Bioinformatics analyses of significant prognostic risk markers for thyroid papillary carcinoma.

This study was aimed to identify the prognostic risk markers for thyroid papillary carcinoma (TPC) by bioinformatics. The clinical data of TPC and their microRNAs (miRNAs) and genes expression profile data were downloaded from The Cancer Genome Atlas. Elastic net-Cox's proportional regression hazards model (EN-COX) was used to identify the prognostic associated factors. The receiver operating characteristic (ROC) curve and Kaplan-Meier (KM) curve were used to screen the significant prognostic risk miRNA and genes. Then, the target genes of the obtained miRNAs were predicted followed by function prediction. Finally, the significant risk genes were performed literature mining and function analysis. Total 1046 miRNAs and 20531 genes in 484 cases samples were identified after data preprocessing. From the EN-COX model, 30 prognostic risk factors were obtained. Based on the 30 risk factors, 3 miRNAs and 11 genes were identified from the ROC and KM curves. The target genes of miRNA-342 such as B-cell CLL/lymphoma 2 (BCL2) were mainly enriched in the biological process related to cellular metabolic process and Disease Ontology terms of lymphoma. The target genes of miRNA-93 were mainly enriched in the pathway of G1 phase. Among the 11 prognostic risk genes, v-maf avian musculoaponeurotic fibrosarcoma oncogene homologue F (MAFF), SRY (sex-determining region Y)-box 4 (SOX4), and retinoic acid receptor, alpha (RARA) encoded transcription factors. Besides, RARA was enriched in four pathways. These prognostic markers such as miRNA-93, miRNA-342, RARA, MAFF, SOX4, and BCL2 may be used as targets for TPC chemoprevention.

[Multiple factor analysis of visual function in hypermetropic children].

OBJECTIVE: To investigate the characteristics of hypermetropic children whose visual acuity (VA) is declined or accompanied by esotropia. METHODS: One hundred and ninety children were given optometry, strabismus degree and binocular vision measurement. RESULTS: Declined VA appeared in 170 children, while esotropia occurred in 173. Sixty-one got binocular single vision, 17 had fusion function, and 11 had stereoaculty. Spherical equivalent had a linear relationship with VA (P < 0.01), but not with the strabismus degree (P > 0.05). The influence factors of binocular vision were age of discovery, VA and the strabismus degree, while the stereoaculty was influenced by the strabismus degree, spherical equivalent and VA. CONCLUSION: Low VA and strabismus are the most common complaint in children. Ametropia and strabismus do great harm to juvenile binocular vision, and stereoaculty is damaged seriously. We suggest an early examination of visual function in children.

Molecular imaging of retinal gliosis in transgenic mice induced by kainic acid neurotoxicity.

PURPOSE: Gliosis is a universal response of the central nervous system to diverse insults. Here the authors aimed to develop a noninvasive fluorescence system to monitor and quantify retinal gliosis in real time. METHODS: Transgenic mice expressing green fluorescent protein (GFP) under the control of the glial fibrillary acidic protein promoter were treated with excitatory neurotoxicant kainic acid (KA) through a single intraperitoneal injection to induce gliosis in the brain and the retina. The expression of the GFAP-GFP transgene as a surrogate reporter for gliosis was noninvasively and longitudinally imaged with a confocal scanning laser ophthalmoscope for 2 weeks to monitor the progression of gliosis. RESULTS: The authors demonstrated that KA-induced gliosis (an elevation in GFP fluorescence intensity [FI]) could be noninvasively detected starting on day 3 and that it peaked on day 7, as quantified for the optic disc astrocytes. A significant increase in the FI in retinal glial cells was also visible on the processed images. Immunohistochemistry in defined regions of the brain (hippocampal CA1, CA3, dentate gyrus) known to be affected by KA neurotoxicity showed that severe gliosis in these regions occurred at day 7, when retinal gliosis peaked. CONCLUSIONS: The current real-time fluorescent imaging method described here is a powerful preclinical tool to directly monitor retinal gliosis caused by various retinopathies. In addition, this molecular imaging method should be useful in assessing retinal neurotoxicity and in therapeutic development in a preclinical setting.