Objective To develop a predictive model for postoperative pulmonary complications (PPC) following video-assisted thoracic surgery (VATS) in lung cancer patients by integrating cardiopulmonary exercise testing (CPET) parameters and machine learning techniques. Methods A retrospective analysis was conducted on patients with early-stage non-small cell lung cancer who underwent CPET and VATS at Guangdong Provincial People’s Hospital between October 2021 and July 2023. Patients were divided into a PPC group and a non-PPC group. The least absolute shrinkage and selection operator (LASSO) regression was used to select important features associated with PPC. Six machine learning algorithms were utilized to construct prediction models, including logistic regression, support vector machine, k-nearest neighbors, random forest, gradient boosting machine, and extreme gradient boosting. The optimal model was interpreted using SHapley Additive exPlanations (SHAP). Results A total of 325 patients were included, with an average age of 60.36 years, and 55.1% were male. Significant differences were observed between the PPC and non-PPC groups in age, diabetes, coronary heart disease, surgical approach, forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FVC% predicted, peak oxygen uptake (peak VO2), anaerobic threshold (AT), and ventilatory equivalent for carbon dioxide slope (VE/VCO2 slope) (P<0.05). In the predictive model constructed by selecting 7 key features using LASSO regression, the random forest model demonstrated the best overall performance across various metrics, with an area under the receiver operating curve of 0.930, an F1 score of 0.836, and a Brier score of 0.133 in the training set. It also exhibited good predictive ability and calibration in the test set. SHAP analysis ranked feature importance as follows: peak VO2, VE/VCO2 slope, age, FEV1, smoking history, diabetes, and surgical approach. Conclusion Integrating CPET parameters, the random forest model can effectively identify high-risk patients for PPC and has the potential for clinical application.

Background Prenatal exposure to fine particulate matter (PM_2.5) is closely associated with cortical damage and neuroinflammation in offspring. The cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS)–stimulator of interferon genes (STING) signaling pathway is a key regulator of inflammation and may be subject to epigenetic regulation. Objective To investigate the role of cGAS-STING pathway activation in PM_2.5-induced cortical damage in offspring mice during pregnancy and the underlying epigenetic regulatory mechanisms. Methods Open field tests were used to assess depressive-like behavior in offspring mice. Morphological analysis was conducted to evaluate cortical damage and microglial activation in offspring brains. Real-time fluorescent quantitative PCR (RT-qPCR) and Western blot (WB) were performed to detect changes in the expression of key molecules in the cGAS-STING pathway in cortical tissue. A PM_2.5-induced microglial cell injury model was established in BV2 cells. Microglial activation was observed, cell viability was measured using the Cell Counting Kit-8 (CCK-8), and the expression levels of inducible nitric oxide synthase (iNOS) and key molecules in the cGAS-STING pathway were detected by RT-qPCR and WB. Bioinformatics analysis was performed to explore the epigenetic regulatory association between the STING signaling pathway and lysine-specific demethylase 5A (KDM5A). Changes in KDM5A mRNA and protein expression, as well as the protein level of histone H3 lysine 4 trimethylation (H3K4me3), were detected in an in vitro PM_2.5 injury model. Using small interfering RNA (siRNA) technology, the KDM5A gene was silenced in BV2 cells exposed to PM_2.5. The protein expression of H3K4me3 was detected to evaluate improvements in microglial activation, changes in inflammatory markers such as iNOS and mannose receptor (CD206), and alterations in the cGAS-STING pathway. Results Compared with the control group, the total distance of offspring mice in the PM_2.5 group was significantly reduced, and both the distance traveled and the time spent in the central area of the open field were significantly decreased (P<0.01, P<0.001), indicating depressive-like behavior in the offspring mice. Compared with the control group, the offspring mice in the PM_2.5 group exhibited disorganized cortical structure and significantly activated microglia (P<0.01), with significantly increased mRNA and protein levels of cGAS and STING (P<0.05, P<0.01, or P<0.001). The in vitro experiments demonstrated that the PM_2.5 treatment induced BV2 cells to polarize toward the M1 phenotype, exhibiting a distinct amoeboid morphology, with upregulated expression of the pro-inflammatory factor iNOS (P<0.05, P<0.01, or P<0.001) and activation of the cGAS-STING pathway (P<0.05, P<0.01). The analysis of RNA-seq data from KDM5A knockout cells revealed significantly downregulated STING expression, suggesting that KDM5A may activate the STING signaling pathway. The in vitro experiments further confirmed that the PM_2.5-treated BV2 cells exhibited significantly elevated mRNA and protein levels of KDM5A (P<0.01), while the H3K4me3 protein levels were markedly reduced (P<0.05). After silencing KDM5A in BV2 cells exposed to PM_2.5, compared with the PM_2.5+siNC group, the PM_2.5+siKDM5A group showed no obvious microglial activation and polarized toward the M2 phenotype, with significantly decreased expression levels of iNOS, cluster of differentiation 16 (CD16), and interleukin-1β (P<0.05, P<0.01), and significantly increased expression levels of anti-inflammatory factors CD206, YM1, and interleukin-10 (P<0.01, P<0.001). Meanwhile, the expression levels of cGAS and STING were also reduced (P<0.05, P<0.01). Conclusion KDM5A activates microglia through the cGAS-STING pathway, thereby contributing to PM_2.5-induced cortical damage in offspring mice during pregnancy.

Chronic obstructive pulmonary disease （COPD） is a chronic respiratory disease that poses a significant threat to global health， exhibiting high morbidity， disability and mortality rate， with its prevention and treatment situation becoming increasingly critical. The pathogenesis of COPD is complex， and the underlying cellular and molecular biological mechanisms remain incompletely elucidated. Programmed cell death （PCD） is the process wherein cells actively undergo demise to maintain internal environmental stability in response to certain signals or specific stimuli. Contemporary medical research indicates that the dysregulation of PCD patterns such as apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis is closely related to the onset and progression of COPD. Clarifying the molecular mechanisms of PCD in COPD may provide novel perspectives for in-depth understanding and prevention of the disease. Traditional Chinese medicine （TCM） is characterized by holistic regulation. In recent years， extensive research has been conducted in the TCM field focusing on modulating apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis for the treatment of COPD， yielding remarkable achievements. Therefore， this study systematically explored the molecular mechanism of PCD in COPD and reviewed the potential mechanisms and intervention status of TCM targeting PCD in COPD， aiming to provide insights and references for the clinical prevention， treatment and in-depth research of COPD.

Chronic obstructive pulmonary disease （COPD） is a chronic respiratory disease that poses a significant threat to global health， exhibiting high morbidity， disability and mortality rate， with its prevention and treatment situation becoming increasingly critical. The pathogenesis of COPD is complex， and the underlying cellular and molecular biological mechanisms remain incompletely elucidated. Programmed cell death （PCD） is the process wherein cells actively undergo demise to maintain internal environmental stability in response to certain signals or specific stimuli. Contemporary medical research indicates that the dysregulation of PCD patterns such as apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis is closely related to the onset and progression of COPD. Clarifying the molecular mechanisms of PCD in COPD may provide novel perspectives for in-depth understanding and prevention of the disease. Traditional Chinese medicine （TCM） is characterized by holistic regulation. In recent years， extensive research has been conducted in the TCM field focusing on modulating apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis for the treatment of COPD， yielding remarkable achievements. Therefore， this study systematically explored the molecular mechanism of PCD in COPD and reviewed the potential mechanisms and intervention status of TCM targeting PCD in COPD， aiming to provide insights and references for the clinical prevention， treatment and in-depth research of COPD.

Modern cataract surgery has completely moved beyond the traditional vision-restoring model and has fully entered a new era of refractive cataract surgery(RCS)centered on precise refractive correction. Its core objective is to provide patients with personalized visual experiences characterized by full-range, clear, and comfortable vision. Currently, although diagnostic and therapeutic technologies for RCS are rapidly evolving, there remain many bottlenecks in the precise management of the entire perioperative process that urgently need to be addressed. Preoperatively, the measurement consistency among ocular biometry devices based on different detection principles remains poor, and systematic measurement errors cannot be completely eliminated. Moreover, the individualized selection of intraocular lenses(IOLs)relies heavily on surgeons' clinical experience, lacking a standardized quantitative decision-making framework, which makes it difficult to achieve precise personalized matching. Intraoperatively, the quality of continuous curvilinear capsulorhexis is affected by multiple factors such as ocular anatomical characteristics and surgical proficiency, and its stability cannot be reliably ensured. Various intelligent surgical navigation systems are compromised by intraoperative ocular conditions, and their clinical performance fails to meet theoretical expectations. At the postoperative stage, existing IOL optical designs and materials have inherent limitations. The longterm prevention and control of posterior capsule opacification(PCO)remains a core factor restricting patients' long-term high-quality visual outcomes. This article systematically reviews the precise diagnostic and therapeutic challenges and core bottlenecks across the preoperative, intraoperative, and postoperative stages of RCS. It further explores frontier technological directions—including cross-device error compensation models, artificial intelligence-assisted decision-making, preoperative VR-based visual simulation, and the construction of intelligent surgical ecosystem platforms—to delineate targeted solutions and optimization pathways. This review aims to provide references and insights for the standardized clinical implementation, technological innovation, and future research endeavors in precision diagnosis and treatment of RCS.

Viral pneumonia is an infectious disease caused by virus invading the lung parenchyma and interstitial tissue and causing lung inflammation， with the incidence rising year by year. Traditional Chinese medicine （TCM） can treat viral pneumonia in a multi-component， multi-target， and holistic manner by targeting the core pathogenesis of pneumonia caused by different respiratory viruses， demonstrating minimal side effects and significant advantages. According to the theory of healthy Qi and pathogenic Qi in TCM， the struggle between healthy Qi and pathogenic Qi and the imbalance between immunity and inflammation run through the entire process of viral pneumonia， and the immunity-inflammation status at different stages of the disease reflects different relationships between healthy Qi and pathogenic Qi. Immune dysfunction leads to the deficiency of healthy Qi， causing viral infections. The struggle between healthy Qi and pathogenic Qi causes immunity-inflammation imbalance， leading to the onset of viral pneumonia. Inflammatory damage causes persistent accumulation of phlegm and stasis， leading to the progression of viral pneumonia. The cytokine storm causes immunodepletion， leading to the excess of pathogenic Qi and diminution of healthy Qi and the deterioration of viral pneumonia. After the recovery from viral pneumonia， there is a long-term imbalance between immunity and micro-inflammation， which results in healthy Qi deficiency and pathogenic Qi lingering. Healthy Qi deficiency and pathogenic Qi excess act as common core causes of pneumonia caused by different respiratory viruses. Clinical treatment should emphasize both replenishing healthy Qi and eliminating pathogenic Qi， helping to restore the balance between healthy Qi and pathogenic Qi as well as between immunity and inflammation， thus promoting the recovery of patients from viral pneumonia. According to the TCM theory of healthy Qi and pathogenic Qi， this article summarizes the immunity-inflammation mechanisms at different stages of viral pneumonia， and explores the application of the method of replenishing healthy Qi and eliminating pathogenic Qi in viral pneumonia. The aim is to probe into the scientific connotation of the TCM theory of healthy Qi and pathogenic Qi in viral pneumonia and provide ideas for the clinical application of the method of replenishing healthy Qi and eliminating pathogenic Qi to assist in the treatment of viral pneumonia.

BackgroundAttention deficit hyperactivity disorder （ADHD） is a neurodevelopmental disorder characterized by age-inappropriate inattention， excessive activities incongruous with setting， and emotional impulsivity. Subthreshold ADHD （sADHD） is clinically defined as the presence of ADHD symptoms that do not meet the full diagnostic criteria for ADHD. Children with sADHD exhibit deficits in executive function， demonstrate more conduct， learning， and anxiety-related problems compared to typically developing children， and show even poorer working memory performance than children diagnosed with ADHD. Currently， there is limited epidemiological research on sADHD in China， with few studies simultaneously investigating the prevalence of both ADHD and sADHD in children. ObjectiveTo investigate the prevalence of ADHD and sADHD among children aged 6–13 years in Chongqing， analyzing their distribution characteristics within this population， with the aim of providing references for developing preventive measures against both ADHD and sADHD. MethodsFrom October to November 2023， a total of 3 398 students in grades 1–6 from six primary schools in Jiangbei District， Chongqing were selected using a stratified cluster random sampling method. The occurrence of ADHD and sADHD was evaluated by using the short version （18-item version） of the Swanson， Nolan， and Pelham IV rating scales （SNAP-IV） and the Chinese vision of Schedule for Affective Disorder and Schizophrenia for School-aged Children-Present and Lifetime Version （K-SADS-PL）. ResultsThe ADHD detection rate among children in Chongqing was 1.90% （95% CI： 0.014–0.024）. Boys showed a significantly higher ADHD detection rate than girls （χ²=7.733， P=0.005）. No statistically significant differences were found in ADHD detection rates across different grades or age groups （χ²=7.347， 12.362， P>0.05）. The sADHD detection rate was 6.32% （95% CI： 0.054–0.072）. Similarly， boys exhibited significantly higher sADHD detection rates than girls （χ²=21.005， P<0.01）. Significant differences emerged across different grades （χ²=20.559， P=0.001）， while no statistically significant difference was observed in age groups （χ²=12.070， P=0.060）. ConclusionThe ADHD detection rates were comparable across all grade levels and age groups from 6–13 years old. Second-grade children demonstrated notably higher sADHD rates compared to other grades， while boys demonstrated higher prevalence rates than girls for both ADHD and sADHD. ［Funded by Science and Health Joint Medical Research Project in Jiangbei District， Chongqing City in the Second Half of 2023 （number， 2023JBKWLH022）］

Sj?gren syndrome(SS)is an immune disease mainly characterized by lymphocytes infiltrate in salivary and lacrimal glands,leading to glandular secretion disorders and dryness in the mouth and eyes.In recent years,clinical application of ultrasound elastography(USE)increased widespread,providing a new imaging method for diagnosis of SS.The research progresses of USE in SS were reviewed in this article.

Objective To explore the clinical efficacy of wrist arthroscopy assisted closed reduction with external fixation in the treatment of intra-articular comminuted fractures of the distal radius(type C3).Methods A retrospective analysis was conducted on 98 patients with type C3 intra-articular comminuted fractures of the distal radius admitted to our hospital from March 2022 to February 2023.Among them,48 patients underwent wrist arthroscopy assisted closed reduction with external fixation with a bracket(arthroscopy group),and another 50 patients underwent open reduction with steel plate internal fixation surgery(control group).The two groups were compared in terms of operation time,intraoperative bleeding volume,incision length,fracture union time,range of motion(ROM)of joint,Visual Analogue Scale(VAS),and Gartland-Werley wrist scores,as well as radiographic parameters(palmar tilt,ulnar inclination,and radial height)evaluated at various follow-up intervals.Results The arthroscopy group had an operation time of(55.3±10.5)min,which was significantly shorter than that in the control group[(83.4±14.6)min;t=-10.979,P=0.000].The intraoperative bleeding volume in the arthroscopy group was(42.3±8.6)ml,which was less than that in the control group[(71.4±10.5)ml;t=-14.953,P=0.000].The incision length of the arthroscopy group was(1.3±0.3)cm,which was shorter than that of the control group[(5.1±1.5)cm;t=-18.550,P=0.000].The arthroscopy group had a fracture healing time of(10.7±1.4)weeks,which was shorter than that in the control group[(12.2±1.6)weeks;t=-4.855,P=0.000].The palmar flexion ROM in the arthroscopy group was 68.8°±8.3°,which was significantly higher than that in the control group(61.5°±9.4°;t=4.002,P=0.000).The dorsiflexion ROM in the arthroscopy group was 63.9°±7.5°,which was significantly higher than that in the comtrol group(59.2°±8.3°;t=2.931,P=0.004).The pronation ROM in the arthroscopy group was 67.4°±10.3°,which was significantly higher than that in the control group(62.1°±9.9°;t=2.604,P=0.011).The supination ROM in the arthroscopy group was 70.5°±7.4°,which was significantly higher than that in the control group(64.4°±8.6°;t=3.777,P=0.000).The VAS score of the arthroscopy group was(1.3±0.6)points,which was significantly lower than that in the control group[(1.7±0.5)points;t=-3.941,P=0.000].After 6 months,the Gartland-Werley wrist scores of the arthroscopy group was significantly higher than that of the control group(Z=-2.614,P=0.009).The wrist joint imaging showed significantly higher radial height,palmar inclination angle,and ulnar deviation angle in the arthroscopy group than the control group(all P=0.000),while there were no significant differences in palmar inclination angle and ulnar deviation angle at different time points within each group(P＞0.05).Except for significant differences in radial height at 3 d,1 month,and 6 months after surgery(P=0.015,P=0.035),there were no significant differences between any other time points(P＞0.05).The interaction between time and group was not significant for palm inclination angle,ulnar deviation angle,and radial height(P＞0.05).Conclusion Wrist arthroscopy assisted closed reduction with external fixation for intra-articular comminuted fractures of distal radius has advantages of short operation time,less intraoperative blood loss,and good recovery of wrist joint functions.

Objective:To explore the impacts of 131I-NaI radiotherapy on the promotion of glycolysis and 18F-fluorodeoxyglucose ( 18F-FDG) uptake in pancreatic cancer cells via the induction of proviral integration moloney murineleukemia virus 2 (PIM2) and 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3). Methods:In the cell experiments, human pancreatic carcinoma cells-1 (PANC-1) were randomly divided into four groups: a control group, an HJ-PI01 group, a 131I-NaI group, and an HJ-PI01 + 131I-NaI group. Their aerobic glycolysis capacity was assessed by measuring glucose uptake, lactate production, and extracellular acidification rate (ECAR). In vivo animal experiments, 12 nu/nu female nude mice were given 100 μl (1 × 10 7 cells) of cell suspension through subcutaneous injection into the left lower limbs. When the tumor volume reached approximately 60 mm 3, these mice were divided into four groups (a control group, a HJ-PI01 group, a 131I-NaI group, and an HJ-PI01+ 131I-NaI group) using a random number table, with three mice in each group. After 14 days of treatment, 18F-FDG PET/CT imaging was performed to calculate the maximum standardized uptake value (SUV max) of the xenografts. Following PET/CT imaging, the tumor tissues were harvested and analyzed for PIM2, PFKFB3, and Ki-67 expressions using immunohistochemistry. Results:In cell experiments, compared to the control group, the HJ-PI01 group exhibited significant reduction in glucose uptake, lactate production, PFKFB3 protein expression, and ECAR in PANC-1 cells ( t = 4.59-13.98, P < 0.05). In contrast, the 131I-NaI group showed significant increases in these parameters ( t = 3.36-13.97, P < 0.05). Compared to the 131I-NaI group, the HJ-PI01+ 131I-NaI group showed significant reduction in glucose uptake, lactate production, PFKFB3 protein expression, and ECAR ( t = 5.14-20.87, P < 0.05). In the animal experiments, compared to the control group, the three groups displayed significant decrease in SUV max of 18F-FDG uptake in tumors ( t = 16.48, 22.49, 32.64, P < 0.001). Moreover, the HJ-PI01 + 131I-NaI group exhibite significantly lower SUV max than the 131I-NaI group ( t = 10.16, P < 0.001). Immunohistochemical analysis revealed that the HJ-PI01+ 131I-NaI group, compared to the 131I-NaI group, showed significantly lower Ki-67 expression and the PIM2/PFKFB3 signaling pathway in tumor tissues ( t = 3.27, 10.73, 14.85, P < 0.05). Conclusions:Glycolysis enhancement of PANC-1 cells, mediated by the PIM2/PFKFB3 signaling pathway inhibition, can significantly improve the anticancer capacity of 131I-NaI, providing a novel strategy for radiotherapy in pancreatic cancer.