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The identification of pollutant source release history in rivers is important for emergency response of pollution accidents and formulating remediation strategies. Space-time radial basis collocation method (RBCM), as a meshless method with strong applicability, can directly estimate the release history from the concentration data measured at downstream observation sites. However, the uncertainty of specific parameters in space-time RBCM is the main factor affecting the accuracy of estimation. Therefore, a way to solve the parameters efficiently and accurately is essential. For this purpose, a new model which combines space-time RBCM and differential evolution algorithm (DEA) is established to identify the source release history. First of all, efficient parameter optimizer DEA is introduced to search the parameters that affect the estimation accuracy of space-time RBCM. Then, a new loss function considering the imbalance configuration of RBCM nodes is designed to ensure the rationality of the parameters obtained by DEA. The results of numerical cases and real field case show that the proposed method can accurately estimate the real release history with low time consumption. It is also demonstrated that DEA is more efficient than k-fold cross-validation in searching the optimal parameters for space-time RBCM, and the parameters obtained from the new loss function can make the estimated release history more precise.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of neurological disability and mortality in newborns, with limited therapeutic options beyond hypothermia. Bromodomain and extra-terminal domain (BET) proteins function as epigenetic readers that regulate gene expression by recognizing acetylated lysine residues on histones. Among BET inhibitors, (+)-JQ1 (JQ1) has recently garnered attention due to its potent anti-inflammatory and antioxidant properties. This study aims to investigate the neuroprotective effects of JQ1 and elucidate the underlying mechanisms in the context of HIE brain injury. We established an in vivo model via the modified Rice-Vannucci method, alongside an in vitro model using oxygen-glucose deprivation (OGD) in HT22 cells. Transcriptomic changes in cortical tissues during the acute phase after HIE were profiled through RNA sequencing. Western blot, immunofluorescence, immunohistochemistry, and transmission electron microscopy were employed to measure the levels of neuroinflammation and ferroptosis. Furthermore, SIRT3-knockdown HT22 cells under OGD conditions were used to validate the JQ1-mediated protective mechanisms. JQ1 treatment significantly reduced cerebral infarction, edema, and neuronal loss, while improving emotional behavior and cognitive functions after HIE. It inhibited the cGAS-STING pathway, and alleviated ferroptosis by restoring GPX4 and system Xc⁻ activity while reducing iron overload. These effects were reversed by the SIRT3 inhibitor 3-TYP or SIRT3 siRNA. JQ1 exerts neuroprotective effects in neonatal hypoxic-ischemic encephalopathy by attenuating neuroinflammation and suppressing ferroptosis. We demonstrate that SIRT3 upregulation in the brain underlies the neuroprotective role of JQ1.

Background Neuroinflammation and oxidative stress, mediated by microglial activation, hinder the development of oligodendrocytes (OLs) and delay myelination in preterm infants, leading to white matter injury (WMI) and long‐term neurodevelopmental sequelae. Peroxisome proliferator‐activated receptor gamma (PPAR‐γ) has been reported to inhibit inflammation and oxidative stress via modulating microglial polarization in various central nervous system diseases. However, the relationship between PPAR‐γ and microglial polarization in neonatal WMI is not well understood. Therefore, this study aimed to elucidate the role and mechanisms of PPAR‐γ in preterm infants affected by WMI. Methods In this study, an in vivo hypoxia‐ischemia (HI) induced brain WMI neonatal mouse model was established. The mice were administered intraperitoneally with either RSGI or GW9662 to activate or inhibit PPAR‐γ, respectively. Additionally, an in vitro oxygen–glucose deprivation (OGD) cell model was established and pretreated with pcDNA 3.1‐PPAR‐γ or si‐PPAR‐γ to overexpress or silence PPAR‐γ, respectively. The neuroprotective effects of PPAR‐γ were investigated in vivo. Firstly, open field test, novel object recognization test, and beam‐walking test were employed to assess the effects of PPAR‐γ on neurobehavioral recovery. Furthermore, assessment of OLs loss and OL‐maturation disorder, the number of myelinated axons, myelin thickness, synaptic deficit, activation of microglia and astrocyte, and blood–brain barrier (BBB) were used to evaluate the effects of PPAR‐γ on pathological repair. The mechanisms of PPAR‐γ were explored both in vivo and in vitro. Assessment of microglia polarization, inflammatory mediators, reactive oxygen species (ROS), MDA, and antioxidant enzymes was used to evaluate the anti‐inflammatory and antioxidative effects of PPAR‐γ activation. An assessment of HMGB1/NF‐κB and NRF2/KEAP1 signaling pathway was conducted to clarify the mechanisms by which PPAR‐γ influences HI‐induced WMI in neonatal mice. Results Activation of PPAR‐γ using RSGI significantly mitigated BBB disruption, promoted M2 polarization of microglia, inhibited activation of microglia and astrocytes, promoted OLs development, and enhanced myelination in HI‐induced WMI. Conversely, inhibition of PPAR‐γ using GW9662 further exacerbated the pathologic hallmark of WMI. Neurobehavioral tests revealed that neurological deficits were ameliorated by RSGI, while further aggravated by GW91662. In addition, activation of PPAR‐γ significantly alleviated neuroinflammation and oxidative stress by suppressing HMGB1/NF‐κB signaling pathway and activating NRF2 signaling pathway both in vivo and in vitro. Conversely, inhibition of PPAR‐γ further exacerbated HI or OGD‐induced neuroinflammation, oxidative stress via modulation of the same signaling pathway. Conclusions Our findings suggest that PPAR‐γ regulates microglial activation/polarization as well as subsequent neuroinflammation/oxidative stress via the HMGB1/NF‐κB and NRF2/KEAP1 signaling pathway, thereby contributing to neuroprotection and amelioration of HI‐induced WMI in neonatal mice. Our findings suggest that PPAR‐γ regulates microglial activation/polarization as well as subsequent neuroinflammation/oxidative stress via the HMGB1/NF‐κB and NRF2 signaling pathway, thereby contributing to myelination and amelioration of WMI after HI insult in neonatal mice.

White matter injury (WMI), the most common type of brain damage in infants born preterm, is characterized by failure in oligodendrocyte progenitor cell maturation and myelination, thereby contributing to long-term neurological impairments. Regrettably, effective therapies for promoting remyelination and improving function are currently lacking for this growing population affected by WMI. Recombinant human fibroblast growth factor (rhFGF) 21 modulated microglial activation and then ameliorated brain damage and improved neurological deficits in several central nervous system diseases. However, the effects of rhFGF21 treatment on WMI in preterm infants remain uncertain. In this study, we established an in vivo mouse model of cerebral hypoxia–ischemia (HI)-induced brain WMI and an in vitro model using oxygen–glucose deprivation (OGD)-treated HMC3 cells to investigate the neuroprotective effects of rhFGF21 against WMI and elucidated the potential mechanism. Our findings demonstrated that administration of rhFGF21 significantly ameliorated the retardation of oligodendrocyte differentiation, promoted myelination, and mitigated axonal deficits, synaptic loss, and GFAP scarring, thereby improving lifelong cognitive and neurobehavioral dysfunction associated with WMI. Moreover, rhFGF21 modulated microglial polarization, promoted a shift from the M1 to the M2 microglial phenotype, and suppressed microglial activation, thus ameliorating inflammatory response and oxidative stress. Additionally, rhFGF21 treatment significantly inhibited the HMGB1/NF-κB pathway linked to inflammation, and activated the NRF2 pathway associated with oxidative stress through the upregulation of PPAR-γ. Importantly, the beneficial effects of rhFGF21 on HI-induced WMI and microglial activation were dramatically inhibited by PPAR-γ antagonist and its siRNA. Our findings provide compelling evidence that rhFGF21 treatment mitigated the inflammatory response and oxidative stress through the modulation of microglial polarization via the PPAR-γ-mediated HMGB1/NF-κB pathway and the NRF2 pathway, respectively, contributes to neuroprotection and the amelioration of WMI in neonatal mice. Thus, rhFGF21 represents a promising therapeutic agent for the treatment of neonatal WMI.

Low-temperature annealing experiments were conducted on high-nitrogen austenitic stainless steel at different temperatures. Microstructural observations and tensile tests were performed to investigate the effects of annealing temperature on the microstructure and mechanical properties of P550 high-nitrogen austenitic stainless steel. Results indicate that, with the holding time unchanged, increasing the annealing temperature did not cause significant changes in the matrix microstructure of high-nitrogen austenitic stainless steel, thereby maintaining the material’s excellent mechanical properties.

Quantum entanglement has emerged as a great resource for studying the interactions between molecules and radiation. We propose a new scheme of stimulated Raman scattering with entangled photons. A quantum ultrafast Raman spectroscopy is developed for condensed-phase molecules, to monitor the exciton populations and coherences. Analytic results are obtained, showing an entanglement-enabled time-frequency scale not attainable by classical light. The Raman signal presents an unprecedented selectivity of molecular correlation functions, as a result of the Hong-Ou-Mandel interference. Our work suggests a new paradigm of using an unconventional interferometer as part of spectroscopy, with the potential to unveil advanced information about complex materials.Proposed set up for entangled photons enabled ultrafast stimulated Raman spectroscopy for molecular dynamics.

In the digital age, patients with type 2 diabetes mellitus (T2DM) are exposed to extensive health information, leading to information overload (IO). This overload results in decision-making difficulties, increased cognitive burden, and reduced health literacy (HL). This study investigates the complex relationship among IO, cognitive fusion (CF), and HL, emphasizing the moderating role of CF. A cross-sectional survey was conducted involving 233 patients with T2DM. Participants completed a general information questionnaire, the Information Overload Scale (IOS), the Cognitive Fusion Questionnaire (CFQ), and the Diabetes Health Literacy Scale (DHLS). A moderated network analysis was used to explore the bidirectional associations between IO and HL and to verify the moderating effect of CF. Network analysis revealed several significant bidirectional relationships between IO and HL, with CF showing a significant moderating effect. Reduced CF strengthened the positive effects of “perceived diabetes information overload” and “multi-channel diabetes information stress” on “functional health literacy”, as well as the effect of “increased diabetes information device maintenance” on “interactive health literacy”. “perceived diabetes information overload” had the highest centrality index in the network model, which demonstrated overall good stability. This study advances understanding of the relationships among IO, CF, and HL in patients with T2DM. The findings suggest that interventions aimed at alleviating cognitive rigidity should adopt comprehensive strategies targeting the IO symptom network to enhance HL in this population.

Rocket launches constitute a major anthropogenic source of disturbance in the near-Earth space environment, inducing significant ionospheric perturbations through both chemical and dynamic mechanisms. This study presents a systematic analysis of ionospheric disturbances—specifically, electron density depletion and traveling ionospheric disturbances (TIDs)—triggered by four rocket launches from China’s Jiuquan Satellite Launch Center between 2023 and 2025. Using high-rate, multi-constellation GNSS data from 370 ground stations and BeiDou GEO satellites, we extracted total electron content (TEC) signals and applied advanced detection methods, including the Multi-Rolling-Multi-Image-Tracking (MRMIT) algorithm for depletion identification and a parametric integration framework for quantitative comparison. Our results reveal that all launches produced rapid TEC depletions, evolving along the rocket trajectory and peaking within approximately 30 min. Launch mass was the dominant factor controlling depletion intensity, while propellant chemistry (UDMH-based vs. liquid oxygen/methane) and local time/background TEC levels modulated the recovery rate and spatial extent. Additionally, distinct TIDs exhibiting wave-like and V-shaped structures were observed, propagating outward from the trajectory with latitudinal variations in amplitude and waveform. These findings highlight the critical roles of rocket attributes and ambient ionospheric conditions in shaping disturbance characteristics. The study underscores the value of multi-source GNSS networks and novel methodologies in monitoring anthropogenic space weather effects, with implications for GNSS performance and sustainable space operations.

Developing mild photocatalytic bromination strategies using sustainable bromo source has been attracting intense interests, but there is still much room for improvement. Full utilization of redox centers of photocatalysts for efficient generation of Br + species is the key. Herein we report heterogenous organophotocatalytic HBr oxidation coupled with oxygen reduction to furnish Br 2 and H 2 O 2 for effective bromination of arenes over Al 2 O 3 supported perylene-3,4,9,10-tetracarboxylic dianhydride (PTCDA). Mechanism studies suggest that O-vacancy in Al 2 O 3 can provide Lewis-acid-type anchoring sites for O 2 , enabling unexpected dual-electron transfer from anchored photoexcited PTCDA to chemically bound O 2 to produce H 2 O 2 . The in-situ generated H 2 O 2 and Br 2 over redox centers work together to generate HBrO for bromination of arenes. This work provides new insights that heterogenization of organophotocatalysts can not only help to improve their stability and recyclability, but also endow them with the ability to trigger unusual reaction mode via cooperative catalysis with supports. Developing mild photocatalytic bromination strategies using sustainable bromo source has been attracting intense interests, but there is still much room for improvement. Here, the authors report heterogenous organophotocatalytic HBr oxidation coupled with oxygen reduction to furnish Br 2 and H 2 O 2 for effective bromination of arenes.

Previous efforts to retrieve thermospheric density using satellite payloads have been limited to a small number of satellites equipped with GNSS (Global Navigation Satellite System) receivers and accelerometers. These satellites are confined to a few orbital planes, and analysis can only be conducted after the data are processed and updated, resulting in sparse and delayed thermospheric density datasets. In recent years, the Starlink constellation, developed and deployed by SpaceX, has emerged as the world’s largest low Earth orbit (LEO) satellite constellation, with over 6000 satellites in operations as of October 2024. Through the strategic use of multiple orbital shells featuring various inclinations and altitudes, Starlink ensures continuous near-global coverage. Due to extensive coverage and frequent maneuvers, SpaceX has publicly released predicted ephemeris data for all Starlink satellites since May 2021, with updates approximately every 8 h. With the ephemeris data of Starlink satellites, we first apply a maneuver detection algorithm based on mean orbital elements to analyze their maneuvering behavior. The results indicate that Starlink satellites exhibit more frequent maneuvers during thermospheric disturbances. Then, we calculate the mechanical energy loss caused by non-conservative forces (primarily atmospheric drag) through precise dynamical models. The results demonstrate that, despite certain limitations in Starlink ephemeris data, the calculated mechanical energy loss still effectively captures thermospheric density variations during both quiet and disturbed geomagnetic periods. This finding is supported by comparisons with Swarm-B data, revealing that SpaceX incorporates the latest space environment conditions into its orbit extrapolation models during each ephemeris update. With a maximum lag of only 8 h, this approach enables near-real-time monitoring of thermospheric density variations using Starlink ephemeris.