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关键词： Land surface phenology   MODIS-like NDVI   spatiotemporal data fusion   global vegetation dynamics   remote sensing  

摘要： As climate change continues to reshape global ecosystems, accurately monitoring and understanding shifts in land surface phenology (LSP) has become increasingly critical for detecting vegetation responses, assessing ecosystem resilience, and improving predictions of climate-biosphere interactions. While several moderate-to-fine spatial resolution global LSP datasets exist, most are constrained to post-2000 records due to the availability of MODIS era observations, leaving a significant gap in long-term phenological information and limiting our ability to investigate multi decadal trends. To address this, we developed the first global 1 km resolution LSP dataset spanning 1982-2018. By integrating MODIS and AVHRR NDVI data through the enhanced Flexible Spatiotemporal Data Fusion (cuFSDAF) model, we reconstructed pre-2000 MODIS-like NDVI time series with improved temporal consistency and reduced cross sensor bias. Using logistic functions and third-order derivatives, we extracted four key phenological metrics, including the start of the growing season (SOS), maturity, senescence, and the end of the growing season (EOS), enabling detailed characterization of vegetation development stages across diverse biomes. In the Northern Hemisphere (NH), SOS, maturity, and EOS advanced significantly from 1982 to 2018, while senescence was delayed, indicating a widespread lengthening of the growing season. In contrast, the Southern Hemisphere (SH) experienced delayed SOS, maturity, and senescence, with EOS occurring earlier, suggesting a shortening of the growing season and revealing contrasting hemispheric sensitivities to climate forcing. These metrics were validated against ground-based observations from multiple networks, demonstrating strong consistency, high accuracy, and reliable reconstruction of long term phenological signals. As the first dataset of its kind at 1 km resolution over such an extended period, it provides an invaluable resource for studying global vegetation d

关键词： Piezo1   TME   mechanical signals   tumour progression   immunotherapy  

摘要： Background/objectivesAs a pivotal mechanosensitive ion channel, Piezo-type mechanosensitive ion channel component 1 (Piezo1) converts mechanical stimuli into biochemical signals that regulate key oncogenic processes, including tumour cell proliferation, migration and invasion. Emerging evidence demonstrates that Piezo1 is widely expressed across various cellular compartments of the tumour microenvironment (TME), and its elevated expression strongly correlates with adverse clinical outcomes. A comprehensive understanding of the complex interactions between Piezo1 activation and cytokine networks in different TME cell populations is therefore essential for developing innovative and effective anti-tumour therapeutic strategies. In this review, we aimed to highlight the molecular mechanisms of Piezo1, systematically elucidating how the mechanical stimulation-Piezo1 signalling pathway within the TME contributes to tumour immune escape and malignant progression. Furthermore, we summarized current research advances in Piezo1-targeting drugs and clinical trials, and discuss strategies to improve tissue specificity while minimizing off-target *** comprehensive literature review was conducted, focusing on the specific mechanisms through which Piezo1 regulates endothelial cells, immune cells, cancer-associated fibroblasts and the extracellular matrix within the TME. Activation of Piezo1 in endothelial and immune cells promotes tumour angiogenesis and immune ***1 plays a critical role in tumour progression and represents a promising therapeutic target for cancer treatment

关键词： Macrophages   Insulin-like growth factor-1   acute lung injury   efferocytosis   acute respiratory distress syndrome  

摘要： BackgroundNo effective treatment strategy for acute respiratory distress syndrome (ARDS) has been established. Conflicting reports on the effects of insulin-like growth factor (IGF)-1 stimulation and the inhibition of IGF-1 receptor (IGF-1R) signalling in tissue injury across several organs have led to hesitation in advancing IGF-1-based treatment strategies for tissue *** aim to examine whether IGF-1/IGF-1R signalling contributes to recovery from acute lung injury in mouse models and to further explore its potential *** (LPS) was intratracheally injected into mice to create acute lung injury models. Experiments were conducted to acquire or inhibit IGF-1 signalling through the intratracheal injection of recombinant IGF-1 or JB1, an IGF-1 receptor antagonist during the recovery phase of the models, starting on day 4 after LPS administration. Bone marrow monocyte-derived macrophages (MDMs) cocultured with IGF-1 and/or JB1 were intratracheally injected during the recovery *** cell counts and lung injury scores were significantly decreased when recombinant IGF-1 was administered in the later phase, while they increased with the administration of JB1. On day 4 after LPS injection, IGF-1 receptor (IGF-1R, also known as CD221) was strongly expressed on macrophages, particularly in CD11c+SiglecF+ alveolar macrophages (AMs). Intratracheal injection of MDMs cocultured with IGF-1 decreased lung neutrophil counts, whereas the addition of JB1 to MDMs cocultured with IGF-1 counteracted the effect of IGF-1. JB1 also reduced efferocytosis capacity of AMs in the later phase. In the phagocytosis assay, LPS decreased the efflux capacity of macrophages, but recombinant IGF-1 improved this capacity regardless of the presence or absence of ***-1/IGF-1R signalling in macrophage facilitates the recovery from acute lung injury via enhancing efferocytosis. IGF-1 delivery potentially offers a new treatment str

关键词： HIF-1 alpha   VEGF   lung   liver   roiler ascites syndrome  

摘要： Broiler ascites syndrome (BAS), a hypoxia-driven metabolic disorder, causes significant economic losses in poultry production. This study aimed to evaluate the pathological changes in the lungs and liver of broiler chickens and the expression of HIF-1 alpha and VEGF. HE, Masson and Van Gieson staining were used to observe histopathological changes in the lungs and liver, and molecular biology methods such as qPCR, Western blotting and immunohistochemistry were used to detect the expression of HIF-1 alpha and VEGF in the lungs and liver. The histopathological results revealed significant thickening and remodelling of the pulmonary artery wall in BAS broiler chickens;the boundaries of the vascular intima, media and adventitia were unclear;and there was a significant increase in the collagen fibre content around the arteries. Additionally, the hepatic cords were loosely arranged liver cords. The molecular biology results revealed that both the mRNA and protein expression levels of HIF-1 alpha and VEGF were significantly increased (p < 0.05) in the lungs and liver of AS broiler chickens. These findings establish an association between HIF-1 alpha/VEGF dysregulation and BAS pathogenesis, providing a foundation for mechanistic investigation.

关键词： Salvianolic acid B   benzoylpaeoniflorin   ischemic stroke   angiogenesis   Nrf2/HO-1/VEGFA signaling axis  

摘要： ContextAngiogenesis is one of the essential protective mechanisms that promote neural repair and regeneration after ischemic stroke (IS). Salvianolic Acid B (SAB) and Benzoyl paeoniflorin (BP) are compounds extracted from the Chinese medicines Salvia miltiorrhiza Bunge and Paeonia suffruticosa Andrews, *** investigated whether SAB combined with BP alleviated IS by promoting micrangium angiogenesis and determined the potential molecular *** and methodsThe impact of SAB-BP on angiogenesis after IS was investigated in middle cerebral artery occlusion (MCAO) rat model, ponatinib-induced ischemic stroke in zebrafish, and human umbilical vein endothelial cells (HUVECs). The neuroprotective effect of SAB-BP in rats was assessed using behavior tests and histopathological staining. The cerebral thrombosis assessment and angiogenesis assay were performed in the zebrafish model. Cell proliferation and angiogenesis in oxygen-glucose deprivation and reperfusion (OGD/R) HUVECs were assessed through cell viability, tube formation, migration, and invasion assays. Western blot analysis and immunofluorescence staining were used to determine the protein expression levels of Nrf2, HO-1, and *** findings indicated that SAB-BP significantly reduced neurological impairment following IS and promoted the formation of functional vessels in the cerebral ischemic penumbra. Furthermore, SAB-BP up-regulated the protein expression of Nrf2, HO-1, HIF-1 alpha, and VEGFA. Intriguingly, the pro-angiogenic effect of SAB-BP markedly restrained by adding the inhibitor of Nrf2 (ML385).Discussion and conclusionOur study demonstrates that SAB-BP enhances angiogenesis following IS by modulating the Nrf2/HO-1/VEGFA signaling axis both in vivo and in vitro. SAB-BP could serve as a promising therapeutic agent for IS recovery.

关键词： Xijiaqi Formula   chronic heart failure   myocardial fibrosis   extracellular matrix remodeling   TGF-beta 1  

摘要： ContextChronic heart failure (CHF) is the common concern following myocardial infarction. Xijiaqi Formula (XJQ) effectively treats CHF clinically while the underlying mechanism remains *** study was designed to investigate the effect and mechanism of XJQ on CHF in rats following *** and methodsUHPLC-Q-TOF-MS/MS was utilized to analyze the constituents of XJQ. Post-MI CHF was induced in rats by permanent ligation of the left anterior descending coronary artery. Cardiac function was assessed by echocardiogram and hemodynamic. Myocardial morphology, fibrosis, and ultrastructure were evaluated through HE staining, Masson staining, and transmission electron microscopy, respectively. Myocardial transcriptomics were employed to identify genes that may be altered in response to XJQ treatment. Consistently, XJQ inhibited TGF-beta 1-induced myofibroblast activation in *** significantly improved cardiac function and structure, mitigating fibrosis, edema, and mitochondrial damage, while reducing key biomarkers (BNP, NT-proBNP, cTnT, Ang II). Transcriptomic analysis indicated that the differentially expressed genes influenced by XJQ were predominantly associated with extracellular matrix (ECM) remodeling. Notably, XJQ inhibited the upregulation of ECM proteins, including Adamts2, Fbln1, Itgbl1, and Ltbp3 mRNAs, as well as the proteins TGF-beta 1, P-Smad2/3, and MMP2. Additionally, in vitro experiments revealed that XJQ significantly suppressed the activation of myofibroblasts induced by TGF-beta *** significantly attenuated the progression from MI to CHF by inhibiting fibroblast activation mediated by TGF-beta 1/Smads signaling. The molecular mechanisms underlying this effect appear to be intricately linked to its regulation of ECM remodeling proteins, specifically Adamts2, Itgbl1, Fbln1, and Ltbp3.