With strikingly high speed, data retention ability and storage density, resistive RAMs have emerged as a forerunning nonvolatile memory. Here we developed a Re-RAM with ultra-high density array of monocrystalline perovskite quantum wires (QWs) as the switching matrix with a metallic silver conducting pathway. The devices demonstrated high ON/OFF ratio of ∼107 and ultra-fast switching speed of ∼100 ps which is among the fastest in literature. The devices also possess long retention time of over 2 years and record high endurance of ∼6 × 106 cycles for all perovskite Re-RAMs reported. As a concept proof, we have also successfully demonstrated a flexible Re-RAM crossbar array device with a metal–semiconductor–insulator–metal design for sneaky path mitigation, which can store information with long retention. Aggressive downscaling to ∼14 nm lateral dimension produced an ultra-small cell effectively having 76.5 nm2 area for single bit storage. Furthermore, the devices also exhibited unique optical programmability among the low resistance states.

The malignant tumor is a multi-etiological, systemic and complex disease characterized by uncontrolled cell proliferation and distant metastasis. Anticancer treatments including adjuvant therapies and targeted therapies are effective in eliminating cancer cells but in a limited number of patients. Increasing evidence suggests that the extracellular matrix (ECM) plays an important role in tumor development through changes in macromolecule components, degradation enzymes and stiffness. These variations are under the control of cellular components in tumor tissue via the aberrant activation of signaling pathways, the interaction of the ECM components to multiple surface receptors, and mechanical impact. Additionally, the ECM shaped by cancer regulates immune cells which results in an immune suppressive microenvironment and hinders the efficacy of immunotherapies. Thus, the ECM acts as a barrier to protect cancer from treatments and supports tumor progression. Nevertheless, the profound regulatory network of the ECM remodeling hampers the design of individualized antitumor treatment. Here, we elaborate on the composition of the malignant ECM, and discuss the specific mechanisms of the ECM remodeling. Precisely, we highlight the impact of the ECM remodeling on tumor development, including proliferation, anoikis, metastasis, angiogenesis, lymphangiogenesis, and immune escape. Finally, we emphasize ECM "normalization" as a potential strategy for anti-malignant treatment.

Phase change memory is widely considered as the most promising candidate as storage class memory (SCM), bridging the performance gaps between dynamic random access memory and flash. However, high required operation current remains the major limitation for the SCM application, even after using defect engineering materials, for example, Ti-doped Sb 2 Te 3 . Here, we demonstrate that ∼87% current can be reduced by spatially separating Sb 2 Te 3 and TiTe 2 layers, thanks to semimetallic TiTe 2 serving as a thermal barrier in the reset process. Moreover, the stable crystalline TiTe 2 layer provides an ordered interface to speed up the crystallization process of the amorphous Sb 2 Te 3 layer, enabling ∼10 ns ultrafast crystallization speed. An outstanding device lifetime, up to ∼2 × 10 7 cycles, has been obtained, which is twice as long as that of alloy-based cells. Correlative electron microscopy and atom probe tomography provide evidence that the TiTe 2 /Sb 2 Te 3 multilayer can keep a layer-stacked structure, avoiding phase segregation found in alloys and strong element intermixing in the GeTe/Sb 2 Te 3 superlattice, which enables excellent cyclability. This study suggests that adding a semimetallic layer in the phase change layer, such as TiTe 2 and TiSe 2 , can yield a phase change memory with superior properties. KEYWORDS: thermal barrier phase change material, atom probe tomography, Ti−Sb−Te, TiTe 2 , TiTe 2 /Sb 2 Te 3 , high endurance, low energy consumption

Metastasis is the main cause of cancer‐related death, yet the underlying mechanisms are still poorly understood. Long noncoding RNAs (lncRNAs) are emerging as crucial regulators of malignancies; however, their functions in tumor metastasis remain largely unexplored. In this study, we identify a lncRNA, termed metabolism‐induced tumor activator 1 (MITA1), which is up‐regulated in hepatocellular carcinoma (HCC) and contributes to metastasis. MITA1, a chromatin‐enriched lncRNA discovered by our nuclear RNA sequencing, is significantly induced by energy stress. This induction of MITA1 is governed by the liver kinase B1–adenosine monophosphate‐activated protein kinase (LKB1‐AMPK) pathway and DNA methylation. Knockdown of MITA1 dramatically inhibits the migration and invasion of liver cancer cells in vitro and HCC metastasis in vivo. Mechanistically, MITA1 promotes the epithelial–mesenchymal transition, an early and central step of metastasis, which may partly attribute to an increase in Slug (snail family zinc finger 2) transcription. MITA1 deficiency reduces the expression of the mesenchymal cell markers, especially Slug, whereas Slug overexpression greatly impairs the effects of MITA1 deficiency on HCC migration and invasion. Correspondingly, there is a positive correlation between the levels of MITA1 and Slug precursors in HCC tissues. Conclusion: Our data reveal MITA1 as a crucial driver of HCC metastasis, and highlight the identified AMPK‐MITA1‐Slug axis as a potential therapeutic strategy for HCC.