Correlations among peripapillary vasculature, macular superficial capillaries, and eye structure in healthy and myopic eyes of Chinese young adults (STROBE).

The correlations between retinal vessel distribution, anterior chamber depth (ACD) and other myopic eye structural parameters remains elusive. This study aims to investigate retinal vasculature and eye structure correlations in healthy and myopic eyes of Chinese young adults.In this cross-sectional study, 181 eyes (97 adults) were recruited. Macular and peripapillary vasculature was quantified by optical coherence tomography angiography. Correlations between retinal vasculature and eye structure were analyzed using multivariable linear regression.There were significant differences in ACD, spherical equivalent, axial length (AL), superficial macular vascular density (MVD), peripapillary vascular density (PVD) and circumference of foveal avascular zone (FAZ) among emmetropia, low-myopia, moderate-myopia, and high-myopia groups (both P < 0.05). Furthermore, ACD had significant positive correlation with AL and FAZ, but negative correlation with PVD. MVD also had a negative correlation with AL (beta = -0.247, P < .001). In addition, there was a significant negative correlation between circumference of the FAZ and spherical equivalent as well as central subfield thickness (beta = -0.20, P = .005; beta = -0.334, P < .001, respectively).The degree of myopia affected ACD, MVD, PVD, and circumference of the FAZ in eyes of young healthy adults. Meanwhile, ACD has a positive, while retinal vascular system measurements have a negative correlation with increasing severity of myopia.

MiR-145-modulated SOX9-mediated hypospadias through acting on mitogen-activated protein kinase signaling pathway.

This study primarily explored how miR-145, mitogen-activated protein kinase (MAPK) signaling and a downstream transcription factor (i.e., SOX9) mediated development of hypospadias. The hypospadias tissues and preputial tissues were isolated from pediatric inpatients postoperatively. Simultaneously, the rat models of hypospadias were established, and spermatogonial stem cells were separated. The expressions of proteins that symbolized cell apoptosis and oxidative stress were quantified via western blot analysis. Furthermore, the apoptosis, proliferation, and viability of cells were evaluated by means of flow cytometry, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assays. The results of microarray indicated miR-145 as a differentially expressed biomarker between hypospadias tissues and normal tissues (p < 0.05). Moreover, rat models of hypospadias were observed with markedly lower vitamins A and E levels, reduced expressions of proteins relevant to oxidative stress (i.e., Nrf2, HO-1, Gpx, and SOD-1), as well as enhanced Bax and cleaved caspase-3 expressions ( p < 0.05). Furthermore, SOX9 was found to be targeted by miR-145, and it was also modified by phosphorylated extracellular-regulated kinase (p-ERK), a portion of MAPK signaling ( p < 0.05). The p-ERK was significantly regulated after altering the expression of miR-145 ( p < 0.05). Moreover, activation of p-ERK and transfection of pcDNA-SOX9 could cause higher expression of apoptins and larger apoptotic proportion of cells ( p < 0.05), yet transfection of miR-145 mimic led to improved cell apoptosis and depressed cell viability ( p < 0.05). In conclusion, SOX9, which was regulated by both miR-145 and miR-145/MAPK signaling, could be involved in the pathogenesis of hypospadias.

Expression of hMSH2 gene and mutant p53 in sporadic digestive tract tumors.

OBJECTIVE: To investigate the role of mutated mismatch repair gene hMSH2 and mutant p53 gene in the carcinogenesis and development of sporadic digestive tract tumors. METHODS: hMSH2 gene in normal and tumor tissue of 30 digestive tract tumor specimens was examined using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) silver staining. The PCR product with an abnormal strand was sequenced directly. Mutant p53 protein in the tumor tissue was analyzed immunohistochemically. RESULTS: Six patients were identified as having mutated strands, three on hMSH2 exon 1 and three on hMSH2 exon 5. DNA sequencing revealed that all 6 patients had mutated basic groups that led to decrease in function of the hMSH2 protein. Forty percent (12/30) of patients were p53 positive. The frequency of mutated hMSH2 in p53 positive patients (41.7%) was significantly higher than in p53 negative patients (5.6%, P < 0.05). CONCLUSION: The mutation of hMSH2 plays an important role in the carcinogenesis and development of digestive tract tumors through stimulating p53 mutation.