Strain insensitive flexible photodetector based on molybdenum ditelluride/molybdenum disulfide heterostructure.

Flexible electronic and optoelectronic devices are highly desirable for various emerging applications, such as human-computer interfaces, wearable medical electronics, flexible display, etc. Layered two-dimensional (2D) material is one of the most promising types of materials to develop flexible devices due to its atomically thin thickness, which gives it excellent flexibility and mechanical endurance. However, the 2D material devices fabricated on flexible substrate inevitably suffer from mechanical deformation, which can severely affect device performances, resulting in function degradation and even failure. In this work, we propose a strain insensitive flexible photodetector based on MoS2/MoTe2heterostructure on polyimide substrate, which provides a feasible approach to cancel unpredicted impacts of strain on the device performances. Specifically, the MoS2/MoTe2heterostructure is deposited with 4 electrodes to form three independent devices of MoS2FET, MoTe2FET and MoS2/MoTe2heterojunction. Among them, the MoS2/MoTe2heterojunction is used as the photodetector, while the MoS2FET is used as a strain gauge to calibrate the photo detection result. Such configuration is enabled by the Schottky barrier formed between the electrodes and the MoS2flake, which leads to obvious and negligible photo response of MoS2/MoTe2heterojunction and MoS2FET, respectively, under low source-drain bias (ex. 10 mV). The experimental results show that the proposed mechanism can not only calibrate the photo response to cancel strain effect, but also successfully differentiate the wavelength (with fixed power) or power (with fixed wavelength) of light illumination.

Pharmacological inhibition of TLR4-NF-κB signaling by TAK-242 attenuates hydrocephalus after intraventricular hemorrhage.

Compelling evidence has confirmed that inflammatory pathways involving TLR4-regulated cytokines and immune cells are vitallyimportant for the pathogenesis of posthemorrhagic hydrocephalus (PHH), hinting that pharmacological prevention of PHH is feasible. TAK-242, as a toll-like receptor 4 (TLR4) inhibitor, downregulates TLR4-induced inflammatory responses and becomes a potent and noveltherapeuticdrugcandidatefor PHH. In the present study, we investigate whether TAK-242 protects against hydrocephalus and improves the prognosis of intraventricular hemorrhage (IVH). We also explore the possible role of TAK-242 for the regulation of TLR4-NF-κB signaling pathway. A model of PHH was conducted in 6-week-old Male Sprague-Dawley (SD) rats. The rats were divided into four main groups, including the sham, IVH + vehicle, IVH + TAK-242 and IVH groups. Magnetic resonance imaging (MRI) was applied to measure the lateral ventricle volume. Western blot (WB) and immunofluorescence (IF) were applied to detect the expression of TLR4, NF-κB, fibronectin and laminin. A combined scoring system and Morris water maze were employed to evaluate neurological functions after IVH. We found that IVH induced heightened activation of TLR4-NF-κB signaling pathway. We observed the increased lateral ventricular volume, elevation of NF-κB in choroidplexus, as well as fibronectin and laminin in the subarachnoid space (SAS) and ventricular wall after IVH. Obviously, TAK-242 treatment effectively inhibited the up-regulation of NF-κB, fibronectin, laminin and significantly alleviated ventriculomegaly after IVH. Importantly, TAK-242 improved neurocognitive deficits after PHH. In conclusion, TAK-242 attenuated IVH-induced hydrocephalus and improved the prognosis of PHH. The underlying mechanism involved the TAK-242-mediated downregulation of TLR4-NF-κB signaling pathway.

miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling.

Objective: Micro-RNA plays a critical role in the pathological process of gliomas. Previous research showed that the level of miR-155 was significantly increased in many cancers, including gliomas. However, the mechanism of glioma is still unknown. Method: To investigate the regulatory function of miR-155 on glioma U87-MG cells and its effects on related signaling pathways. After transfection of miR-155 mimic and inhibitor, the level of miR-155 were applied to detect cell proliferation, apoptosis, senescence index, invasive ability and cell migration at different time points (0, 24, 24 h, respectively) by CCK8 assay, flow cytometry, ß-galactosidase (ß-gal) staining, transwell and scratch test, respectively. The effect of miR-155 on PI3K/AKT signal pathway was observed at meantime. Results: Compared with the control group, after miR-155 mimic transfection, U87-MG cell viability, cell migration rate and invasiveness were increased, while apoptosis and senescence were significantly decreased, which was the opposite on miR-155 inhibitor transfection. The phosphorylation levels of miR-155, PI3K, AKT, PI3K, and AKT in U87-MG cells intervened with miR-155 mimic also increased significantly, while the levels of PTEN, Caspase-3, Caspase-9 mRNA, and protein declined significantly, with statistically significant difference. Meanwhile, compared with the control group, miR-155 inhibitor group were on the contrary. Conclusion: The study indicated that miR-155 take charge a key function in regulating the proliferation, migration, and invasion of glioma U87-MG cells through PI3K/AKT signaling pathway, and has anti-glioma effects by inhibition of miR-155, which provided ideas for further clinical treatment of glioma patients.