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Baryon Electromagnetic Form Factors are essential for testing ground state models of nucleon internal structures. At the BESIII experiment, a comprehensive study has been conducted on the electromagnetic form factors of various baryons. The electromagnetic form factor ratio of the nucleon (proton and neutron), denoted as | G E / G M |, has been determined with high precision. And the study at BESIII has explored the cross sections of various baryon pairs, including Λ, Λ c , Σ, Ξ, Ω and Δ from their respective thresholds. In the study conducted at BESIII, threshold effects have been observed in some baryon pairs, enhancing our understanding of these baryon interactions.

Lung cancer is a malignant tumor characterized by a rapid proliferation rate, less survivability, high mortality, and metastatic potential. This review focuses on updated research about the clinical application of traditional Chinese medicine (TCM) as an adjuvant therapy to lung cancer treatment and the mechanisms of TCM effect on lung cancer in vitro and in vivo. We summarized the recent 5 years of different research progress on clinical applications and antitumor mechanisms of TCM in the treatment of lung cancer. As a potent adjuvant therapy, TCM could enhance conventional treatments (chemotherapy, radiation therapy, and epidermal growth factor receptors [EGFRs] tyrosine kinase inhibitors [TKIs]) effects as well as provide synergistic effects, enhance chemotherapy drugs chemosensitivity, reverse drug resistance, reduce adverse reactions and toxicity, relieve patients' pain and improve quality of life (QOL). After treating with TCM, lung cancer cells will induce apoptosis and/or autophagy, suppress metastasis, impact immune reaction, and therapeutic effect of EGFR-TKIs. Therefore, TCM is a promisingly potent adjuvant therapy in the treatment of lung cancer and its multiple mechanisms are worthy of an in-depth study.

In this paper, the terminal guidance problem of unpowered lifting reentry vehicle to stationary target is studied. Based on the requirement of attacking the target with high precision and high impact angle constraint, a fractional-order theory combined sliding mode guidance law is proposed. Its sliding surface is specially designed to satisfy the requirements in the terminal guidance phase. The novel fractional-order sliding mode guidance law is established in both two-dimensional environment and three-dimensional environment; then, the systems are proved to be asymptotically stable according to the Lyapunov stability principle. Finally, compared with the one without fractional-order term, experiments show the novel guidance law has better stability. Monte Carlo simulation verifies that the designed guidance law is more robust against the disturbance of random noise and ensures higher precision in terms of impact angle error and miss distance.

Acinar metaplasia is an initial step in a series of events that can lead to pancreatic cancer. Here we perform single-cell RNA-sequencing of mouse pancreas during the progression from preinvasive stages to tumor formation. Using a reporter gene, we identify metaplastic cells that originated from acinar cells and express two transcription factors, Onecut2 and Foxq1. Further analyses of metaplastic acinar cell heterogeneity define six acinar metaplastic cell types and states, including stomach-specific cell types. Localization of metaplastic cell types and mixture of different metaplastic cell types in the same pre-malignant lesion is shown. Finally, single-cell transcriptome analyses of tumor-associated stromal, immune, endothelial and fibroblast cells identify signals that may support tumor development, as well as the recruitment and education of immune cells. Our findings are consistent with the early, premalignant formation of an immunosuppressive environment mediated by interactions between acinar metaplastic cells and other cells in the microenvironment. Pancreatic ductal adenocarcinoma may be initiated by acinar metaplasia, but the molecular and cellular insights during this transition are unclear. Here the authors show, using single cell RNA-sequencing analyses, that mouse metaplastic acinar cells can be clustered into six cell types or states that are heterogeneous and have unique transcription programs.

Despite the diverse etiologies of drug-induced liver injury (DILI), innate immunity activation is a common feature involved in DILI progression. However, the involvement of innate immunity regulation in inflammation resolution and liver regeneration in DILI remains obscure. Herein, we identified the chemokine CCL5 as a central mediator of innate immunity regulation in the pathogenesis of DILI. First, we showed that serum and hepatic CCL5 levels are elevated in both DILI patients and an APAP-induced liver injury (AILI) mouse model. Interestingly, both nonparenchymal cells and stressed hepatocytes are cell sources of CCL5 induction in response to liver injury. Functional experiments showed that CCL5 deficiency has no effect on the early phase of AILI but promotes liver repair in the late phase mainly by promoting inflammation resolution and liver regeneration, which are associated with an increased number of hepatic M2 macrophages. Mechanistically, CCL5 can directly activate M1 polarization and impede M2 polarization through the CCR1- and CCR5-mediated activation of the MAPK and NF-κB pathways. We then showed that CCL5 inhibition mediated by either a CCL5-neutralizing antibody or the antagonist Met-CCL5 can greatly alleviate liver injury and improve survival in an AILI mouse model. Our data demonstrate CCL5 induction during DILI, identify CCL5 as a novel innate immunity regulator in macrophage polarization, and suggest that CCL5 blockage is a promising therapeutic strategy for the treatment of DILI.

Perovskite solar cells with an inverted architecture provide a key pathway for commercializing this emerging photovoltaic technology because of the better power conversion efficiency and operational stability compared with the normal device structure. Specifically, power conversion efficiencies of the inverted perovskite solar cells have exceeded 25% owing to the development of improved self-assembled molecules 1 – 5 and passivation strategies 6 – 8 . However, poor wettability and agglomeration of self-assembled molecules 9 – 12 cause interfacial losses, impeding further improvement in the power conversion efficiency and stability. Here we report a molecular hybrid at the buried interface in inverted perovskite solar cells that co-assembled the popular self-assembled molecule [4-(3,6-dimethyl-9 H -carbazol-9-yl)butyl]phosphonic acid (Me-4PACz) with the multiple aromatic carboxylic acid 4,4′,4″-nitrilotribenzoic acid (NA) to improve the heterojunction interface. The molecular hybrid of Me-4PACz with NA could substantially improve the interfacial characteristics. The resulting inverted perovskite solar cells demonstrated a record certified steady-state efficiency of 26.54%. Crucially, this strategy aligns seamlessly with large-scale manufacturing, achieving one of the highest certified power conversion efficiencies for inverted mini-modules at 22.74% (aperture area 11.1 cm 2 ). Our device also maintained 96.1% of its initial power conversion efficiency after more than 2,400 h of 1-sun operation in ambient air. High efficiency in perovskite solar cells is achieved by using a molecular hybrid of a self-assembled monolayer with nitrilotribenzoic acid.

Background RC48-antibody-drug conjugates (ADC) link humanized anti-HER2 immunoglobulin with monomethyl auristatin E (MMAE). Clinical trials suggest promising antitumor activity in HER2-expressing solid tumors. This study probes RC48-ADC’s efficacy and safety in patients with HER2-expressing advanced or metastatic solid tumors. Method Data was collected from 23 advanced cancer patients treated with RC48-ADC at our oncology center between July 2021 and December 2022. These patients exhibited at least 1 + expression of HER2 immunohistochemistry, had previously experienced at least one failed systemic chemotherapy, and were treated with RC48-ADC until the occurrence of intolerable adverse reactions or disease progression. The primary endpoint was the disease control rate (DCR), and secondary endpoints included progression-free survival (PFS), objective response rate (ORR), and safety. Results 23 of 25 screened patients received RC48 treatment. The ORR was 43.5% (95% CI, 23.2-63.7%) with a median PFS of 6.0 months (95% CI, 4.8–7.4). In the low-to-medium HER2 expression subgroup, ORR was 37.5%, median PFS 5.75 months. In the high HER2 expression subgroup, ORR was 57.1%, median PFS 7 months. For the cohort combining RC48 with PD-1 inhibitors, ORR was 53.8%, median PFS 8 months. In the concurrent local radiation therapy subgroup, ORR was 40.0%, median PFS 6.0 months. Treatment-related adverse events (TRAEs) were anemia (60.8%), leukopenia (56.2%), raised transaminases (52.17%), and neutropenia (43.5%). Five patients (21.7%) experienced Grade 3 symptoms, including anemia (21.7%) and neutropenia (14.0%). No Grade 4 adverse reactions or deaths were reported. Conclusion RC48-ADC shows promising efficacy and manageable safety in HER2-expressing advanced or metastatic solid tumor patients.

Regiella insecticola is a bacterial endosymbiont in insects that exhibits a negative effect on the fitness of hosts. Thus, it is not clear why this costly endosymbiont can persist in host populations. Here, we tested a hypothesis that the infection pattern and negative roles of the endosymbiont were not constant but environmentally dependent. The grain aphids Sitobion avenae , belonging to different genotypes and infected with Regiella or not, were used in this study. We found that S . avenae populations were infected with Regiella , Hamiltonella defensa , Serratia symbiotica and Rickettsia . The predominant endosymbionts in the aphid populations varied with season. Serratia and Rickettsia were predominant from December to February while Regiella predominated from March to May. The vertical transmission of Regiella was poorer at high temperature, but following conditioning for seven generations, the transmission rate improved. Regiella inhibited the production of winged aphids at 25 °C, but it did not affect winged morph production at the higher temperatures of 28 °C and 31 °C. Regiella infection decreased the intrinsic rate of increase ( r m ) of aphids at 25 °C and 28 °C. However, at 31 °C, the effect of Regiella on the r m varied depending on the aphid genotype and density. Thus, the negative effects of this endosymbiont on its host were environmentally dependent.

Asymmetric dearomatization reactions have recently emerged as a powerful tool for the rapid build-up of the molecular complexity. Chiral three-dimensional polycyclic molecules bearing contiguous stereogenic centers can be synthesized from readily available planar aromatic feedstocks. Here we report that an intermolecular asymmetric dearomatization reaction of α -naphthols bearing a tethered nucleophile at the C4 position of the naphthol ring is achieved by a chiral phosphoric acid. The reaction proceeds via a highly chemo- and regioselective aminative dearomatization/Michael addition sequence, affording a wide array of functionalized cyclic ketones in good yields (up to 93%) with excellent enantioselectivity (up to >99% ee). The catalyst loading can be reduced to 0.1 mol%. Preliminary mechanistic investigations identify that the enantioselectivity is established in the dearomatization step, while the Michael addition is the rate-limiting step. A working model accounting for the origin of the stereochemistry is proposed based on DFT calculations. Catalytic asymmetric dearomatization (CADA) reactions readily convert common aromatic compounds to diverse 3D chiral, polycyclic molecules. Here, the authors report an intermolecular asymmetric dearomatization of nucleophile-tethered α-naphthols affording functionalized cyclic ketones with high enantioselectivity.

C1q/TNF-related protein 6 (CTRP6) is emerging as a critical regulator of cancer biology with direct implications for clinical outcomes. Across a wide spectrum of malignancies, CTRP6 plays a central role in coordinating key oncogenic processes and linking metabolic, inflammatory, and signaling pathways that drive tumor progression. While CTRP6 generally promotes oncogenic behavior in cancers such as hepatocellular carcinoma, lung cancer, and clear cell renal cell carcinoma, conflicting findings have been reported in gastric cancer and oral or head and neck squamous cell carcinoma, where its tumor-promoting versus tumor-suppressive roles remain unresolved. CTRP6 has been shown to modulate fundamental processes including angiogenesis, ferroptosis, proliferation, apoptosis, migration, invasion, and inflammation. These effects are primarily mediated through activation of the PI3K/AKT and MEK/ERK signaling pathways, which are central to tumor growth, metastasis, and therapeutic resistance. Beyond its mechanistic roles, CTRP6 demonstrates potential as a diagnostic and prognostic biomarker, with altered expression patterns linked to cancer initiation, progression, and patient survival. Inhibition of CTRP6 in preclinical models enhances ferroptotic cell death and suppresses tumor progression, highlighting its promise as a therapeutic target. By consolidating current evidence from multiple cancer models, this review provides a comprehensive overview of CTRP6’s contributions to oncogenesis and underscores its dual potential as both a biomarker and a therapeutic target. Advancing a deeper understanding of CTRP6 in specific tumor contexts will be critical for unlocking its clinical utility and may open new opportunities to improve diagnosis, optimize therapeutic strategies, and ultimately enhance patient outcomes.