Background: Microtia is a congenital anomaly of the external ear that can appear in isolation or in association with other congenital anomalies. In this study, the authors identify the prevalence and phenotypes of associated congenital malformations in patients with microtia in a Chinese specialty clinic population. Methods: Data were collected from 672 patients seen between December of 2014 and February of 2016 in the Department of Auricular Reconstruction at the Plastic Surgery Hospital of Peking Union Medical College. All patients were examined by trained clinicians and classified into one of three grades of microtia. Co-occurring congenital anomalies were detected and recorded. Results: The majority of study participants were male patients (72 percent), and most participants had unilateral microtia (93 percent, 68 percent of whom had right-side microtia). Two hundred ninety-three patients (44 percent) had one or more associated anomalies. The most commonly occurring comorbid malformations were those of the ear, face, and neck (40 percent of all associated malformations); musculoskeletal system (35 percent); and cardiovascular system (11 percent). Conclusions: These data represent the first detailed and thematic study of microtia and associated congenital anomalies in a Chinese clinical population. Substantial clinical heterogeneity was observed, and the prevalence of comorbid congenital malformations was high. Future studies investigating congenital anomalies associated with microtia are needed to improve understanding of its cause.

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Inducible nitric oxide synthase (iNOS) produces NO from l-arginine and plays critical roles in inflammation and immune activation. Selective and potent iNOS inhibitors may be potentially used in many indications, such as rheumatoid arthritis, pain, and neurodegeration. In the current study, five new compounds, including a dibenzo-α- pyrone derivative ellagic acid B (5) and four α-pyrones diaporpyrone A–D (9–12), together with three known compounds (6–8), were isolated from the endophytic fungus Diaporthe sp. CB10100. The structures of these new natural products were unambiguously elucidated using NMR, HRESIMS or electronic circular dichroism calculations. Ellagic acid B (5) features a tetracyclic 6/6/6/6 ring system with a fused 2H-chromene, which is different from ellagic acid (4) with a fused 2H-chromen-2-one. Both 2-hydroxy-alternariol (6) and alternariol (7) reduced the expression of iNOS at protein levels in a dose-dependent manner, using a lipopolysaccharide (LPS)-induced RAW264.7 cell models. Also, they decreased the protein expression levels of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6 and monocyte chemotactic protein 1. Importantly, 6 and 7 significantly reduced the production of NO as low as 10 μM in LPS-induced RAW264.7 cells. Molecular docking of 6 and 7 to iNOS further suggests that both of them may interact with iNOS. Our study suggests that 6 and 7, as well as the alternariol scaffold may be further developed as potential iNOS inhibitors.

The role of lncRNA miR503HG has been investigated in several types of cancer, but its functions in ovarian cancer (OC) is unclear. Analysis of TCGA dataset revealed a 50-fold lower expression level of miR503HG in OC tissues than that in non-tumor tissues, indicating the involvement of miR503HG in OC. Results in this study showed that miR503HG was downregulated in OC and predicted poor survival. Expression of miR503HG negatively correlated with the expression of miR-31-5p across OC and non-tumor tissues. RNA-RNA interaction analysis revealed that miR503HG can interact with miR-31-5p. Dual-luciferase assay showed that miR-31-5p and miR503HG may directly interact with each other. Methylation specific PCR (MSP) showed that overexpression of miR503HG led to increased methylation level of miR-31-5p gene. Transwell assay showed that overexpression of miR-31-5p resulted in increased invasion and migration rates of OC cells. Overexpression of MiR503HG played an opposite role and attenuated the effects of overexpressing miR-31-5p. Therefore, miR503HG may promote the methylation of miR-31-5p and serve as its sponge to inhibit OC cell invasion and migration.

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