Design of a hazard prediction system with intelligent multimodal fusion based on artificial intelligence & internet of things technology: taking a crib as an example.

Problem: How to design an intelligent multimodal fusion hazard prediction system using AIoT (Artificial Intelligence & Internet of Things) technology to predict some potential dangers. This article will provide some ideas and methods.

Introduction: This article designs an intelligent multimodal fusion hazard prediction system based on AIoT technology.

Disturbed Flow-Facilitated Margination and Targeting of Nanodisks Protect against Atherosclerosis.

Disturbed blood flow induces endothelial pro-inflammatory responses that promote atherogenesis. Nanoparticle-based therapeutics aimed at treating endothelial inflammation in vasculature where disturbed flow occurs may provide a promising avenue to prevent atherosclerosis. By using a vertical-step flow apparatus and a microfluidic chip of vascular stenosis, herein, it is found that the disk-shaped versus the spherical nanoparticles exhibit preferential margination (localization and adhesion) to the regions with the pro-atherogenic disturbed flow.

Vitexin inhibits APEX1 to counteract the flow-induced endothelial inflammation.

Vascular endothelial cells are exposed to shear stresses with disturbed vs. laminar flow patterns, which lead to proinflammatory vs. antiinflammatory phenotypes, respectively.

Rational Construction of an Exceptionally Stable MOF Catalyst with Metal-Adeninate Vertices toward CO Cycloaddition under Mild and Cocatalyst-Free Conditions.

CO is considered as the primary greenhouse gas, resulting in a series of serious environmental problems that affect people's life and health. Carbon capture and sequestration has been implemented as one of the most appealing pathways to control and use CO . Here, we rationally integrate various functional sites within the confined nanospace of a microporous metal-organic framework (MOF) material, which is constructed by mixed-ligand strategy based on metal-adeninate vertices.

STAT3 down-regulation induces mitochondria-dependent G2/M cell cycle arrest and apoptosis in oesophageal carcinoma cells.

STAT3 is persistently activated in a wide variety of human tumours, and aberrant STAT3 activity promotes tumour growth, invasion and metastasis. To explore STAT3 down-regulation in human oesophageal cancer cells, cell proliferation, apoptosis and mitochondrial mechanisms were explored in oesophageal carcinoma TE1 cell cultures. We demonstrate for the first time that STAT3 down-regulation by RNAi is sufficient to inhibit oesophageal cancer cell proliferation inducing cell apoptosis.