In this study, three chromophores-p-nitroaniline, 4-(4-nitrophenylazo)aniline, and 4-[(E)-2-{4-[(E)-2-(4-nitrophenyl)-1-diazenyl]phenyl}-1-diazenyl]anilinewere intercalated into layered aluminosilicate saponite and then dispersed into the polyurethanes matrix. The intercalated chromophore/saponite complexes were examined by inductively coupled plasma emission and element analysis technologies. The molecular orbital package computation simulation and X-ray diffraction (XRD) analysis showed that possible configurations of chromophore ions on the gallery surfaces of saponite suggest that the chromophore molecules lie parallel to the basal planes of silicate as an inclined paraffin structure or as pseudo-multilayers. The XRD and transmission electron microscopy analysis indicated that the delamination of organoclay in the polyurethanes matrix exhibited nanolayers, exfoliated structure, or both. In particular, even at high doping levels up to 15 wt % of organoclay, the [chromophore] ϩsaponite/polyurethanes film did not display a macroscopic aggregation of layered silicates and showed high transparency. The thermal stability of chromophore was significantly enhanced as intercalated into the layered aluminosilicate saponite, and the glass-transition temperature of [chromophore] ϩ -saponite/polyurethanes nanocomposites proportionally increased with increased clay content.

The pivotal role of dysregulated miRNAs in development of papillary thyroid carcinoma has been emphasized in recent research. miR-671-5p was previously documented to function as a tumor suppressor. However, the role and mechanism of miR-671-5p in progression of papillary thyroid carcinoma remain to be further studied. Data from functional assays indicated that forced expression of miR-671-5p decreased cell viability, repressed cell proliferation, migration, and invasion in papillary thyroid carcinoma cells. In vivo study showed that miR-671-5p overexpression inhibited tumor growth, downregulated Ki67, and decreased tumor volume and weight. Tripartite motif containing 14 (TRIM14) was verified as downstream target of miR-671-5p. The expression of TRIM14 was suppressed by miR-671-5p in papillary thyroid carcinoma. Overexpression of TRIM14 increased cell viability, and promoted the proliferation, migration, and invasion of papillary thyroid carcinoma. Moreover, TRIM14 counteracted the suppressive effect of miR-671-5p overexpression on papillary thyroid carcinoma cell growth. In conclusion, miR-671-5p repressed progression of papillary thyroid carcinoma through downregulation of TRIM14, providing a promising target for therapy of papillary thyroid carcinoma.

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Objective: Early exposure to general anesthesia in children might be a potentially high-risk factor for learning and behavioral disorders. The mechanism of neurotoxicity induced by general anesthesia was not defined. miR-496 could regulate cerebral injury, while the roles of miR-496 in neurotoxicity were not elucidated. Therefore, we aimed to investigate the effects of miR-496 in neurotoxicity induced by propofol. Methods: Primary prefrontal cortical (PFC) neurons were isolated from neonatal rats and treated with propofol to induce neurotoxicity. Cell viability was detected by (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The target relationship of miR-496 and Rho Associated Coiled-Coil Containing Protein Kinase 2 (ROCK2) was explored using luciferase assays. Results: Propofol decreased cell viability, promoted cell apoptosis, and decreased the expression of miR-496 in PFC neurons in a dose-dependent manner. Overexpression of miR-496 attenuated neurotoxicity induced by propofol in PFC neurons. ROCK2 was a target of miR-496, and miR-496 oppositely modulated the expression of ROCK2. Besides, propofol increased the expression of ROCK2 through inhibiting miR-496 in PFC neurons. Overexpression of miR-496 attenuated propofolinduced neurotoxicity by targeting ROCK2 in PFC neurons. Conclusion: miR-496 was decreased in PFC neurons treated with propofol, and overexpression of miR-496 attenuated propofol-induced neurotoxicity by targeting ROCK2. miR-496 and ROCK2 may be promising targets for protecting propofol-induced neurotoxicity.

Intratracheal ectopic thyroid (ITET) is a rare disease, with limited cases reported in the literature. ITET is an unusual congenital abnormality and can be easily mistaken for a respiratory illness. We present a case of a 61-year-old man with a history of slight discontinuous hemoptysis for 2 years. A tracheal mass, which appeared to be connected to the left thyroid gland, was found by chest computed tomography scan. Ultrasound revealed one suspiciously malignant, solid and hypoechoic nodule in the left thyroid gland. After the thyroid origin of the mass was confirmed by bronchoscopic biopsy, the patient underwent segmental resection and anastomosis of the trachea, together with left thyroidectomy. Histopathology of the tracheal tumor showed adenomatous hyperplastic ITET, and the orthotopic left thyroid gland showed nodular goiter with atypical adenomatous hyperplasia. Clinical suspicion is warranted in patients presenting with a tracheal tumor seemingly connected to the thyroid gland, particularly in patients who have imaging features suggestive of a malignant tumor in the orthotopic thyroid but without confirmative histopathology of malignancy before surgery.