The constituents of coal tar pitch (CTP) significantly impact the wettability of calcined coke (CC) and the performance of prebaked anodes (PA) used in aluminum electrolysis. However, balancing wettability and carbon residue within CTP remains a central challenge in material applications. In addition, limited pore permeability and structural stability in these composites hinder the effective utilization of PA. Enhancing CTP fluidity is crucial for overcoming these challenges. In this work, a novel method was developed to modify CTP utilizing various coal tar fractions, enabling controlled modulation of CTP composition and wettability. Incorporating different fractions allowed for substantial control over interfacial bonding and pore structure. The chemical composition, functional groups, and elemental content of the CTP were analyzed via X-ray photoelectron spectroscopy (XPS), Fourier transform infrared spectroscopy (FT-IR), and proton nuclear magnetic resonance (1H NMR). Subsequently, systematic comparisons of PA materials produced from different CTP formulations demonstrated improved wettability and enhanced mechanical properties. Moreover, DFT calculations were performed to compare the adsorption energies of small molecules from different coal tar fractions with coke, reflecting the interaction strength between the molecules and the solid surface. Using micro-computed tomography (μ-CT), the refined pore structure was examined, resulting in a PA composite with an optimized balance of high strength and toughness.

The endoplasmic reticulum (ER) is a major storage medium for intracellular calcium (Ca²⁺). Changes in ER Ca²⁺ homeostasis can lead to endoplasmic reticulum stress (ER stress), which, in turn, activates the unfolded protein response (UPR). However, the mechanisms involved remain unclear. This paper investigates the pathways involved in ER stress, ER Ca²⁺ homeostasis, Ca²⁺ channels, and related oral diseases. A systematic search of the literature up to April 8, 2025, was performed using PubMed and Google Scholar with specific terms for ER stress, Ca²⁺ homeostasis, and oral disease. The findings are summarized in both graphical and narrative forms. Disruption of ER Ca²⁺ homeostasis leading to ER stress and UPR can cause cellular dysfunction and inflammation in oral tissues. Understanding the relationship between ER Ca²⁺ homeostasis and ER stress in oral diseases could provide new targets for oral disease treatment.