4 research outputs found
Continuous Transformations of the Nucleation Mechanism in the Undercooled State
Studies
on nucleation have relied for many decades on the classical
nucleation theory. Within that picture, thermal fluctuations govern
the formation of critically sized, homogeneous nuclei of the newly
developing phase. At the same time, structural inhomogeneities or
impurities or extrinsic substrates such as surfaces or container walls
can favor the formation of a critical-sized nucleus, leading to so-called
heterogeneous nucleation. Specifically, according to this theoretical
framework, a kinetic nucleation transition between heterogeneous and
homogeneous is predicted to happen at a critical cooling rate. This
underlying picture of nucleation has been applied since the development
of classical nucleation theory, but this transition has rarely been
observed experimentally for simple metallic systems. Now, with the
development of fast scanning chip calorimetry and careful selection
of a model alloy, we have been able to experimentally map the kinetic
transition between these two fundamental modes of nucleation
Additional file 3: Figure S2. of Impaired aldehyde dehydrogenase 1 subfamily member 2A-dependent retinoic acid signaling is related with a mesenchymal-like phenotype and an unfavorable prognosis of head and neck squamous cell carcinoma
ALDH1A2 expression in HNSCC cell lines and morphological phenotype upon inhibition of ALDH1A2-RAR signaling. Western blot analysis with whole cell lysate demonstrates protein expression of ALDH1A2 and key regulators of RA signaling in UMSCC-17B, Detroit562, FaDu, Cal27 and SCC25 cells (A), and ALDH1A2 protein levels in newly established HNSCC cell lines from Lausanne (B). Detection of β-Actin served as control for quantity and quality of protein lysates. Relative RA levels were determined by HPLC analysis with whole cell lysate of untreated (C), and DMSO-treated control or WIN18.446-treated Cal27 and FaDu cells (D). Bars represent mean values ¹ SD of three independent replicates. Graphs indicate relative survival fraction of Cal27 and FaDu cells, which were treated with the indicated concentration of Adapalene (E) or Fenretinide (F). Data represent mean values ¹ SD of three independent replicates. (TIF 301 kb
Additional file 1: Figure S1. of Impaired aldehyde dehydrogenase 1 subfamily member 2A-dependent retinoic acid signaling is related with a mesenchymal-like phenotype and an unfavorable prognosis of head and neck squamous cell carcinoma
Association between subgroups with high or low protein expression of CRABP2 (A), FABP5 (B), RARα (C), RARβ (D) or PPARα/δ (E) and overall survival of OPSCC patients was assessed by univariate Kaplan-Meier analysis. (F) Kaplan-Meier analysis demonstrates overall survival probability for subgroups with indicated staining patterns for ALDH1A2, CRABP2 and FABP5. Number at risk indicates the total amount of patients per subgroup, which were alive and not censored at the indicated time points and were considered to calculate the overall survival probability. P values were calculated by log-rank tests. (TIF 1257 kb
Additional file 5: Figure S4. of Impaired aldehyde dehydrogenase 1 subfamily member 2A-dependent retinoic acid signaling is related with a mesenchymal-like phenotype and an unfavorable prognosis of head and neck squamous cell carcinoma
(A) Representative phase contrast pictures of FaDu, Detroit562 and UMSCC-17B cells, which were treated with DMSO, 3 μM WIN18.446 or 3 μM BMS493 for four days. (B) Representative fluorescent pictures of FaDu and Detroit562 cells, which were treated as described in (A), and were stained with Phalloidin-Alexa488 (green signal). Nuclear staining was done with H33342 (blue signal). Migration of Detroit562 (C) and FaDu cells (D), which were treated with DMSO (white bars), 3 μM WIN18.446 (grey bars) or 3 μM BMS493 (black bars), in a scratch wounding assay was determined by the relative gap closure at the indicated time points. * p value ≤ 0.05. (TIF 4129 kb