Nanointegrative In Situ Reprogramming of Tumor-Intrinsic Lipid Droplet Biogenesis for Low-Dose Radiation-Activated Ferroptosis Immunotherapy.

Low-dose radiotherapy (LDR) has shown significant implications for inflaming the immunosuppressive tumor microenvironment (TME). Surprisingly, we identify that FABP-dependent lipid droplet biogenesis in tumor cells is a key determinant of LDR-evoked cytotoxic and immunostimulatory effects and developed a nanointegrated strategy to promote the antitumor efficacy of LDR through cooperative ferroptosis immunotherapy. Specifically, TCPP-TK-PEG-PAMAM-FA, a nanoscale multicomponent functional polymer with self-assembly capability, was synthesized for cooperatively entrapping hafnium ions (Hf) and HIF-1α-inhibiting siRNAs (siHIF-1α).

Using Highly Electronegative Zn to Regulate the Superlattice Structure for the Na-Ion Layered Oxide Cathode with Superior Electrochemical Performance.

The introduction of a superlattice structure into layered oxide cathode materials is a novel strategy to improve the structural stability of sodium-ion batteries (SIBs). However, the superlattice structure gradually disappears during cycling, which shortens the long life of SIBs. Here, the highly electronegative Zn is introduced into a P2-type layered oxide to regulate the superlattice structure.

Mechanotransduction in response to ECM stiffening impairs cGAS immune signaling in tumor cells.

The tumor microenvironment (TME) plays decisive roles in disabling T cell-mediated antitumor immunity, but the immunoregulatory functions of its biophysical properties remain elusive. Extracellular matrix (ECM) stiffening is a hallmark of solid tumors. Here, we report that the stiffened ECM contributes to the immunosuppression in TME via activating the Rho-associated coiled-coil-containing protein kinase (ROCK)-myosin IIA-filamentous actin (F-actin) mechanosignaling pathway in tumor cells to promote the generation of TRIM14-scavenging nonmuscle myosin heavy chain IIA (NMHC-IIA)-F-actin stress fibers, thus accelerating the autophagic degradation of cyclic guanosine monophosphate (GMP)-AMP synthase (cGAS) to deprive tumor cyclic GMP-AMP (cGAMP) and further attenuating tumor immunogenicity.

High-efficient capture and degradation of formaldehyde based on the electric-field-enhanced catalytic effect.

Enhancing the generation of active groups is of great significance for alleviating the catalyst deactivation of formaldehyde (HCHO) by accelerating the decomposition of intermediate products. Herein, an electric-field-enhanced catalytic effect was proposed for the efficient capture and degradation of HCHO base on carbon cloth loaded manganese oxide catalyst (MnO-CC). Under the action of electric field, MnO can generate more hydroxyl radicals (•OH) and superoxide radicals (•O), thus accelerating the degradation of HCHO and intermediates at room temperature.

Catalytic removal of toluene using MnO-based catalysts: A review.

Volatile organic compounds (VOCs) have serious hazard to human health and ecological environment. Due to its low cost and high activity, the catalytic oxidation technology considered to be the most effective method to remove VOCs. Toluene is one of the typical VOCs, hence its catalytic elimination is crucial for the regulation of VOCs.

Modulating tumor physical microenvironment for fueling CAR-T cell therapy.

Chimeric antigen receptor (CAR) T cell therapy has achieved unprecedented clinical success against hematologic malignancies. However, the transition of CAR-T cell therapies for solid tumors is limited by heterogenous antigen expression, immunosuppressive microenvironment (TME), immune adaptation of tumor cells and impeded CAR-T-cell infiltration/transportation. Recent studies increasingly reveal that tumor physical microenvironment could affect various aspects of tumor biology and impose profound impacts on the antitumor efficacy of CAR-T therapy.

YTHDF1 upregulation mediates hypoxia-dependent breast cancer growth and metastasis through regulating PKM2 to affect glycolysis.

N6-methyladenosine modification is the most common RNA modification mechanism in mammals. YTHDF1, a mA reader, can recognize the mA of mRNAs to facilitate the interaction with the mRNA ribosome assembly and recruitment of translation initiators to promote translation. From a clinical perspective, YTHDF1 upregulation is frequently observed in breast cancer, but its involvement in those cancer-related events is still unclear.

Emerging Roles of Energy Metabolism in Ferroptosis Regulation of Tumor Cells.

Ferroptosis is a new form of regulated cell death, which is characterized by the iron-dependent accumulation of lethal lipid peroxides and involved in many critical diseases. Recent reports revealed that cellular energy metabolism activities such as glycolysis, pentose phosphate pathway (PPP), and tricarboxylic acid cycle are involved in the regulation of key ferroptosis markers such as reduced nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and reactive oxygen species (ROS), therefore imposing potential regulatory roles in ferroptosis. Remarkably, tumor cells can activate adaptive metabolic responses to inhibit ferroptosis for self-preservation such as the upregulation of glycolysis and PPP.

Investigation of the structural, optical and electrical properties of Ca doped CuCoO nanosheets.

In this work, we present the hydrothermal synthesis of delafossite oxide Ca-doped CuCoO2 (CCCaO) nanosheets at a low temperature of 100 °C. The crystal phase, morphology and chemical composition of these CuCoO2 (CCO) based samples were comprehensively characterized by powder X-ray diffraction (XRD), field-emission scanning electron microscopy (FESEM), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), and Raman spectroscopy. The size of CCCaO nanosheets decreased with increasing Ca dopant concentration, and the optimized CCCaO nanosheets (∼490 nm in lateral size and ∼15 nm in thickness) were much smaller than CCO nanocrystals (∼540 nm in lateral size and 85 nm in thickness).

UB-311, a novel UBITh amyloid β peptide vaccine for mild Alzheimer's disease.

Introduction: A novel amyloid β (Aβ) synthetic peptide vaccine (UB-311) has been evaluated in a first-in-human trial with patients of mild-to-moderate Alzheimer's disease. We describe translational research covering vaccine design, preclinical characterization, and phase-I clinical trial with supportive outcome that advances UB-311 into an ongoing phase-II trial.

Methods: UB-311 is constructed with two synthetic Aβ-targeting peptides (B-cell epitope), each linked to different helper T-cell peptide epitopes (UBITh) and formulated in a Th2-biased delivery system.