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Solar activity induces ionospheric irregularities that degrade Global Navigation Satellite System (GNSS) performance through amplitude and phase scintillation. Although numerous studies have investigated event‐driven or regional responses, the nonlinear coupling between solar radiation, ionospheric scintillation, and precise point positioning (PPP) degradation remains insufficiently quantified. This study presents a multi‐year observational analysis integrating GNSS measurements, ionospheric scintillation monitoring data, and solar activity indices from 2017 to 2024, covering high‐, mid‐, and low‐latitude regions. By jointly examining extreme ultraviolet (EUV) radiation, coronal mass ejection activity, scintillation indices (S4 and σφ${\\sigma }_{\\varphi }$ ), cycle‐slip occurrences, and PPP errors, a distinct nonlinear response of ionospheric scintillation to solar radiation is identified. Results reveal an approximately “inverted V‐shaped” dependence of scintillation intensity on EUV flux, with a critical threshold near 0.35 W/m2. In addition, enhanced solar radiation can suppress ionospheric scintillation, leading to transient improvements in positioning accuracy. On the day of peak solar flare activity, GNSS positioning accuracy exhibits a slight improvement as a result of reduced scintillation effects. Both scintillation occurrences and cycle slips aligned more closely with variations in EUV radiation flux. Results also indicate that low‐latitude regions exhibited a higher frequency of amplitude scintillation events (S4 > 0.2) than high‐latitude areas. The results refine the understanding of sun–ionosphere–positioning coupling and offer potential insights for assessing GNSS reliability and anti‐interference strategies during periods of elevated solar activity.

How to determine the earth’s external gravity field with the accuracy of O(T2) by making use of GPS data and gravity values measured on the earth’s surface is dealt with in this paper. There are two main steps: to extend these measured values on the earth’s surface onto the reference ellipsoid at first and then to seek for the integral solution of the external Neumann problem outside the ellipsoid. In addition, the corresponding judging criteria of accuracy to solve the GPS-gravity boundary value problem are established. The integral solution given in the paper not only contains all frequency-spectral information of the gravity field with the accuracy of O(T 2), but is also easily computed. In fact, the solution has great significance for both theory and practice.

The least-squares collocation harmonic analysis method, which is used to determine the earth geopotential coefficients from the radial satellite gravity gradient, is deeply studied. The principle of the least-squares collocation is firstly dissertated, and the covariance and self-covariance matrix between the disturbing gravity gradients and spherical harmonics are derived. When the disturbing gravity gradients are in the regularized equi-longitude grid, the covariance matrix between geopotential and disturbing gravity gradients has the configuration of blocked Toeplitz circulation matrix, and its degree can be lowered by using the fast Fourier transform technology effectively. Truncated singular value decomposition (TSVD) which is used to solve the ill-posed problem of covariance matrix is studied. The complete formula of least-squares collocation harmonic analysis of the radial gravity gradient is finally obtained. The simulation experiment results show that the least-squares collocation harmonic analysis based on TSVD can recover the global gravity field in a rather high precision and validity and practicability of algorithms in this paper are also testified.

Background Adipose-derived stem cells (ADSCs) have provided promising applications for Crohn’s disease (CD). However, the practical efficacy of ADSCs remains controversial, and their mechanism is still unclear. Based on the pathogenesis of dysregulated immune responses and abnormal lymphatic alterations in CD, vascular endothelial growth factor-C (VEGF-C) is thought to be a favourable growth factor to optimize ADSCs. We aimed to investigate the efficacy of VEGF-C-stimulated ADSCs and their dual mechanisms in both inhibiting inflammation “IN” and promoting inflammation “OUT” in the intestine. Methods Human stem cells isolated from adipose tissues were identified, pretreated with or without 100 ng/ml VEGF-C and analysed for the secretion of cell culture supernatants in vitro. Lymphatic endothelial cells (LECs) were treated with ADSCs-conditioned medium or co-cultured with ADSCs and VEGF-C stimulated ADSCs. Changes in LECs transmigration, and VEGF-C/VEGFR-3 mRNA levels were assessed by transwell chamber assay and qRT–PCR. ADSCs and VEGF-C-stimulated ADSCs were intraperitoneally injected into mice with TNBS-induced chronic colitis. ADSCs homing and lymphatic vessel density (LVD) were evaluated by immunofluorescence staining. Lymphatic drainage was assessed using Evans blue. Cytokines and growth factors expression was detected respectively by ELISA and qRT–PCR. The protein levels of VEGF-C/VEGFR-3-mediated downstream signals and the NF- κ B pathway were assayed by western blot. Faecal microbiota was measured by 16S rRNA sequencing. Results ADSCs stimulated with VEGF-C released higher levels of growth factors (VEGF-C, TGF-β1, and FGF-2) and lower expression of cytokines (IFN-γ and IL-6) in cell supernatants than ADSCs in vitro (all P  < 0.05). Secretome released by VEGF-C stimulated ADSCs exhibited a stronger LEC migratory capability and led to elevated VEGF-C/VEGFR-3 expression, but these effects were markedly attenuated by VEGFR-3 inhibitor. VEGF-C-stimulated ADSCs homing to the inflamed colon and mesenteric lymph nodes (MLNs) can exert stronger efficacy in improving colitis symptoms, reducing inflammatory cell infiltration, and significantly enhancing lymphatic drainage. The mRNA levels and protein concentrations of anti-inflammatory cytokines and growth factors were markedly increased with decreased proinflammatory cytokines in the mice treated with VEGF-C-stimulated ADSCs. Systemic administration of VEGF-C-stimulated ADSCs upregulated the colonic VEGF-C/VEGFR-3 pathway and activated downstream AKT and ERK phosphorylation signalling, accompanied by decreased NF- κ B p65 expression. A higher abundance of faecal p-Bacteroidetes and lower p-Firmicutes were detected in mice treated with VEGF-C-stimulated ADSCs (all P  < 0.05). Conclusion VEGF-C-stimulated ADSCs improve chronic intestinal inflammation by promoting lymphatic drainage and enhancing paracrine signalling via activation of VEGF-C/VEGFR-3-mediated signalling and inhibition of the NF- κ B pathway. Our study may provide a new insight into optimizing ADSCs treatment and investigating potential mechanisms in CD.

Creeping fat (CrF) has been recognized to play a positive role in Crohn's disease (CD) progression, yet the cellular compositions within mesenteric adipose tissue (MAT) and their potential mechanism in CrF formation are poorly understood. Analysis of 10X single-cell RNA sequencing was performed on 67 064 cells from 3 pairs of surgically resected samples of CrF and their uninvolved MAT. The results were validated in another cohort with 6 paired MAT samples by immunofluorescence. All samples manifested excellent consistency and repeatability in our study, and 10 cell types from the transcriptome atlas, including 20 clusters, were identified. In CrF, a specific vascular endothelial cell subpopulation highly expressing lipoprotein lipase was first identified, with a significantly increased proportion. This vascular endothelial cell subpopulation manifested robust peroxisome proliferator-activated receptor γ (PPARγ) transcription activity and an upregulated PPAR signaling pathway and was involved in lipid metabolism and the antibacterial response. A novel fibroblast subpopulation (FC3) with remarkable GREM1 and RFLNB expression was identified and validated to predominantly accumulate in the CrF. The FC3 was annotated as inflammation-associated fibroblasts, which are characterized by inflammatory responses and the regulation of Smad phosphorylation related to intestinal fibrosis. The trajectory of fibroblasts revealed their pro-inflammatory and profibrotic conversion tendency during CrF formation with corresponding gene dynamics. Additionally, we unprecedently dissected the different origins and functions of 6 macrophage subclusters within the myeloid compartment. Our results uncover the cellular heterogeneity in the MAT of CD and the role of these various cellular compositions in CrF development. This comprehensive understanding of CrF provides future directions for in-depth research on and potential targets for MAT-based treatment.

The development of efficient and broadly applicable n‐doping strategies for organic semiconductors (OSCs) is crucial for advancing the performance of various organic electronic devices. Here, a novel nucleophilic‐attack n‐doping mechanism is unveiled that achieves exceptionally high conductivity in doped OSC films and demonstrates broad applicability across OSCs. The remarkable efficacy of n‐Butyl lithium (n‐BuLi) is highlighted in n‐doping C60 and PC61BM, achieving a conductivity of 1.27 S cm−1 and 2.57 S cm−1, respectively, which are among the highest reported values for these materials. The investigation reveals that the n‐BuLi anion interacts with electron‐deficient units in OSCs, generating a carbanion that facilitates efficient electron transfer for n‐doping. This mechanism is further validated across diverse fullerenes, polymeric, and small molecule OSCs, and is extendable to other high‐performance dopants such as tert‐Butyllithium (tert‐BuLi) and sodium ethoxide (NaOEt). Device studies show that n‐BuLi‐doped C60 enables substantially improved diode rectification, attributed to greater junction built‐in potential. These findings establish a unified chemical‐bonding‐based n‐doping paradigm, complementing existing electrophilic‐attack p‐doping concepts, and pave the way for achieving efficient doping of OSCs for advanced organic electronic applications. A novel n‐doping mechanism for organic semiconductors (OSCs) is revealed, based on a nucleophilic‐attack reaction. Using n‐Butyl lithium (n‐BuLi) as a model dopant, this strategy achieves exceptionally high conductivity in C60 and PC61BM. The mechanism is broadly applicable to various OSCs and other nucleophilic dopants, establishing a new chemical‐bonding paradigm for efficient n‐doping OSCs.

Adipose-derived stem cells (ADSCs) have provided promising applications for Crohn's disease (CD). However, the practical efficacy of ADSCs remains controversial, and their mechanism is still unclear. Based on the pathogenesis of dysregulated immune responses and abnormal lymphatic alterations in CD, vascular endothelial growth factor-C (VEGF-C) is thought to be a favourable growth factor to optimize ADSCs. We aimed to investigate the efficacy of VEGF-C-stimulated ADSCs and their dual mechanisms in both inhibiting inflammation \"IN\" and promoting inflammation \"OUT\" in the intestine. Human stem cells isolated from adipose tissues were identified, pretreated with or without 100 ng/ml VEGF-C and analysed for the secretion of cell culture supernatants in vitro. Lymphatic endothelial cells (LECs) were treated with ADSCs-conditioned medium or co-cultured with ADSCs and VEGF-C stimulated ADSCs. Changes in LECs transmigration, and VEGF-C/VEGFR-3 mRNA levels were assessed by transwell chamber assay and qRT-PCR. ADSCs and VEGF-C-stimulated ADSCs were intraperitoneally injected into mice with TNBS-induced chronic colitis. ADSCs homing and lymphatic vessel density (LVD) were evaluated by immunofluorescence staining. Lymphatic drainage was assessed using Evans blue. Cytokines and growth factors expression was detected respectively by ELISA and qRT-PCR. The protein levels of VEGF-C/VEGFR-3-mediated downstream signals and the NF-κB pathway were assayed by western blot. Faecal microbiota was measured by 16S rRNA sequencing. ADSCs stimulated with VEGF-C released higher levels of growth factors (VEGF-C, TGF-[beta]1, and FGF-2) and lower expression of cytokines (IFN-[gamma] and IL-6) in cell supernatants than ADSCs in vitro (all P < 0.05). Secretome released by VEGF-C stimulated ADSCs exhibited a stronger LEC migratory capability and led to elevated VEGF-C/VEGFR-3 expression, but these effects were markedly attenuated by VEGFR-3 inhibitor. VEGF-C-stimulated ADSCs homing to the inflamed colon and mesenteric lymph nodes (MLNs) can exert stronger efficacy in improving colitis symptoms, reducing inflammatory cell infiltration, and significantly enhancing lymphatic drainage. The mRNA levels and protein concentrations of anti-inflammatory cytokines and growth factors were markedly increased with decreased proinflammatory cytokines in the mice treated with VEGF-C-stimulated ADSCs. Systemic administration of VEGF-C-stimulated ADSCs upregulated the colonic VEGF-C/VEGFR-3 pathway and activated downstream AKT and ERK phosphorylation signalling, accompanied by decreased NF-κB p65 expression. A higher abundance of faecal p-Bacteroidetes and lower p-Firmicutes were detected in mice treated with VEGF-C-stimulated ADSCs (all P < 0.05). VEGF-C-stimulated ADSCs improve chronic intestinal inflammation by promoting lymphatic drainage and enhancing paracrine signalling via activation of VEGF-C/VEGFR-3-mediated signalling and inhibition of the NF-κB pathway. Our study may provide a new insight into optimizing ADSCs treatment and investigating potential mechanisms in CD.