Immunotherapies represented by immune checkpoint inhibitors and CAR−T cell therapy have fundamentally transformed the cancer treatment landscape, yet they have repeatedly failed against the most lethal brain tumor, glioblastoma (GBM). Why does this "immunological storm" that has swept through oncology suddenly "extinguish" within the brain This review addresses a core scientific question: Are our current immunotherapy strategies trapped in a "whack−a−mole" predicament when confronting GBM's fortress−like immunosuppressive tumor microenvironment (TME), lacking a comprehensive battle blueprint Through critical examination of the root causes underlying current therapeutic failures, we identify fundamental limitations in drug delivery, target selection, and microenvironment remodeling across three critical dimensions. We propose that future breakthroughs must pivot from "single−target approaches" toward "multi−step, sequential TME holistic remodeling." This requires developing more intelligent delivery systems to "breach the fortress walls," implementing metabolic interventions and targeted suppressive cell elimination to "purify the battlefield," and ultimately "create winning opportunities" for immune effector cells. This review also explores how novel preclinical models and dynamic biomarkers can guide the implementation of this complex strategy, aiming to provide new insights and inspiration for igniting this "immunological desert" of GBM.

Gene editing refers to the process of specifically modifying organism's genome using specific technical approaches to regulate its genetic information and phenotypic characteristics. Among them, large−fragment gene integration technology enables the accurate insertion or replacement of large exogenous DNA fragments in the organismal genome, which provides core technical support for the development of innovative therapeutic strategies against severe diseases. Starting from the historical origin of this technology, this paper systematically sorts out its developmental trajectory and analyzes the current technical bottlenecks of large−fragment gene integration technology, including exogenous DNA dependence, delivery challenges and prominent immune risks. Given that the novel large−fragment integration techniques based on R2 retrotransposons are expected to become a key solution to break through these limitations, the study further introduces the structural characteristics and retrotransposition mechanisms of R2 retrotransposons, and reviews the research advances in its structural analysis and engineering modification, and summarizes the technical breakthroughs and application prospects of R2 retrotransposon−mediated large−fragment integration tools, which provides theoretical insights and practical references for the application of R2 retrotransposon tools in gene therapy.

Liver transplantation is the only effective treatment for various end−stage liver diseases. However, immune injury after liver transplantation, such as acute rejection (AR), chronic rejection (CR), hepatic ischemia−reperfusion injury (HIRI), and opportunistic infection, still seriously affects the prognosis of patients. Although great progress has been made in the research of immune injury after liver transplantation, there are still many deficiencies in clinical practice. In this article, the functional changes of hepatocytes and non−parenchymal cells after liver transplantation were used as the breakthrough point to summarize and clarify the potential molecular mechanisms of immune injury after liver transplantation, systematically review the latest progress in the prevention and treatment of immune injury after liver transplantation, and focus on emerging prevention and treatment strategies and their clinical application prospects. The application of artificial intelligence and big data technology in the prediction, diagnosis, treatment and management of immune injury in liver transplantation is prospected, in order to provide reference for related basic research and clinical application.

Small cell lung cancer (SCLC) is the most aggressive lung cancer subtype. With approximately 70% of patients presenting with distant metastasis at initial diagnosis, the 5−year survival rate for these individuals remains below 3%. This high metastatic propensity is the primary driver of poor prognosis. Focusing on SCLC metastasis, this article systematically reviews recent progress across clinical features, molecular mechanisms, and advanced preclinical models. Specifically, it outlines target organ metastasis patterns and current interventions, while exploring the core regulatory networks driving the metastatic cascade, including genetic alterations, pathway activations, and tumor−microenvironment interactions. Furthermore, the review evaluates advanced models—such as cell lines, organoids, and genetically engineered mouse models (GEMMs)—and highlights the application of multi−omics technologies in deciphering spatiotemporal heterogeneity. Future research should prioritize metastasis−specific molecular signatures and therapeutic targets to foster the translational integration of basic and clinical research. Such efforts are essential to address tumor heterogeneity, overcome therapeutic limitations, and ultimately improve patient survival.

Gastric cancer peritoneal metastasis (GCPM) carries a poor prognosis, and the local immune microenvironment is central to disease progression and treatment response. Here, we analyzed paired peritoneal lavage samples collected before and after intraperitoneal chemotherapy (IPC) using bulk RNA sequencing (bulk RNA−seq) and single−cell RNA sequencing (scRNA−seq) to characterize IPC associated immune changes. Bulk RNA−seq showed post−IPC upregulation of immune−related genes, including IL1B, IRAK2, ICAM1, and NLRP3. Pathway enrichment of differentially expressed genes indicated that immune/inflammatory programs—chemokine signaling, and Toll−like receptor signaling—were enriched after IPC, whereas pre−treatment samples were relatively enriched for stromal−remodeling processes, including epithelial−mesenchymal transition (EMT), complement and coagulation cascades, and angiogenesis. CIBERSORT deconvolution further suggested an increase in CD8⁺T cells and a decrease in Treg cells and overall myeloid proportions after IPC. Consistently, scRNA−seq showed higher T/NK−cell proportions and lower myeloid proportions post−treatment. Cell−cell communication analysis further revealed strengthened interactions between CD8_CTL cells and myeloid subsets, most notably along the CCL4−CCR5 and NECTIN2−CD226 axes—consistent with enhanced recruitment and activation of effector lymphocytes. Overall, IPC was associated with increased effector T−cell activity and attenuation of myeloid suppressive features, indicating partial remodeling of the peritoneal immune microenvironment. These findings provide a transcriptomic basis for optimizing local therapeutic strategies in GCPM.

With the transition of China's animal husbandry towards intensification, investigating physiological regulatory mechanisms at the cellular level is of great significance for ensuring animal health and improving production efficiency. As a key intracellular energy sensor, AMP−activated protein kinase (AMPK) plays a multidimensional regulatory role in the process of mitophagy to maintain cellular homeostasis. AMPK can not only directly regulate mitophagy but also influence it through downstream signaling pathways such as ULK1, PGC−1α, and mTOR. This review systematically summarizes the molecular mechanisms by which AMPK mediates mitophagy and its role in animal physiological health. It elaborates on the structure, function, and activation mechanisms of AMPK, as well as its regulation of mitophagy through both direct (e.g., phosphorylating MFF, activating TBK1) and indirect pathways (modulating ULK1, PGC−1α, and mTOR signaling). The synergistic protective effects of AMPK and mitophagy under conditions such as nutrient deficiency, oxidative stress, and disease infection are analyzed. Furthermore, the positive impacts of this regulatory axis on animal muscle development, meat quality, antioxidant capacity, and immune function are discussed. The aim is to provide a scientific theoretical basis for promoting healthy animal growth through the exploration of physiological regulatory mechanisms..

In the digital era, online gaming exhibits a notable double−edged sword effect. As the world's largest gaming market, China's gaming industry has evolved since the 1990s into a core driver of economic growth, technological innovation, and cultural export. It also plays an active role in constructing virtual social ecosystems and promoting gamification in education. However, its associated health risks cannot be overlooked, including physiological issues such as visual impairment, metabolic abnormalities, and circadian rhythm disruptions; psychological challenges like emotional dysregulation, cognitive confusion, and reduced sense of reality; as well as socioeconomic burdens at the familial and societal levels, including financial strain, and tendencies toward violent behavior. Severe addiction may progress into Internet Gaming Disorder (IGD), characterized by excessive prioritization of gaming, impaired self−control, and persistence gaming despite negative consequences. Although anti−addiction systems have been widely implemented, significant gaps remain in IGD prevention and control. Therefore, it is essential to establish a three−tier hierarchical intervention system covering the entire process of addictive behavior development to balance industrial growth with public risk mitigation. The sustainable development of online gaming should focus on three core directions: in the area of source governance, adopting a "Technology for Good" approach by systematically integrating anti−addiction mechanisms into game design and expanding the positive applications of "gaming+" in fields such as education and healthcare; in precise prevention and control, leveraging multimodal biometric and behavioral data to establish an AI−driven dynamic risk assessment and tiered intervention system; through mechanism exploration, enhancing interdisciplinary research integrating neuroscience, psychology, and epidemiology to elucidate the mechanisms underlying IGD development, identify key intervention targets, and enhance clinical outcomes. Through these approaches, the innovation of the gaming industry and the protection of public health can be synergistically advanced, achieving a harmony between social benefits and economic gains.

Continuous−variable quantum key distribution (CV−QKD) technology has emerged as a pivotal direction in quantum secure communication due to its inherent compatibility with classical optical communication systems and high key rates within metropolitan areas. However, the secret key rates of existing CV−QKD systems remain insufficient to meet the practical requirements of one−time pad encryption within metropolitan areas. This work innovatively integrates orthogonal frequency−division multiplexing (OFDM) technology into CV−QKD systems. We experimentally demonstrated, for the first time, a multi−carrier CV−QKD system operating at a 10 GHz repetition rate. Moreover, this experimental system respectively achieves secret key rates of 1819.32, 1078.48, 374.19, 112.96, and 34.63 Mbps over transmission distances of 5, 10, 25, 50, and 75 km by developing a high−precision dual−stage phase noise compensation algorithm, establishing an excess noise theoretical model, and designing a high−throughput data post−processing scheme. Notably, our work realizes the first instance of Gbps−level secret key rates within 10 km and 100 Mbps−level secret key rates within 50 km for metropolitan−area CV−QKD. Compared to traditional single−carrier CV−QKD system with 10 GHz repetition rate under identical experimental conditions, the multi−carrier key rate gains at different transmission distances can respectively reach 1.09@5 km, 1.10@10 km, 1.13@25 km, 1.54@50 km, and 5.55@75 km. These results confirm that the multi−carrier CV−QKD system scheme can significantly enhance quantum key distribution performance, providing an effective solution for future broadband and long−distance quantum secure communication.

Under carbon neutrality targets, understanding the spatial heterogeneity of agricultural carbon mitigation and its linkage with resource endowments and economic constraints is of critical importance. This study constructs baseline and mitigation scenarios and applies global and local spatial autocorrelation methods, including Moran's I, Local Indicators of Spatial Association (LISA), and spatial difference Moran's I, to investigate the spatial patterns and dynamic evolution of cropland distribution, mitigation cost, and emission reduction potential in China's agricultural system. The results show that: (1) Key variables exhibit significant spatial clustering, with global Moran's I ranging from 0.218 to 0.363, indicating a stable positive spatial dependence overall. This positive spatial correlation implies that high−value regions tend to be adjacent to other high−value regions, reflecting the spatial aggregation of areas with similar resource endowments; (2) Local spatial patterns show pronounced regional heterogeneity, with high–high clusters of cropland decreasing from about 8.8% to 2.9%, while low−cost clusters shrink from approximately 14.7% under the baseline scenario to about 5.9% under the mitigation scenario, indicating an overall optimization of the spatial structure; (3) Significant spatial coupling exists between variables, as the bivariate Moran's I between cropland and net cost decreases from approximately 0.431 to 0.192, suggesting that policy interventions weaken the spatial association between resource endowment and cost; (4) Spatial difference analysis indicates that the spatial dependence of cropland change becomes insignificant (from 0.385), whereas that of net cost change remains significantly positive. Overall, the mitigation scenario improves the spatial configuration of the agricultural system to some extent, although regional disparities and structural imbalances persist.

Cirrhosis is highly prevalent among patients with hepatitis B virus (HBV)−related hepatocellular carcinoma (HCC). In HCC patients with cirrhosis, hepatic resection is technically more challenging and is associated with a higher risk of postoperative complications. Moreover, surgical trauma and postoperative complications may further adversely affect long−term prognosis. Compared with open liver resection (OLR), robotic liver resection (RLR) has theoretical minimally invasive advantages; however, systematic evidence remains lacking as to whether RLR can improve short−term postoperative outcomes as well as long−term prognosis in patients with cirrhosis. This study aimed to compare the short−term postoperative outcomes and recurrence and survival outcomes between RLR and OLR in patients with HBV−related HCC and cirrhosis. Patients with HBV−related HCC and cirrhosis who underwent their first R0 liver resection at our center between 2019 and 2021 were retrospectively enrolled. All patients underwent either RLR or OLR. Patients were grouped according to surgical approach, and propensity score matching (PSM) was performed. Short−term postoperative outcomes were compared between the two groups. Kaplan−Meier analysis and the Log−rank test were used to compare recurrence−free survival (RFS) and overall survival (OS) between the RLR and OLR groups. A total of 198 patients were included in this study, including 74 patients in the OLR group and 124 patients in the RLR group. After 1:2 PSM between the OLR and RLR groups, 50 patients in the OLR group and 82 patients in the RLR group were included in the matched cohort. Before PSM, compared with the OLR group, the RLR group had shorter operative time and postoperative length of stay, less intraoperative blood loss, a lower intraoperative transfusion rate, and lower incidences of overall postoperative complications, postoperative ascites, and Clavien−Dindo grade I–II complications (all P<0.05). After PSM, the RLR group still showed less intraoperative blood loss (100 mL vs. 200 mL, P = 0.001), a shorter postoperative length of stay (5.0 days vs. 9.5 days, P<0.001), and a lower incidence of postoperative ascites (4.88% vs. 18.00%, P = 0.031). Regarding long−term prognosis, no significant differences in RFS (P = 0.706) or OS (P = 0.624) were observed between the RLR and OLR groups after PSM. In patients with HBV−related HCC and cirrhosis, RLR was associated with less intraoperative blood loss, a shorter postoperative length of stay, and a lower incidence of postoperative ascites compared with OLR, while no significant differences were observed between the two approaches in postoperative recurrence or survival outcomes.

Against the backdrop of rapidly growing global data volumes and the escalating demand for high−performance computing, storage technologies have continuously evolved as a critical component of information infrastructure. This study systematically reviews the development trajectories and key breakthroughs of mature storage technologies, including magnetic storage, semiconductor storage, and optical storage, and provides an in−depth analysis of the potential, development paths, and challenges associated with emerging storage technologies such as phase−change memory, resistive RAM, ferroelectric RAM, magnetic RAM, and DNA storage. The study further summarizes the current challenges faced by China's storage industry, including high investment risks, intense market competition, dependence on externally supplied critical materials and equipment, and the "performance–cost–ecosystem" constraints that limit the advancement of new storage technologies. Finally, it proposes development strategies such as enhancing strategic focus, cultivating localized supply chains for materials and equipment, and strengthening core technology research, aiming to provide decision−making references for promoting technological innovation and strategic planning in China's storage industry.

Chen−Hsiang Huang (1910–1987), a renowned medical scientist and virologist, was one of the principal founders of modern virology in China and a member of the Chinese Academy of Sciences. In his early career, Professor Huang pioneered the technique of in vitro tissue culture for viruses internationally, laying the methodological foundation for the global leap in virology from qualitative to quantitative research. After returning to China, he devoted his life to fundamental and applied research in virology. His globally acclaimed achievements included establishing the etiology and epidemiology of epidemic Japanese encephalitis, developing and promoting live attenuated measles vaccines, and pioneering explorations in viral immunology and tumor biotherapy during his later years. As an outstanding scientist and educator, Chen−Hsiang Huang not only built a scientific defense for safeguarding the health and lives of the nation through his outstanding research achievements but also mentored a large number of key medical professionals. More importantly, with his rigorous, pragmatic, and pioneering scholarly attitude, as well as his noble character of unwavering dedication to the country and willingness to contribute, he vividly embodied the spirit of Chinese scientists and erected an immortal monument in the field of Chinese virology.