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X-ray “ghost” imaging has drawn great attention for its potential to obtain images with a high resolution and lower radiation dose in medical diagnosis, even with only a single-pixel detector. However, it is hard to realize with a portable x-ray source due to its low flux. Here, we demonstrate a computational x-ray ghost imaging scheme where a real bucket detector and specially designed high-efficiency modulation masks are used, together with a robust deep learning algorithm in which a compressed set of Hadamard matrices is incorporated into a multi-level wavelet convolutional neural network. With a portable incoherent x-ray source of ∼37 µm diameter, we have obtained an image of a real object from only 18.75% of the Nyquist sampling rate. A high imaging resolution of ∼10 µm has been achieved, which is required for cancer detection and so represents a concrete step toward the realization of a practical low cost x-ray ghost imaging camera for applications in biomedicine, archeology, material science, and so forth.

The nonpeptide AVE0991 is expected to be a putative new drug for cardiovascular diseases. However, the mechanisms for the cardioprotective actions of AVE0991 are still not fully understood. We planned to determine whether AVE0991 attenuates the angiotensin II (AngII)-induced myocardial hypertrophy and whether these AVE0991 effects involved transforming growth factor β1 (TGF-β1) and Smad2. A rat model of neonatal myocardial hypertrophy was induced by AngII. The AngII group significantly increased in protein content, surface area, and [3H]leucine incorporation efficiency by cardiomyocytes, compared to those of the control group ( P < 0.01). The AngII group also had elevated TGF-β1 and Smad2 expression ( P < 0.01). These AngII-induced changes were significantly attenuated by AVE0991 in a dose-dependent manner. In our study, these actions of AngII (10−6 mol/l) were significantly inhibited by both concentrations of AVE0991 (10−5 mol/l and 10−7 mol/l). Moreover, the high AVE0991 group had significantly better inhibition of myocardial hypertrophy than the low AVE0991 group. Meanwhile, the beneficial effects of AVE0991 were completely abolished when the cardiomyocytes were pretreated with Ang-(1–7) receptor antagonist A-779 (10−6 mol/l). These results suggested that AVE0991 prevented AngII-inducing myocardial hypertrophy in a dose-dependent fashion, a process that may be associated with the inhibition of TGF-β1/Smad2 signaling. [ABSTRACT FROM AUTHOR]

We theoretically study the high-order harmonic generation (HHG) in a two-color laser field using the Bohmian mechanics. Our results show that, for the case of a weak second-color laser field, the simulation of the HHG with only one central Bohmian trajectory is in a good agreement with the ab initio time-dependent Schrödinger equation (TDSE) results. In contrast, with the increase of the amplitude of the second-color laser field, the HHG spectra from the single central Bohmian trajectory deviate from the TDSE results more and more significantly. By analyzing the Bohmian trajectories, we find that the significant deviation is due to the fact that the central Bohmian trajectory leaves the core quickly in the two-color laser field with the breaking of inversion symmetry. Interestingly, we find that another Bohmian trajectory with different initial position, which keeps oscillating around the core, could qualitatively well reproduce the TDSE results. Furthermore, we study the HHG spectrum in a two-color laser field with inversion symmetry and find that the HHG spectrum in TDSE can be still well simulated with the central Bohmian trajectory. These results indicate that, similar to the case of one color laser field, the HHG spectra in a two-color laser field can be also reproduced with a single Bohmian trajectory, although the initial position of the trajectory is dependent on the symmetry of the laser field. Our work thus demonstrates that Bohmian trajectory theory can be used as a promising tool in investigating the HHG process in a two-color laser field. [ABSTRACT FROM AUTHOR]

We experimentally study the above-threshold ionization (ATI) spectra of noble gas argon in an intense laser field and focus on a novel suppression structure in the high-order ATI (HATI) spectra. It is found that, when a well-documented resonancelike enhancement feature appears in the HATI spectra, a significant suppression structure is followed in a higher energy region of the spectra. The observation is well reproduced by a numerical solution of the time-dependent Schrödinger equation. In terms of quantum-orbit theory, the observed suppression structure can be ascribed to the destructive interference from longer quantum orbits. Furthermore, an intrinsic relation between the ionization suppression and the ionization enhancement in the HATI spectra is well established. [ABSTRACT FROM AUTHOR]

The nonpeptide AVE0991 is an agonist of the angiotensin-(1-7) (Ang-(1-7)) Mas receptor and is expected to be a putative new drug for treatment of cardiovascular disease. However, the mechanisms involved in the antiproliferative effects of AVE0991 are not fully understood. We saw that the compound attenuated proliferation in an angiotensin II-induced rat vascular smooth muscle cells (VSMC) proliferation model. Moreover, treatment with AVE0991 (10(-5) mol/L or 10(-7) mol/L) significantly attenuated reactive oxygen species (ROS) production, phosphorylation of p38 MAPK, and dose-dependently (10(-8) to 10(-5) mol/L) inhibited Ang II-induced VSMC proliferation. Meanwhile, heme oxygenase-1 (HO-1) expression increased in the AVE0991 + Ang II group (10(-5) mol/L or 10(-6) mol/L). However, the beneficial effects of AVE0991 were completely abolished when the VSMC were pretreated with A-779 (10(-6) mol/L). Furthermore, treatment with the HO-1 inhibitor ZnPPIX attenuated the inhibitory effect of AVE0991 on Ang II-induced p38MAPK phosphorylation. These results suggest that AVE0991 attenuates Ang II-induced VSMC proliferation in a dose-dependent fashion and that this effect is associated with the Mas/HO-1/p38 MAPK signaling pathway.