Tricolor narrowband planar perovskite photodetectors based on FP microcavity structure.

This paper presents a novel tunable narrowband photodetector based on Ag-MgF2-Ag (metal-dielectric-metal: MDM) Fabry-Perot (FP) microcavity structure. The tunability is achieved through precise adjustment of the thickness of the metal and intermediate dielectric layers of the FP microcavity, taking into account the response spectral range of planar perovskite. After optimizing the parameters mentioned above, the prototype devices were prepared by combining the perovskite layer and MDM layer. The center wavelength of the planar detector can be tuned from 430 nm to 680 nm within the detection band of 400-800 nm, with a narrow FWHM about 30 nm and a relatively high response of 0.05 A/W @ 5 V bias voltage for 500 nm. Meanwhile the rise and fall times of the detector are 375 ms and 550 ms, respectively. The experimental results are corroborated by the theory. Our design is highly beneficial to such applications as hyperspectral photography and color-related active optical devices, which paves the way to design this kind of triple structure.

Airy-type X-ray states generated using 3/2 flat diffractive optics.

X-rays have developed into an essential tool in variety of fields, such as biology, materials, chemistry, and physics etc. Numerous X-ray types, including the orbital angular momentum (OAM), the Laguerre-Gauss, and the Hermite-Gauss states, have been proposed. This greatly enhances the depth of application of X-ray. The X-ray states described above are mostly produced by binary amplitude diffraction elements. In light of this, this paper proposes a flat X-ray diffraction grating based on caustic theory to generate Airy-type X-ray. It is proved by the simulation of multislice method that the proposed grating can generate the Airy beam in the X-ray field. The results show that the generated beams have a secondary parabolic trajectory deflection with the propagation distance, which is consistent with the theory. Inspired by the success of Airy beam in light-sheet microscope, the Airy-type X-ray can be anticipated to enable novel image capability for bio or nanoscience.

Mechanical strain regulates osteoclastogenesis via modulating the PTEN/PI3K/Akt signal pathway through miR-21.

Mechanical strain regulated osteoclastic differentiation and angiogenesis are crucial for bone modeling and remodeling, and previous data indicate that high-magnitude strain within physiological load regulates osteoclastic differentiation. However, the underlying mechanisms are still not fully understood. In the present study, the RAW264.7 mouse monocyte/macrophage was used as an osteoclast precursor, and the bone marrow-derived macrophages (BMMs) were isolated and cultured in vitro. The above cells were subjected to macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kB ligand (RANKL) for the induction of osteoclast differentiation. Subsequently, the above cells were stretched by differential strain magnitudes to simulate the mechanical stimuli in the physiological conditions, and we found that low-magnitude strain (100 µÎµ) increased the expression levels of Acp5, Clcn7, MMP9 and Ctsk to promote osteoclastogenesis, while high-magnitude strain (3000 µÎµ) had opposite effects. In addition, we noticed that high-magnitude strain upregulated PTEN to inactivate the PI3K/Akt signaling pathway, and silencing of PTEN abrogated the suppressing effects of high-magnitude strain on osteoclastic differentiation. Next, we screened out that high-magnitude strain downregulated miR-21 to promote PTEN expressions in a competing endogenous RNA (ceRNA)-dependent manner. Finally, upregulation of miR-21 recovered osteoclastic differentiation in RAW264.7 and BMMs cells stimulated with high-magnitude strain. Collectively, our findings suggested that high-magnitude mechanical strain affected osteoclastic differentiation through modulating the miR-21/PTEN/PI3K/Akt signaling cascade, which provided potential strategies for the treatment of bone-related diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-021-00507-x.