Ectopic expression of RMRP promoted lung adenocarcinoma cell proliferation, colony formation and invasion.

<p>(A) The expression of RMRP was measured in the H1299 cell after treated with RMRP vector. (B) Ectopic expression of RMRP promoted H1299 cell proliferation. (C) Overexpression of RMRP enhanced the cyclin D1 expression in the H1299 cell. (D) Ectopic expression of RMRP promoted ki-67 expression in the H1299 cell. (E) Overexpression of RMRP promoted the H1299 cell colony formation. (F) Overexpression of RMRP enhanced the H1299 cellinvasion. *p<0.05, **p<0.01 and ***p<0.001.</p

RMRP suppressed expression of miR-206 and increased the expression of KRAS, FMNL2 and SOX9.

<p>(A) Overexpression of RMRP inhibited theexpression of miR-206 in the H1299 cell. (B) Ectopic expression ofRMRP promoted the KRAS mRNA expression in the H1299 cell. (C) The protein expression of KRAS was determined using western blot. (D) Ectopic expression ofRMRP promoted the FMNL2 mRNA expression in the H1299 cell. (E) The protein expression ofFMNL2 was determined using western blot. (F) Ectopic expression ofRMRP promoted the SOX9 mRNA expression in the H1299 cell. (G) The protein expression ofSOX9 was determined using western blot.</p

The expression of RMRP was upregulated in the lung adenocarcinoma tissues.

<p>(A) RMRP expression was measured in the lung adenocarcinoma tissues and the matched adjacent normal tissues using qRT-PCR. (B) The RMRP was upregulated in 25 cases (25/35; 71.4%) compared to the adjacent normal tissues. (C) The RMRP expression was upregulated in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) compared to the bronchial epithelial cell line (16HBE).</p

RMRP exhibited an oncogenic activity through targeting miR-206.

<p>(A) miR-206 expression was upregulated in H1299 cell after treated with the miR-206 mimic. (B) miR-206 expression was decreased in the RMRP-induced H1299 cell after treated with RMRP vector. (C) Restoration of miR-206 suppressed cell proliferation in the RMRP-induced H1299 cell after treated with miR-206 mimic. (D) Restoration of miR-206 inhibited the cell invasion in the RMRP-induced H1299 cell after treated with miR-206 mimic.*p<0.05, **p<0.01 and ***p<0.001.</p

miR-206 expression was downregulated in the lung adenocarcinoma tissues.

<p>(A) The miR-206 expression was measured in lung adenocarcinoma cell lines (A549, SPC-A1, H1299 and H23) and the bronchial epithelial cell line using qRT-PCR. (B) The miR-206 expression was detected in lung adenocarcinoma tissues and the matched adjacent normal tissues by using qRT-PCR. (C) miR-206 expression was downregulated in 21 cases (21/35; 60%) compared to the adjacent normal tissues. (D) The expression of RMRP was negative correlated with the expression of miR-206 in lung adenocarcinoma tissues.</p

Facile Construction of Inorganic Phosphorus/Boron-Layered Double Hydroxide Complexes for Highly Efficient Fire-Safety Epoxy Resin

For inorganic flame retardants, facile fabrication and high-efficiency fire safety without compromising the mechanical property of the matrix are still significant challenges. Here, nanolayered double hydroxide containing boron constructed on the surface of ammonium polyphosphate (APP) complexes (B-LDH@APP) is prepared by a simple in situ coprecipitation technology to reduce the fire hazard and improves the mechanical performances of epoxy resin (EP). The as-obtained 4B-LDH@APP/EP achieves the UL-94 V-0 rating and presents superior flame-safety performance. With respect to the 4APP/EP, the fire growth rate (FIGRA), the peak heat release rate (pHRR), and the peak smoke production rate (pSPR) of 4B-LDH@APP/EP decrease by 77.8, 57.3, and 52.6%, respectively. This is mainly attributed to the excellent synergistic flame-retardant effect among boron, LDH, and APP, which can accelerate the generation of compact charring residual with a good microstructure during combustion of B-LDH@APP/EP composites. Furthermore, B-LDH@APP slightly affects the mechanical performances of the EP matrix due to the upgraded interfacial interaction

Cu(II)/Proline-Catalyzed Reductive Coupling of Sulfuryl Chloride and P(O)–H for P–S–C Bond Formation

A considerably improved method for the Cu-catalyzed coupling of sulfuryl chloride with P­(O)–H was described. Using commercially available l-proline as the ligand decreased the precatalyst loading, broadened the substrate scope and greatly promoted the efficiency of the coupling reaction. Moreover, gram-scale preparation, easy-to handle and recyclable catalyst featured this transformation

Additional file 1 of Construction of a risk stratification model integrating ctDNA to predict response and survival in neoadjuvant-treated breast cancer

Additional file 1: sTable 1. The pCR rate in different molecular subtype. stable 2. Patient Clinical Characteristics (Train and Test Datasets). stable 3. Patient Clinical Characteristics (Extra Test Datasets). stable 4. Patient SNV Characteristics (Train and Test Datasets). stable 5. Patient CNV Characteristics (Train and Test Datasets). stable 6. significant SNV and CNV. stable 7. Patient ctDNA Characteristics