Browse Articles

Spontaneous Room-Temperature Polymerization of Carbon Disulfide in Water Microdroplets

Research on refined classification method of surrounding rock based on game theory combination weighting - fuzzy cloud model

Dynamic Solvation Structure Regulation Enables Long-Life Li–Organic Batteries

Nature Counts to Three: Universal Mg-Pinch Motif Polarizes the Cleaved Bond in NTP-Processing Enzymes

General Oxidative Chemical Activation of Neutral Exciton Emission in Colloidal MoS ₂ Monolayers

Structure Sensitivity in CH ₄ Oxidation: Switching C ₁ to C ₂ Selectivity on Mn Single Atoms Versus Nanoparticles

Steric Hindrance of Proton Donors Modulates Heterogeneous Electrochemical Nitrogen Reduction Reaction Selectivity in Nonaqueous Electrolytes

Photoinduced Copper-Catalyzed Site- and Stereoselective Desymmetrizing β-C(sp ³ )-H Alkynylation of Cycloalkyl Amines

Biomimetic D–A1–A2 Organic Cages with Recombination-Suppressed Sequential Charge Transfer for Hydrogen Peroxide Photosynthesis

A Ce ⁴⁺ Aluminum Hydride Complex

Highly Selective and Modular Assembly of Densely Substituted Tetrahydrofurans

Dynamic Kinetic Resolution-Based Asymmetric Hydrogenation of Pyridines

Electrolyte Engineering Enables Selective Electrocatalytic Hydrogenation of Furfural to 2-Methylfuran

How I Treat Thrombotic Microangiopathy in the Setting of Triggers

Complement-mediated thrombotic microangiopathy can be difficult to recognize when it presents in the setting of an apparent clinical trigger, such as pregnancy, severe hypertension, or kidney transplantation. These conditions can each cause endothelial injury directly, but may also unmask complement dysregulation in susceptible individuals. In these situations, the critical question is not whether a trigger exists but whether it fully explains the syndrome and whether urgent complement blockade is warranted to prevent irreversible kidney injury. In this How I Treat article, we use three real-world cases to illustrate how we approach this decision in practice. We emphasize the bedside features that most influence our threshold to treat, including the pattern and severity of kidney injury, tempo of disease progression, and lack of improvement with supportive or trigger-directed care. We also address the interpretation of complement genetic findings, pregnancy- and transplant-specific risk stratification, and individualization of treatment duration. Functional assays can support mechanistic assessment in selected cases but remain an adjunct to the diagnosis and should not drive management decisions.

A General Approach to <i>geminal</i> -Dimethyl <i>trans</i> -Decalin Terpenoids

CD70 Overexpression at Diagnosis Predicts Relapse and supports dual CD19-CD70 CAR-T Therapy in Follicular Lymphoma

Although first-line immunotherapy achieves remission in most patients with follicular lymphoma (FL), improved biomarkers and therapeutic strategies are required to identify and manage those who relapse. We investigated the immune microenvironment at diagnosis in uniformly treated FL patients with extended follow-up (&amp;gt;11 years), comparing relapsed and relapse-free cases. Transcriptomic profiling revealed enrichment of inflammatory response pathways in relapsed patients, including cytokine overexpression and upregulation of CD70, a molecule implicated in immune activation and inflammation. Multiplex immunofluorescence confirmed CD70 overexpression at diagnosis in tumor cells as well as in CD8⁺ and CD4⁺ T follicular helper (TFH) cells, correlating with inferior progression-free survival. Functional studies demonstrated that CD70⁺ tumor cells were more proliferative and induced CD70 expression in T cells, suggesting a feed-forward loop sustaining immune activation. To target these cells and enhance current CAR-T approaches, we engineered dual CD19-CD70 chimeric antigen receptor (CAR) T cells by co-transducing the CD19-CAR-T ARI-0001 with a CD27-based anti-CD70 CAR. Dual CAR-T cells exhibited enhanced in vitro cytotoxicity against patient-derived spheroids of FL, diffuse large B-cell lymphoma, and mantle cell lymphoma. In FL xenograft models, dual CAR-T treatment achieved superior disease control compared to monotargeted CAR-T cells, inducing complete tumor clearance in spleen and bone marrow. Collectively, these findings provide strong preclinical rationale for the clinical development of CD19-CD70 dual CAR-T therapy to improve outcomes in high-risk FL and potentially other B-cell non-Hodgkin lymphomas.

A Hydrocarbon Organic Cage-Based Porous Liquid for Ethylene/Ethane Separation

IL-6 receptor inhibition promotes expansion of cytolytic CD4+ T cells after cellular immunotherapy.

Graft-versus-host disease (GVHD) remains a major barrier to the success of allogeneic hematopoietic stem cell transplantation (HSCT). In preclinical models, dysregulation of IL-6 in the peri-transplant period promotes GVHD via STAT3-dependent T cell differentiation and monocyte activation but the nature of immunological effects invoked in patients remains unclear. To advance our understanding of IL-6 signaling in humans during HSCT, we performed single-cell RNA sequencing on circulating CD14+ monocytes and CD4+ T cells from patient samples within a clinical trial of IL-6R inhibition (tocilizumab (TCZ) or placebo) on a backbone of calcineurin inhibition (CNI) and short-course methotrexate. We studied patients who did not develop acute GVHD and included a placebo-treated group analyzed prior to the development of acute GVHD. IL-6R inhibition promoted Type-I IFN-associated transcriptional programs in both CD4+ T cells and CD14+ monocytes. Surprisingly, IL-6R-inhibition with TCZ profoundly enhanced cytolytic CD4+ T cell differentiation. In experimental HSCT and chimeric antigen receptor T cell systems, genetic deletion of IL-6 signaling in donor T cells enhanced the expansion of cytolytic Eomes+ CD4+ regulatory T cell subsets whilst attenuating Th1 and Th17 differentiation. Consistent with the promotion of this cytolytic CD4+ phenotype, anti-tumor effects were improved in the absence of IL-6 signaling. In summary, these data demonstrate that IL-6R inhibition during cell therapy imprints Type-I IFN programs and cytolytic CD4+ T cell differentiation, including the Eomes+ fraction associated with favorable immunotherapy outcomes.

Pressure-Induced Crossover from Antiferromagnetism to Single-Band Superconductivity via Multiband Superconductivity in Quasi-1D CrZr ₄ Te ₁₄

Force-Accelerated Autocatalysis in a Knoevenagel Condensation Reaction during Ball Milling