Parkinson’s disease is expected to cause a substantial economic burden from 2020 to 2040, amounting to 473 billion CNY in constant 2024 prices, which represents 0.017% of projected GDP in China. Utilizing a health-augmented macroeconomic model across 31 provinces, researchers found that disease-induced reductions in physical capital accumulation outweigh labor supply declines in most regions. The findings support tailored prevention and long-term care strategies.

The cutting-edge advances in multivalent mRNA–exosome vaccines provides a mechanistic blueprint showing how these customized mRNA payloads can systematically reprogram the immunosuppressive architecture of “cold” tumor microenvironments and mobilize potent, antigen-specific cytotoxic T-lymphocyte responses to overcome cancer immunotherapy resistance.A primary challenge in oncology vaccinology is delivering payloads to lymphoid-resident antigen-presenting cells (APCs) without triggering systemic toxicities or rapid hepatic clearance. While synthetic lipid nanoparticles (LNPs) are standard for systemic delivery, they face hepatocyte sequestration driven by blood-borne apolipoprotein E (ApoE) binding, which limits extrahepatic bioavailability. To bypass this constraint, engineered exosomes offer a biological alternative. These cell-derived vesicles feature a native lipid bilayer enriched with cholesterol and sphingomyelin that shields mRNA from ribonuclease degradation. By presenting surface markers like CD47—a “don’t eat me” signal blocking macrophage phagocytosis via SIRPα—exosomes achieve extended circulation half-lives (Figure 1).

Glioblastoma (GBM) remains the most aggressive and lethal primary brain tumor, with a dismal prognosis despite decades of intensive research. While immunotherapy has revolutionized treatment for many cancers, GBM has proven remarkably refractory to immune-based interventions due to the absence of effective immunotherapeutic targets and the profoundly immunosuppressive tumor microenvironment. In this groundbreaking study, researchers employed CRISPR screening to systematically identify novel drivers of GBM progression, uncovering Niemann-Pick C1-like 1 (NPC1L1) as a previously unrecognized key regulator of GBM pathogenesis. Mechanistically, NPC1L1 modulates cholesterol metabolism to concurrently enhance tumor cell stemness and suppress CD8+ T-cell activation, creating a dual mechanism that drives tumor progression while evading immune surveillance. Most notably, combined treatment with ezetimibe, an FDA-approved NPC1L1 inhibitor, and anti-PD-1 antibody elicited potent antitumor activity in GBM orthotopic mouse models, offering a promising translational strategy. These findings establish NPC1L1 as a critical regulator of GBM pathogenesis and underscore the therapeutic potential of targeting NPC1L1-mediated cholesterol metabolism for developing novel GBM immunotherapies, opening new avenues for treating this devastating disease.

Researchers in China developed a novel two-terminal β-Ga₂O₃ photo-synapse based on self-trapped holes engineering, achieving low weight update nonlinearity and excellent anti-interference characteristics. The device enables diversified in-sensor computing tasks from image classification to motion recognition, demonstrating great potential for neuromorphic machine vision systems in the artificial intelligence era.

Indolent B-cell non-Hodgkin lymphomas (iNHLs) represent a biologically heterogeneous group of hematological malignancies characterized by slow progression and extended survival, yet most cases remain incurable with frequent relapses. This prospective, multicenter, single-arm clinical trial evaluated the efficacy and safety of obinutuzumab plus bendamustine (GB) as first-line treatment for 220 Chinese patients with newly diagnosed indolent B-cell lymphoma across eight centers. The study encompassed multiple iNHL subtypes including follicular lymphoma (FL), marginal zone lymphoma, Waldenström macroglobulinemia, hairy cell leukemia variant, and unclassified B-cell lymphoproliferative disorder. Patients received six induction cycles of GB followed by two years of obinutuzumab maintenance in responders. At a median follow-up of 13.1 months, the regimen demonstrated remarkably high overall response rates across all subtypes, with particularly impressive complete response rates. The FL and non-FL groups showed comparable overall response rates, although the FL group achieved a significantly higher complete response rate. Treatment-emergent adverse events were generally manageable, though infections were more frequent in the non-FL group. Multivariate analysis identified elevated beta-2 microglobulin levels and failure to complete all planned treatment cycles as independent predictors of shorter progression-free survival.

Hepatocellular carcinoma (HCC) remains one of the most lethal malignancies worldwide, ranking as the third leading cause of cancer-related mortality, with limited therapeutic targets and dismal prognosis for advanced disease. This study identifies P53 and DNA damage-regulated gene 1 (PDRG1) as a novel oncogenic driver in HCC, revealing a previously unrecognized regulatory axis promoting tumor progression. The researchers demonstrate that PDRG1 expression is significantly upregulated in HCC tissues compared with normal liver, and that high PDRG1 expression correlates with advanced tumor stage, higher histological grade, and poor patient survival, establishing PDRG1 as a potential prognostic biomarker. Functional studies reveal that PDRG1 knockdown suppresses HCC cell proliferation, migration, and invasion in vitro, and inhibits tumor growth and lung metastasis in vivo, while PDRG1 overexpression exerts opposite effects. Mechanistically, PDRG1 activates Wnt/β-catenin signaling, elevating levels of β-catenin, c-Myc, and phosphorylated GSK-3β, and the oncogenic effects of PDRG1 are reversed by the Wnt pathway inhibitor XAV939, confirming functional dependence on this pathway. Furthermore, the study identifies transcription factor Specificity Protein 1 (SP1) as an upstream regulator that binds directly to the PDRG1 promoter and activates its transcription, with rescue experiments confirming that SP1 exerts its pro-tumor effects through PDRG1.

Researchers at Beijing Institute of Technology developed a spatially shaped femtosecond-laser method for patterning quantum-dot colour-conversion pixels. The approach creates microholes down to 100 nm and produces red and green CdSe quantum-dot pixels as small as approximately 700 nm, yielding monochromatic and dual-colour arrays with high uniformity. This mask-free strategy offers a promising route toward high-resolution full-colour micro-LED displays for AR/VR and other advanced applications.