Xiaodan Wu

The longstanding trade‐off between spatial resolution and detection sensitivity has hindered X‐ray imaging in high‐speed nondestructive testing. Here, we present a synergistic strategy that integrates time‐delay integration (TDI) linear scanning with a waveguide‐structured pixelated Cs ₃ Cu ₂ I ₅ scintillator array to overcome this limitation. The pixelated architecture effectively suppresses lateral photon scattering while maintaining high light output from a 400‐µm‐thick scintillator layer, achieving a spatial resolution of 27.9 lp mm ⁻¹ in X‐ray imaging. By incorporating a multistage TDI configuration, we amplify the collected scintillation photons without compromising spatial resolution, achieving a 29.8‐fold enhancement in sensitivity. Notably, the TDI‐based linear scanning system supports a continuous high‐speed readout rate of 22.3 mm s ⁻¹ , enabling real‐time, high‐fidelity X‐ray chip inspection with a throughput exceeding 130 chips per minute. This work establishes a viable pathway for advancing X‐ray imaging toward high‐precision and real‐time X‐ray inspection.

Background: Myocardial injury is a major contributor to mortality in sepsis, yet the mechanisms underlying gut‐heart communication in sepsis‐induced myocardial injury remain insufficiently defined. Natriuretic peptide B (NPPB) is a cardiac stress‐responsive gene, but its involvement in mitochondrial homeostasis and metabolic regulation is unclear. This study investigated how gut microbiota and aldosterone influence myocardial mitophagy and metabolic reprogramming through NPPB in sepsis‐induced myocardial injury. Methods: A sepsis‐like myocardial injury model was induced in mice by intraperitoneal lipopolysaccharide (LPS). Fecal microbiota transplantation from septic mice into pseudo‐germ‐free recipients assessed microbial contributions. Metagenomic, metabolomic, and transcriptomic analyses identified disrupted metabolites and cardiac gene signatures. Heart‐specific NPPB‐knockout mice were used to determine its in vivo role. Mitochondrial function and metabolic alterations were evaluated by energy metabolism assays. In vitro, aldosterone‐treated AC16 cardiomyocytes were used to examine NPPB‐mediated mitophagy and metabolic changes. Molecular docking, dynamics simulation, and machine‐learning screening identified Lestaurtinib, whose therapeutic effects were validated pharmacologically. Results: Sepsis caused pronounced microbial dysbiosis and elevated aldosterone levels. Multi‐omics analysis identified NPPB as a central regulator of mitophagy and metabolic remodeling. NPPB deficiency mitigated mitochondrial impairment and metabolic disturbances in vivo. Aldosterone upregulated NPPB in cardiomyocytes, promoting mitophagy and metabolic reprogramming. Lestaurtinib, identified as a candidate targeting the aldosterone‐NPPB axis, improved cardiac structure and function while partially restoring microbial and metabolic homeostasis. Conclusions: This study uncovers a novel gut microbiota‐aldosterone‐NPPB axis driving LPS‐induced myocardial injury through dysregulated mitophagy and metabolism and highlights Lestaurtinib as a potential therapeutic strategy for sepsis‐induced myocardial injury.

Postoperative atrial fibrillation (POAF) is a common and serious complication following video-assisted thoracoscopic surgery (VATS), which affects patients

Patients with sleep disorders often suffer from gastrointestinal diseases such as abdominal pain and diarrhea, which severely affect their quality of life. Therefore, identifying interventions to mitigate sleep deprivation (SD)-induced intestinal barrier damage is an important clinical objective. The potential of stellate ganglion block (SGB) to improve gut health in this context and its underlying mechanisms remain unclear. In phase one, rats were randomly allocated to CON, SD1, SD3, SD5, and SD7 groups (n = 4-6 per group), undergoing SD for 0, 1, 3, 5, or 7 days respectively. The time point of peak intestinal injury was determined by Evans blue staining. Based on these results, a second phase assigned rats to six groups (n = 5-6 per group): CON, SD, SD + SGB, antibiotics (ABX), ABX + SD, and ABX + SD + SGB. Intestinal barrier function was assessed via crypt depth, mucosal thickness, and expression of tight junction proteins (Occludin, ZO-1). Gut microbiota composition was analyzed by 16S rRNA gene sequencing, and microbial metabolites were profiled using LC-MS-based non-targeted metabolomics. Evans blue staining showed that intestinal permeability was significantly increased after 7 days of SD, reaching approximately fourfold higher levels compared with the control (CON) group (p < 0.0001). Consistent with this functional impairment, morphological analysis revealed that the SD group exhibited substantial reductions in crypt depth (by ~ 56%), mucosal thickness (by ~ 59%), and goblet cell count (by ~ 45%) relative to CON (all p < 0.01). Treatment with SGB markedly attenuated these alterations, restoring mucosal thickness and goblet cell count to about 78% and 97% of the CON levels, respectively. At the molecular level, the expression of the tight junction protein Occludin, which was significantly lower in the SD group (~ 38% of CON, p < 0.05), was also recovered after SGB intervention. Notably, the therapeutic effects of SGB were absent in pseudo-germ-free conditions, suggesting a microbiota-dependent mechanism. 16S rRNA gene sequencing confirmed that SGB altered the gut microbiota composition. Furthermore, untargeted metabolomics revealed that SGB counteracted SD-induced shifts in the fecal metabolome, specifically altering the relative abundance of metabolites associated with inflammatory lipids and microbial amino acid metabolism. SGB was associated with the attenuation of SD-induced intestinal barrier dysfunction, and this effect was absent under antibiotic treatment, suggesting a microbiota-dependent component. These findings offer theoretical support for its clinical application.

Purpose: Postoperative pain sensitivity is a key target for perioperative analgesic care, linked to acute severe pain and chronic pain risk. This study aimed to investigate whether perioperative subanesthetic esketamine attenuates early postoperative pain sensitivity in patients undergoing emergency laparoscopic salpingectomy for ectopic pregnancy. Methods: This randomized controlled trial enrolled patients with ectopic pregnancy undergoing laparoscopic salpingectomy, randomly assigned 1:1 to esketamine or control. Patients in the esketamine group received an intravenous bolus of esketamine 0.25 mg/kg during surgery, followed by a patient-controlled intravenous analgesia (PCIA) solution containing esketamine (1 mg/kg) and sufentanil (1 μg/kg). The control group received a PCIA solution containing a higher dose of sufentanil (2 μg/kg) with equivalent volumes of normal saline instead of esketamine. The primary outcome was postoperative pain sensitivity, assessed by the Pain Sensitivity Questionnaire (PSQ) at postoperative day 1, 2, and 7. Secondary outcomes included the Numeric Rating Scale (NRS) pain scores, the 17-item Hamilton Depression Rating Scale (HAMD-17) scores, serum prostaglandin E2 (PGE2), brain-derived neurotrophic factor (BDNF) levels, and adverse events. Results: A total of 84 patients were enrolled and randomized (42 per group), with 80 completing the trial (42 in the esketamine group, 38 in the control group). For the primary outcome, repeated-measures ANOVA revealed a significant main effect of group on PSQ-total scores (F(1,78) = 9.881, P = 0.002). These beneficial effects were consistently observed across both PSQ subscales (PSQ-minor: P = 0.002; PSQ-moderate: P = 0.002). Dynamic NRS pain scores were significantly lower at 30 minutes post-surgery (median [IQR]: 3.0 [2.0– 4.0] vs. 4.0 [2.0– 5.0]; 95% CI for difference: 0.57– 2.42; P< 0.001). HAMD-17 scores showed a downward trend without significant difference (P=0.125). Serum BDNF levels were significantly higher in the esketamine group compared with controls (P < 0.05), whereas PGE2 levels showed no significant between-group difference (P > 0.05). Conclusion: Perioperative subanesthetic esketamine may provide modest improvement in early postoperative pain sensitivity, and may serve as a useful adjunct in multimodal postoperative analgesia for emergency laparoscopic salpingectomy.

Fetal acidosis (FA) is a prevalent clinical symptom in newborns during the perinatal period, which can lead to higher risks of hypoxic ischemic encephalopathy, seizures, intraventricular hemorrhage and delayed developmental milestones. However, there is no effective tool for the risk assessment and prediction of FA in neonates. Therefore, our objective is to develop a FA prediction model in newborns by using machine-learning algorithms. Parturients and their neonates who delivered at the Fuzhou University Affiliated Provincial Hospital between January 2018 and December 2023 were included to identify optimal predictors and develop a prediction model for FA. To prospectively validate the model’s predictive performance, an independent cohort of newborns delivered at the Fujian Maternal and Child Health Hospital between June 2023 and March 2024 was enrolled. Model interpretability was assessed using the Shapley Additive Explanations (SHAP) method. Eventually, a total of 1,587 neonates at the Fuzhou University Affiliated Provincial Hospital constituted the development dataset (1110 cases were assigned to the training cohort, and 477 were included in the internal validation cohort), while 333 neonates from the Fujian Maternal and Child Health Hospital formed the prospective validation cohort. Among various machine learning algorithms evaluated, the Gaussian Naive Bayes (GNB) algorithm demonstrated the best performance across all validation types. The model achieved an area under the receiver operating characteristic curve (AUC) of 0.749 [95% CI: 0.679–0.818] in internal validation, and 0.763 [95% CI: 0.719–0.807] in external validation. This algorithm will be instrumental for identification of high-risk perinatal populations and it will facilitate targeted interventions in neonates. Trial registration: Chinese Clinical Trial Registry Identifier ChiCTR2300074180.

Autism Spectrum Disorder (ASD) presents a substantial global challenge, yet no pharmacological treatments effectively target its core symptoms, especially in individuals with severe cognitive or adaptive impairments. This double-blind, sham-controlled, randomized clinical trial assessed accelerated intermittent theta burst stimulation (iTBS) targeting the personalized fronto-parietal network (FPN) in ASD. Participants (6–30 years) were randomized in a 2:1 ratio to active or sham iTBS (three daily sessions, 1800 pulses/session) over 12 weeks (324k pulses) alongside behavioral training. The primary outcome was defined as the response rate, charaterized by a ≥ 1-point reduction in ADOS-2 SA at week 12. Of 132 individuals screened, 67 were randomized (mean age 10.04 ± 4.22 years; 88.1% male; all with cognitive/adaptive delays), with 59 completing the study. Active iTBS resulted in a significantly higher response rate (55% vs. 29%) and higher symptom improvement than sham (cohen’s d = −0.53), with mild local pain in only 5% of iTBS group. In the profound autism subgroup, the active group exhibited language improvement alongside amelioration of core symptoms. These findings suggest that prolonged, accelerated FPN-targeted iTBS is a safe and efficacious intervention for severe ASD, offering a promising therapeutic approach. Registration ClinicalTrials.gov Identifier: NCT05890846