Human salivary histatin 1 regulating IP3R1/GRP75/VDAC1 mediated mitochondrial-associated endoplasmic reticulum membranes (MAMs) inhibits cell senescence for diabetic wound repair.

Rationale: Difficulty in skin wound healing is a concern for diabetic patients across the world. Impaired mitochondrial dysfunction and aging-related vascular dysfunction in human umbilical vein endothelial cells (HUVECs) caused by oxidative stress are major impediments to diabetic wound healing. However, research on skin repair at the mechanistic level by improving mitochondrial function and inhibiting oxidative stress-induced HUVEC senescence remains lacking.

Bus arrival and departure time updates in the Greater Sydney Area.

Public Transport Authorities generate large quantities of data as part of their daily operations, including vehicle positions, arrival times, and dynamic routing options. This information is essential feedback into the system for planning routes and timetables, modelling passenger demand growth and evaluating operational performance. The General Transit Feed Specification (GTFS) is a data format that allows public transport data to be consumed by a wide variety of software applications.

Identification of a novel protein Hq023 of the hard tick Haemaphysalis qinghaiensis and preliminary evaluation of its analgesic effect in mice model.

Tick saliva contains a range of critical biological molecules which could inhibit host defenses and guarantee their food supply. Hq023, a novel cDNA sequence, was cloned from a cDNA library constructed from salivary glands of partially-engorged Haemaphysalis qinghaiensis. Hq023 has an open reading frame (ORF) of 408 bp coding a protein containing 135 amino acid residues with a molecular mass of 15 kDa.

The YY1-CPT1C signaling axis modulates the proliferation and metabolism of pancreatic tumor cells under hypoxia.

Carnitine palmitoyltransferase 1C (CPT1C) is an enzyme that regulates tumor cell proliferation and metabolism by modulating mitochondrial function and lipid metabolism. Hypoxia, commonly observed in solid tumors, promotes the proliferation and progression of pancreatic cancer by regulating the metabolic reprogramming of tumor cells. So far, the metabolic regulation of hypoxic tumor cells by CPT1C and the upstream mechanisms of CPT1C remain poorly understood.