Atomic Force Microscopy Nanomechanics Visualizes Molecular Diffusion and Microstructure at an Interface

Here we demonstrate a simple, yet powerful method, atomic force microscopy (AFM) nanomechanical mapping, to directly visualize the interdiffusion and microstructure at the interface between two polymers. Nanomechanical measurements on the interface between poly­(vinyl chloride) (PVC) and poly­(caprolactone) (PCL) allow quantification of diffusion kinetics, observation of microstructure, and evaluation of mechanical properties of the interdiffusion regions. These results suggest that nanomechanical mapping of interdiffusion enables the quantification of diffusion with high resolution over large distances without the need of labeling and the assessment of mechanical property changes resulting from the interdiffusion

Nanorheological Mapping of Rubbers by Atomic Force Microscopy

A novel atomic force microscopy (AFM) method is used for nanometer-scale mapping of the frequency dependence of the storage modulus, loss modulus, and loss tangent (tan δ) in rubber specimens. Our method includes a modified AFM instrument, which has an additional piezoelectric actuator placed between the specimen and AFM scanner. The specimen and AFM cantilever are oscillated by this actuator with a frequency between 1 Hz and 20 kHz. On the basis of contact mechanics between the probe and the sample, the viscoelastic properties were determined from the amplitude and phase shift of the cantilever oscillation. The values of the storage and loss moduli using our method are similar to those using bulk dynamic mechanical analysis (DMA) measurements. Moreover, the peak frequency of tan δ corresponds to that of bulk DMA measurements

Figure 9

<p>A summary schematic of the lansoprazole-induced AhR/Cyp1a1/Nrf2 pathway in the liver. XRE, xenobiotic response elements; ARE, antioxidant response element.</p

Up-regulation of HO-1 IR in hepatocytes following single oral treatment with lansoprazole.

<p>A) Up-regulation of HO-1 IR in the liver at 6 h. ** P<0.01 compared with control. Representative photographs showing an increase of HO-1 IR. B) Immunohistochemistry for HO-1 in the liver at 6 h. Signals for HO-1 IR were detected in macrophages in the control. <i>De novo</i> signals for HO-1 IR were observed in hepatocytes in response to treatment with lansoprazole. Upper panel bar = 100 µm. Lower panel bar = 20 µm.</p

Histology of the liver stained with hematoxylin-eosin.

<p>A) Control (group A). B) TAA-treated liver (group C). C) TAA-treated liver pretreated by lansoprazole (group D), Bar = 250 µm. D) Lesion index (%). * P<0.05.</p

Validation of gene expression changes in the liver at 3 h following oral administration of lansoprazole (100 mg/kg).

<p>A) Up-regulation of AhR mRNA. ***P<0.0001. B) No significant change (P = 0.068) of Pparα mRNA levels. C) Up-regulation of Cyp1a1 mRNA. ***P<0.0001.</p

Up-regulation of Nrf2 and HO-1 following successive subcutaneous treatments with lansoprazole.

<p>A) No significant changes in the levels of mRNA for Nrf2, Keap1 and HO-1. B) Up-regulation of IR levels for Nrf2 and HO-1, with no change of Keap1 IR. *P<0.05, ***P<0.001 compared with control. Representative photographs showing an increase of Nrf2 and HO-1 IR. C) Nuclear translocation of Nrf2 in hepatocytes as demonstrated by double fluorescence immunohistochemistry and western blotting of cytosol fraction (C; Calpain-positive) and nuclear fraction (N; Histone H1-positive). Blue indicates DAPI-positive nuclei, red indicates Nrf2 IR, and pink indicates the nuclear localization of Nrf2. Bar = 20 µm.</p

Up-regulation of mRNA for Nrf2-dependent antioxidant and phase II enzymes following single oral treatment with lansoprazole.

<p>A) Up-regulation of HO-1 mRNA in the liver at 3 h. B) Up-regulation of NAD (P) H dehydrogenase, quinone 1 (Nqo1) mRNA in the liver at 3 h. C) Up-regulation of glutathione S-transferase A2 (Gsta2) mRNA in the liver at 3 h. D) Up-regulation of UDP glucuronosyltransferase 1 family polypeptide A6 (Ugt1a6) mRNA in the liver at 3 h. *P<0.05, ** P<0.01, ***P<0.001 compared with control.</p

List of oligonucleotide primers used for RT-PCR.

<p>List of oligonucleotide primers used for RT-PCR.</p

Serum levels and the % inhibition of AST and ALT in TAA-induced acute hepatic damage.

<p>A) Serum AST levels. * P<0.001 compared with group A (control). B) Serum ALT levels * P<0.0001 compared with group A (control). # P<0.01 compared with group C (acute hepatic damage). C) The % inhibition of TAA-induced increase of serum AST levels between group D (acute hepatic damage with lansoprazole) and group F (acute hepatic damage with lansoprazole and SnMP). D) The % inhibition of TAA-induced increase of serum ALT levels between group D (acute hepatic damage with lansoprazole) and group F (acute hepatic damage with lansoprazole and SnMP).</p