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Background & aims Sarcopenia is associated with poor clinical outcomes of patients who underwent esophagectomy. The current diagnostic criteria for sarcopenia are complex and laborious. We aimed to employ the simple and economic indicator sarcopenia index (SI = creatinine/cystatin C ×100) to screen for sarcopenia and to evaluate its prognostic value in patients with esophageal cancer (EC). Methods Older participants in the National health and nutrition examination survey (NHANES) database (1999–2002) were divided into three groups according to tertiles of the SI value to explore the feasibility of SI in the diagnosis of sarcopenia. Restricted cubic spline (RCS) was utilized to show the non-linear relationship between all-cause mortality and SI. Patients with EC admitted to Jinling Hospital were enrolled to validate the efficacy and prognostic value of SI. Cut-off values of SI were determined using receiver operating characteristic curves. Multivariable logistic analyses and Cox analyses were used to identify the independent factors of postoperative complications and long-term survival, respectively. Results A total of 989 participants were identified from the NHANES database. SI showed the diagnostic value of sarcopenia (tertile 1 vs. tertile 3: odds ratio [OR]=3.67, 95% confidence interval [CI]: 1.52–8.87, p =0.004; tertile 2 vs. tertile 3: OR=1.79, 95% CI: 0.75–4.28, p =0.191) adjusted for race, gender, and body mass index (BMI). Individuals with SI ≤ 68 had a poorer overall survival (OS) (hazard ratio [HR]=2.14, 95% CI: 1.71–2.68, p <0.001), and the RCS plot showed that the all-cause mortality risk gradually decreased with the increase in SI. Then, 203 patients with EC were enrolled, of which 76 patients were diagnosed with sarcopenia. There was a linear correlation between SI and skeletal muscle index and prealbumin, indicating that SI was reliable for diagnosing sarcopenia. Patients in the high sarcopenia risk group (Male: SI < 62; Female: SI < 55) showed a higher incidence of complications (OR=3.50, 95% CI: 1.85–6.61, p <0.001) and poorer long-term survival (HR=2.62, 95% CI: 1.02–6.77, p =0.046). Conclusion SI could be used to identify sarcopenia in patients with EC, and it is a useful prognostic factor of postoperative complications and long-term survival.

Neuroinflammation is a key immunological driver of spinal sensitization and the transition from acute to chronic pain. Although mechanical interventions can reduce pain, the immuno-inflammatory mechanisms linking mechanical cues to resolution of spinal neuroinflammation remain poorly integrated and inconsistently defined. A major gap is the lack of a mechanobiological framework that connects mechanotransduction with glial activation, cytokine/chemokine signaling, and neuroimmune synaptic plasticity, and translates these mechanisms into measurable biomarkers and reproducible protocols. Here, we synthesize preclinical and clinical evidence showing how mechanical stimuli may modulate neuroinflammation-driven sensitization. We summarize mechanotransduction pathways that shape microglial and astrocytic reactivity, inflammatory signaling, and downstream remodeling of ion channels, receptors, and synaptic circuits. We also discuss how mechanical interventions may shift the spinal inflammatory microenvironment by improving perfusion and metabolic homeostasis. Finally, we outline candidate biomarker panels and highlight key limitations, including heterogeneity in dosing, outcomes, and translational models. Overall, mechanical forces may act as immunomodulatory cues that reprogram neuroinflammation and weaken spinal sensitization, supporting a mechanistic basis for non-pharmacological analgesia. Future progress requires standardized mechanical dosing, mechanism-informed biomarkers, and rigorous translational pipelines to enable quantifiable, personalized mechanotherapy for chronic pain.

Chronic pain frequently coexists with adverse emotions, including anxiety and depression, significantly affecting patients’ physical and psychological health as well as their quality of life. Changes in hippocampal synaptic architecture, neuronal injury, and diminished neurogenesis significantly contribute to pain-related emotions. Microglia in the hippocampus are implicated in these pathologies. Stimulation or injury leads to microglial activation, which causes pain; prolonged pain causes microglia to continuously release pro-inflammatory factors that induce astrocyte activation, which mediates the apoptosis of hippocampal neurons and abnormal neurogenesis. Concurrently, microglia exhibit aberrant phagocytosis and augmented pruning of hippocampal dendritic spines, which disrupts synaptic plasticity and influences hippocampal long-term potentiation, hence contributing to the emergence of negative emotions. Inflammatory responses in the brain are a prevalent pathological foundation for mood disorders and pain, and the activation or inhibition of microglia M1 polarization can influence pain-related emotions. This review elucidates the significance of hippocampal microglia activation, and their interactions with neurons in the hippocampus and astrocytes, in pain-related emotions.

Light-Burned Magnesia (LBM) activated Ground Granulated Blast Furnace Slag (GGBS) is established as a promising and robust binder for soil stabilization. However, its durability in saline environments subjected to freeze-thaw (F-T) cycles lacks systematic investigation. To validate its potential for subgrade engineering in seasonally frozen regions, this study evaluates the mechanical and microscopic properties of LBM-GGBS solidified saline soil under F-T cycling. The effects of LBM and GGBS on the unconfined compressive strength (UCS), permeability coefficient, Cl − leaching and microstructures of solidified saline soil after different F-T cycles (0, 2, 4, 6, 8, and 10) were examined. The results showed that increasing the LBM-GGBS content significantly enhanced the soil’s resistance to F-T cycles. With a 12% LBM-GGBS content and a GGBS/LBM ratio of 7 (determined as the optimal mix proportion), the solidified soil reached a residual strength of 3 MPa after 10 F-T cycles, which was four times the strength required for the upper base layer of highway pavement subgrade. Microscopic analysis revealed that the LBM-GGBS solidified soil exhibited a dense structure with calcium silicate hydrate (C-S-H), magnesium silicate hydrate (M-S-H), hydrotalcite, and Kuzel salt as the primary reaction products. The formation of these hydration products significantly densified the structure, thereby increasing the strength and improving the F-T resistance of the solidified soil. Furthermore, ~ 75% of Cl − in the original saline soil could be stabilized even after multiple F-T cycles. These findings elucidate the micro-mechanism of chloride stabilization under freezing conditions and provide a robust theoretical foundation for utilizing LBM-GGBS to mitigate saline soil hazards in seasonally frozen regions.

Background Synaptic abnormalities are hallmark pathological features of autism spectrum disorders (ASD), contributing to the behavioral impairments frequently observed in these neurodevelopmental conditions. Microglia, as the brain’s primary immune cells, are essential for synaptic refinement during adolescent development. Disrupted microglia-dependent synapse remodeling has been implicated in pathophysiology of ASDs, however, the underlying mechanisms remain incompletely elucidated. In this context, repetitive unidirectional spinal tactile stimulation (RSTS) has emerged as a promising non-invasive therapeutic strategy. This study aims to explore whether and how RSTS enhances microglia-dependent synapse remodeling in the medial prefrontal cortex (mPFC) during adolescent development in ASD mice, with a specific focus on the role of Brain and Muscle ARNT-Like 1 ( Arntl1 ), a core circadian protein crucial for regulating this process. Methods ASD mice underwent RSTS treatment during adolescent brain for 21 days, administered twice daily for 10 min per session. Behavioral changes were evaluated using the three-chamber social interaction and open field tests. Synapse number and morphology were assessed through Golgi staining. Microglia-dependent synapse remodeling ability was analyzed using immunofluorescence and Western blot. Furthermore, the molecular mechanism was investigated using single-nucleus RNA sequencing (snRNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq). Finally, the role of Bmal1 was validated, confirming its involvement in the enhancement of RSTS during adolescent brain in ASD. Results RSTS was found to alleviate autistic-like behaviors in adolescent ASD mice. Results from snRNA-seq and ChIP-seq indicated that the therapeutic effects of RSTS may be mediated through microglial Bmal1 and its role in the transcriptional regulation of microglia-dependent synapse remodeling. Furthermore, in vivo experiments confirmed that RSTS enhances microglia-dependent synapse remodeling in mPFC of adolescent ASD mice via Bmal1. These findings suggested that Bmal1 serves as a critical target of RSTS in facilitating microglia-dependent synapse remodeling during the adolescent brain developmental period in ASD mice. Conclusion Our findings suggest that the therapeutic effects of RSTS are potentially mediated through the modulation of microglial Bmal1 -dependent synapse remodeling and the regulation of synaptic proteins and the complement system. These results provide novel empirical evidence for RSTS in restoring synaptic balance and offer valuable insights into its potential as an intervention for ASD. Graphic abstract A diagram of the proposed mechanism by which RSTS promotes microglia-dependent synapse remodeling during adolescent brain development in ASD through Bmal1. ① ASD mice exhibit an excess of immature synapses; ②RSTS is applied as a therapeutic intervention; ③RSTS increases the expression of Bmal1 enhances its transcriptional regulatory activity in ASD mice brain; ④RSTS upregulates the expression of CD68, CR3, C1q, and C3b in ASD mice microglia; ⑤Bmal1 promotes expression of Wnt/β-catenin downstream targets (e.g., CyclinD1, C-Myc, Prox1) and interacts with TCF4 to modulate transcription;⑥RSTS lowers the expression of synaptic markers (e.g., PSD95, Syn1), reduces total synapse number, and decreases the proportion of immature synapses, indicating synaptic normalization in VPA-exposed mice.

OBJECTIVES Esophagectomy is the most effective treatment for oesophageal cancer, although the incidence of postoperative complications remains high. Severe major complications, such as intrathoracic anastomotic leakage, are costly and life-threatening to patients. Therefore, early identification of postoperative complications is essential. The surgical Apgar score (SAS) was introduced by Gawande and colleagues to predict major complications after oesophagectomy. Several studies were carried out with inconsistent results. METHODS PubMed, Embase, Web of Science, ClinicalTrials.gov and the Cochrane Library were searched for studies regarding SAS and oesophagectomy. Forest plots were generated using a random-effects model to investigate the actual predictive value of SAS in identifying major complications after oesophagectomy. RESULTS Nine retrospective cohort studies were finally identified from selected electronic databases. The meta-analysis demonstrated that SAS could forecast the incidence of postoperative complications (odds ratio = 1.82, 95% confidence interval: 1.43–2.33, P < 0.001). Subgroup analysis validated the predictive value of SAS whether as continuous or discrete variables. In addition, a meta-analysis of 4 studies demonstrated that SAS could predict the incidence of pulmonary complications (odds ratio = 2.32, 95% confidence interval: 1.61–3.36, P < 0.001). Significant heterogeneity but no publication bias was found. CONCLUSIONS Lower SAS scores could predict the incidence of major morbidities and pulmonary complications after oesophagectomy. Significant heterogeneity limits the reliability of the results, even if publication bias is not observed. More high-quality prospective research should be conducted to verify the findings. PROSPERO registration ID: CRD42020209004.

Cement-based stabilization/solidification (S/S) is a practical treatment approach for hazardous waste with anthropogenic As sources; however, its applicability for geogenic As-containing soil and the long-term leaching potential remain uncertain. In this study, semi-dynamic leaching test was performed to investigate the influence of S/S binders (cement blended with fuel ash (FA), furnace bottom ash (FBA), or ground granulated blast furnace slag (GGBS)) on the long-term leaching characteristics of geogenic As. The results showed that mineral admixtures with higher Ca content and pozzolanic activity were more effective in reducing the leached As concentrations. Thus, cement blended with FBA was inferior to other binders in suppressing the As leaching, while 20% replacement of ordinary Portland cement by GGBS was considered most feasible for the S/S treatment of As-containing soils. The leachability of geogenic As was suppressed by the encapsulation effect of solidified matrix and interlocking network of hydration products that were supported by scanning electron microscopy (SEM), X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS) results. The long-term leaching of geogenic As from the monolithic samples was diffusion-controlled. Increasing the Ca content in the samples led to a decrease in diffusion coefficient and an increase in feasibility for “controlled utilization” of the S/S-treated soils.

There is accumulating evidence to implicate the importance of EphBs receptors and ephrinBs ligands were involved in modulation of spinal nociceptive information. However, the downstream mechanisms that control this process are not well understood. In the present study, we investigated whether phosphatidylinositol 3-kinase (PI3K), as the downstream effectors, participates in modulation of spinal nociceptive information related to ephrinBs/EphBs. Intrathecal injection of ephrinB1-Fc produced a dose- and time-dependent thermal and mechanical hyperalgesia, accompanied by the increase of spinal PI3K-p110γ, phosphorylation of AKT (p-AKT) and c-Fos expression. Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of spinal AKT induced by ephrinB1-Fc. Inhibition of spinal PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal c-Fos protein expression induced by intrathecal injection of ephrinB1-Fc. Inhibition of EphBs receptors by intrathecal injection of EphB1-Fc reduced formalin-induced inflammation and chronic constrictive injury-induced neuropathic pain behaviors accompanied by decreased expression of spinal PI3K,p-AKT and c-Fos protein. Furthermore, pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented ephrinB1-Fc-induced ERK activation in spinal. These data demonstrated that PI3K and PI3K crosstalk to ERK signaling contributed to modulation of spinal nociceptive information related to ephrinBs/EphBs.

This study aimed to find an effective, inexpensive, and safe washing treatment for municipal solid waste incineration bottom ash (MSWIBA) in order to reduce its potential harmful effects in disposal and recycling. The washing solutions, namely tap water (TW), saturated lime water (SLW), and wastewater from concrete batching plant (WW) were used to wash MSWIBA at different liquid–solid (L/S) ratios and for different durations. Leaching behavior of some heavy metals, chloride, and sulfate from MSWIBA was tested and evaluated. From the TCLP leaching test, when the L/S ratio was above 5, WW was the most effective solution in reducing As, Cd, Se, and Sb emissions from MSWIBA. The calcium and iron ions present in the WW were essential for controlling the leaching of As, Cd, and Sb from MSWIBA due to the formation of stable crystalline pharmacosiderite, cadmium hydroxide sulfate, and hydromeite during the washing process. Using WW showed the best effect in removing sulfate from MSWIBA. At a L/S ratio of 10, about 83% of the sulfate could be removed from MSWIBA after 20 min of washing. The L/S ratio was most influential in removing chloride from MSWIBA. The three washing treatments chosen were effective in reducing the chloride level in MSWIBA to below the level of hazardous waste. Nevertheless, there were still substantial amounts of chloride remaining in the treated MSWIBA. Under the Dutch Building Materials Decree, the treated MSWIBA may be used as a building material in parts which allow isolation, control, and monitoring (ICM).

Objective To explore the mechanism of An-pressing manipulation in improving post-stroke muscle spasticity, by observing the changes of γ-aminobutyric acid (GABA) and glycine (Gly) in plasma and gray matter of L 1 -L 3 spinal cord anterior horn in post-stroke rats with muscle spasticity after An-pressing manipulation intervention. Methods Ten of 80 adult male Sprague-Dawley (SD) rats were randomly selected as the blank group, and the remaining 70 were used for modeling. The middle cerebral artery occlusion (MCAO) rat model was established by insertion suture occlusion method in the left external carotid artery. Thirty rats with a Longa neurological score of 2-3 points and a modified Ashworth spasticity scale score of 1 − , 1 + , or 2 were included in the experiment. Using the random number table method, the 30 successfully modeled rats were randomly divided into a model group, an An-pressing tendon group and an An-pressing muscle belly group. Two days after modeling, rats in the An-pressing tendon group and An-pressing muscle belly group received An-pressing manipulation on the tendon and belly of quadriceps femoris muscle respectively, with the pressure of (350±50) g and the frequency of 5 s/time, 15 min per session, once a day for 5 continuous days. After the 5th treatment, the tension of the rat quadriceps femoris muscle was evaluated using the modified Ashworth spasticity scale. The Gly levels in rat plasma and L 1 -L 3 segments of spinal cord were determined by enzyme-linked immunosorbent assay (ELISA). The GABA levels in rat plasma and L 1 -L 3 segments of spinal cord were measured by high performance liquid chromatography (HPLC). Results The decrease in rat muscle tension scored by the modified Ashworth spasticity scale in the An-pressing tendon group was more significant than that in the An-pressing muscle belly group ( P <0.01); the increases in Gly and GABA levels in the rat plasma and L 1 -L 3 segments of spinal cord were more significant in the An-pressing tendon group than those in the An-pressing muscle belly group (all P <0.01). Conclusion Based on the theory of ‘anti-stretch reflex’ of tendon organs, the use of An-pressing manipulation to induce the ‘anti-stretch reflex’ by stimulating the tendon organs can improve the muscle spasticity of rats, which is better than An-pressing the muscle belly. Increased levels of Gly and GABA in rat plasma and L 1 -L 3 segments of spinal cord may be one mechanism of An-pressing manipulation to improve muscle spasticity by stimulating tendon organs.