An Investigation into High-Accuracy and Energy-Efficient Novel Capacitive MEMS for Tire Pressure Sensor Application.

Tire pressure monitoring systems (TPMSs) are essential for maintaining driving safety by continuously monitoring critical tire parameters, such as pressure and temperature, in real time during vehicle operation. Among these parameters, tire pressure is the most significant, necessitating the use of highly precise, cost-effective, and energy-efficient sensing technologies. With the rapid advancements in micro-electro-mechanical system (MEMS) technology, modern automotive sensing and monitoring systems increasingly rely on MEMS sensors due to their compact size, low cost, and low power consumption.

How does globally accumulated tropical cyclone energy vary in response to a changing climate?

How tropical cyclone (TC) activity varies in response to a changing climate is widely debated. The accumulated cyclone energy (ACE) is one of the indicators of TC activity and has attracted considerable attention because of its close relationship with the damages caused by TCs. Previous studies have focused on detecting long-term trends in global ACE; however, the results are inconclusive.

Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling.

The transmembrane protein Synapse Differentiation Induced Gene 4 (SynDIG4) functions as an auxiliary factor of AMPA receptors (AMPARs) and plays a critical role in excitatory synapse plasticity as well as hippocampal-dependent learning and memory. Mice lacking SynDIG4 have reduced surface expression of GluA1 and GluA2 and are impaired in single tetanus-induced long-term potentiation and NMDA receptor (NMDAR)-dependent long-term depression. These findings suggest that SynDIG4 may play an important role in regulating AMPAR distribution through intracellular trafficking mechanisms; however, the precise roles by which SynDIG4 governs AMPAR distribution remain unclear.

Helicobacter pylori infection promotes M1 macrophage polarization and gastric inflammation by activation of NLRP3 inflammasome via TNF/TNFR1 axis.

Background: Macrophages play a crucial role in chronic gastritis induced by the pathogenic Helicobacter pylori (H. pylori) infection. NLRP3 inflammasome has emerged as an important component of inflammatory processes.

The epitranscriptional factor PCIF1 orchestrates CD8 T cell ferroptosis and activation to control antitumor immunity.

T cell-based immunotherapies have revolutionized cancer treatment, yet durable responses remain elusive. Here we show that PCIF1, an RNA N 2'-O-dimethyladenosine (mA) methyltransferase, negatively regulates CD8 T cell antitumor responses. Whole-body or T cell-specific Pcif1 knockout (KO) reduced tumor growth in mice.