Dual-Asymmetric Solid Additive Enables Eco-friendly All-Polymer Solar Cells with Over 19% Efficiency and Excellent Stability.

The optimization of morphology in all-polymer solar cells (all-PSCs) often relies on the use of solvent additives. However, their tendency to remain trapped in the device due to high boiling points leads to performance degradation over time. In this study, we introduce a novel approach involving the design and synthesis of one dual-asymmetric solid additive featuring mono-brominated-asymmetric dithienothiophene (SL-1).

A powerful organic photosensitizer for effective treatment of malignant tumor via activating antitumor immune response.

Photodynamic therapy (PDT) has emerged as an innovative approach in cancer treatment, effectively inducing tumor cell death through light-triggered reactive oxygen species (ROS) generation. Additionally, PDT can also trigger antitumor immune responses, thereby reducing the risk of postoperative tumor recurrence. However, the development of highly efficient photosensitizers aimed at activating immune responses for comprehensive tumor eradication remains at an early stage.

Enhanced Efficiency and Light Stability of Conventional Organic Solar Cells with a p-Type Polymeric Thin Layer on PEDOT:PSS.

Simultaneous improvement in power conversion efficiency (PCE) and device stability is very important for organic solar cells (OSCs). Herein, oligothiophene-based polymer W19 with excellent solvent resistance is exploited as a polymer thin layer to optimize the active layer morphology and then device efficiency and stability. Polymer W19 possesses a simple skeleton of trifluromethyl-substituted dithienoquinoxaline and quaterthiophene, whose thin layer shows suitable energy level, low surface energy, and strong interchain aggregation, leading to outstanding solvent resistance and excellent hole transport ability.

Epigenetic regulation of macrophage function in kidney disease: New perspective on the interaction between epigenetics and immune modulation.

The interaction between renal intrinsic cells and macrophages plays a crucial role in the onset and progression of kidney diseases. In recent years, epigenetic mechanisms such as DNA methylation, histone modification, and non-coding RNA regulation have become essential windows for understanding these processes. This review focuses on how renal intrinsic cells (including tubular epithelial cells, podocytes, and endothelial cells), renal cancer cells, and mesenchymal stem cells influence the function and polarization status of macrophages through their own epigenetic alterations, and how the epigenetic regulation of macrophages themselves responds to kidney damage, thus participating in renal inflammation, fibrosis, and repair.

Binding mechanism and antagonism of the vesicular acetylcholine transporter VAChT.

The vesicular acetylcholine transporter (VAChT) has a pivotal role in packaging and transporting acetylcholine for exocytotic release, serving as a vital component of cholinergic neurotransmission. Dysregulation of its function can result in neurological disorders. It also serves as a target for developing radiotracers to quantify cholinergic neuron deficits in neurodegenerative conditions.