Polarization-Sensitive Sum-Frequency Generation Microscopy of Collagen Fibers

Point-scanning sum-frequency generation (SFG) microscopy enables the generation of images of collagen I fibers in tissues by tuning into specific vibrational resonances of the polypeptide. It is shown that when collagen-rich tissues are visualized near the 2954 cm^–1 stretching vibration of methylene groups, the SFG image contrast is higher compared to the contrast seen in nonresonant second-harmonic generation (SHG) imaging. Polarization and spectrally resolved analysis of the SFG signal as a function of fiber orientation in the CH-stretching range of the vibrational spectrum enabled a comparative characterization of the achiral tensor elements of collagen’s second-order susceptibility. This analysis reveals that selected on-resonance tensor elements are enhanced over other elements, giving rise to a much stronger anisotropy ρ of the signal for SFG (ρ ≈ 15) compared to SHG (ρ ≈ 3). The improved anisotropy of the vibrationally resonant signal contributes to the higher contrast seen in the SFG tissue images

RT-PCR analysis of ABCG2 and SMO mRNA levels.

<p>A, Representative RT-PCR gel images. M, marker; lane 1, NCI-H460 cells normally cultured in serum-containing medium; lane 2, the H460 spheres; lane 3, purified SP cells; lane 4, purified non-SP cells; lane 5, the Tomatidine control group; lane 6, the Cyclopamine experimental group; lane 7, SP tumors; lane 8, non-SP tumors. B, Quantitative presentation of ABCG2 and SMO mRNA levels as determined by densitometry (<i>P</i><0.001, except ABCG2 mRNA lane 6 vs. lane 8 and SMO mRNA lane 1 vs. lane 5 and lane 4 vs. lane 6).</p

SP re-analysis in various samples.

<p>A–B, SP re-analysis when the SP spheres were disaggregated and dissociated cells cultured in normal serum-containing medium for one week. C–D, SP re-analysis in the SP cell-derived tumors. E–F, SP re-analysis in non-SP cell-derived tumors. A, C, E, without verapamil. B, D, F, with verapamil.</p

Sphere formation and proliferative capacity of H460 SP and non-SP cells.

<p>A–B, Purified SP and non-SP cells were cultured in serum-free medium in anchorage-independent conditions. The SP cells formed typical floating spheres within 4 days (A) whereas the non-SP cells largely established adherent growth (B). C, The SP cells displayed higher proliferative ability than non-SP cells as determined by CCK-8 kit (<i>P</i><0.05 for all time points, Student <i>t</i>-test).</p

SP analysis in cultured H460 lung cancer cells.

<p>A–B, Hoechst staining of H460 cells. Note that although the majority of cells were stained in the nucleus, some cells (indicated by arrows) apparently lacked nuclear Hoechst staining. C–D, SP phenotypes in the absence (C) or presence (D) of verapamil.</p

Cyclopamine inhibits H460 cell proliferation.

<p>A–C, Representative photomicrographs of H460 cells 72 h after treatment with vehicle control (A), Tomatidine (B), or Cyclopamine (C). Original maginifications: ×200. D, Cyclopamine dose-dependently inhibited H460 cell proliferation (<i>P</i><0.05; one-way ANOVA). E, Time course of Cyclopamine inhibition of H460 cells (<i>P</i><0.05, one-way ANOVA). Cyclopamine was used at 20 µmol/L. F, Effects of Cyclopamine on the cell cycle of H460 cells.</p

High tumorigenicity in SP cells.

<p>A, Table presentation of the tumorigenic potential of H460 SP and non-SP cells. Three parameters of tumorigenicity, i.e., tumor incidence, latency, and volume (*<i>P</i><0.01) were shown. All animals were terminated (term.) 28 days after implantation. B, The SP cells regenerated larger tumors than corresponding non-SP cells at every cell dose. C, Gross tumor images when tumors were harvested at day 28 after s.c. injection of the SP and non-SP cells into NOD/SCID mice. D, Representative HE-stained photomicrographs of SP and non-SP tumors.</p

Selective Ethylene Oligomerization with Chromium-Based Metal–Organic Framework MIL-100 Evacuated under Different Temperatures

MIL-100­(Cr) was synthesized and evacuated under different temperatures to generate a series of heterogeneous catalysts for ethylene oligomerization. These catalysts showed moderate catalytic activities for ethylene oligomerization but high selectivities to low carbon olefins C6, C8, and C10. Moreover, the oligomer distribution was different depending on the evacuation temperature. The XPS results showed the reduction of some Cr^III active sites in the MIL-100­(Cr) structure to Cr^II active sites, which made the catalysts show polymerization activities. The MIL-100­(Cr)-250 catalyst evacuated at 250 °C exhibited the highest oligomerization and polymerization activities up to 9.27 × 10⁵ g/(molCr·h) and 0.99 × 10⁵ g/(molCr·h) respectively. The oligomerization selectivity to low carbon olefins C6, C8, and C10 was about 99%. The byproduct polymer from MIL-100­(Cr)-250 belonged to linear polyethylene with ultrahigh molecular weight and broad molecular weight distributions. This work demonstrated that MOFs containing coordinatively unsaturated metal sites might be a promising selective catalyst for ethylene slurry oligomerization

Image1_Feiyanning formula modulates the molecular mechanism of osimertinib resistance in lung cancer by regulating the Wnt/β-catenin pathway.TIF

Feiyanning Formula (FYN), a Chinese herbal formula derived from summarized clinical experience, is proven to have anti-tumor effects in lung cancer patients. Osimertinib, a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), can improve progression-free survival and overall survival of patients but drug resistance is inevitable. The current study evaluated the effects of FYN in osimertinib-resistant HCC827OR and PC9OR cells. FYN preferentially inhibited the proliferation and migration of HCC827OR and PC9OR cells. Moreover, FYN and osimertinib exhibited synergistic inhibitory effects on proliferation and migration. Real-time qPCR (RT-qPCR) and western blotting results indicated that FYN downregulated gene and protein levels of GSK3β and SRFS1, which are enriched in the Wnt/β-catenin pathway. Besides, FYN inhibited tumor growth and exhibited synergistic effects with osimertinib in vivo. Collectively, the results suggested that FYN exerted an anti-osimertinib resistance effect via the Wnt/β-catenin pathway.</p

MOESM1 of MicroRNA-125b promotes tumor metastasis through targeting tumor protein 53-induced nuclear protein 1 in patients with non-small-cell lung cancer

Additional file 1: Figure S1. Expressions of miR-125b and TP53INP1 in isolated NSCLC cells were determined by qPCR and analyzed for their negative correlation