post-treatment, and the eyes attached with optic nerves were removed for histology. The morphological changes of optic nerve axons and retinal ganglion cells (RGCs) were assessed under light microscope (LM) and transmission electromicroscope (TEM). The numbers of axons and RGCs were counted. RESULTS: In this study we demonstrate the potential for Mecobalamin as a neuroprotective agent following optic nerve crush injury. We show here that the axons of optic nerves were loose in structure or destroyed. The mitochondria of the RGCs was swollen, and the Nissel body was less evident after the crush injury. Moreover, the number of axons and RGCs was significantly reduced (P < 0.001). However, these changes were less dramatic after the Mecobalamin-treatment. More axons and RGCs were remained in the group than those in the untreated injury group (P = 0.010 and 0.003 respectively), and those in the VitaminB12-treated group (P = 0.037 and 0.035 respectively). More significantly, there were newly formed axons found in the Mecobalamin-treated group. CONCLUSIONS: Optic nerve crush injury in rats causes the loss of the axons and RGCs but this may be ameliorated by treatment with Mecobalamin.

Animals↗

[Glaucoma valve devices for refractory glaucoma following vitrectomy].

OBJECTIVE: To evaluate the surgical effectiveness of glaucoma valve devices for refractory glaucoma following vitrectomy surgery. METHODS: Sixteen eyes of 15 patients suffering from secondary glaucoma following vitrectomy were treated with glaucoma valve implantation, all of the eyes were in critical condition, and the intraocular pressure failed to control after the silicone oil removal and/or with glaucoma medication. Among them, 13 eyes underwent Ahmed valve implantation and 3 eyes underwent Krupin disk implantation. RESULTS: The mean follow-up was 18.5 months. The total success rate was 76.9% at 3 months, 70.0% at 6 months and 66.7% at one year or longer. The postoperative complications included transient hyphema, early postoperative hypotony, choroidal detachment, shallow anterior chamber and obstruction of the tube tip. CONCLUSION: The glaucoma valve device is a safe and effective method for refractory glaucoma following vitrectomy, especially for the patients who have a certain level of visual acuity.

Adult↗