According to the Qi-blood-body fluid theory and the association between the spleen in visceral manifestation theory of traditional Chinese medicine （TCM） and mitochondria in modern cellular biology， it is proposed that the role of the spleen in generating and transforming Qi and blood is analogous to the energy-producing function of mitochondria—both serving as fundamental power sources for vital activities of the human body. The spleen governs transportation and transformation， playing a critical role in energy metabolism and the digestion and absorption of nutrients. Similarly， mitochondria are vital for maintaining physiological functions such as cellular energy supply， cell survival， and overall human metabolism. Furthermore， spleen deficiency is closely linked to mitochondrial dysfunction. Accordingly， mitochondrial energy conversion and substance metabolism are regarded as the microscopic essence of the spleen's function in transportation and transformation. Spleen deficiency and mitochondrial dysfunction contribute to the formation of pathological products such as phlegm-turbidity and blood stasis. This aligns with the pathogenesis of chronic obstructive pulmonary disease （COPD）， with Qi deficiency as the root cause and phlegm-turbidity and blood stasis as the manifestations. Therefore， the integrative treatment of COPD should follow the therapeutic principle of invigorating the spleen and reinforcing healthy Qi， while also resolving phlegm and removing blood stasis to address both root cause and manifestations. This approach can improve the mitochondrial function， regulate energy metabolism， and reduce oxidative stress levels to alleviate COPD symptoms， slow down disease progression， and improve prognosis. By integrating the holistic concept of TCM with molecular mechanisms of modern medicine， this paper explores the pathogenesis and therapeutic principles of COPD from the spleen-mitochondria correlation. It not only provides a new direction for the modern development of TCM and the integration of Chinese and Western medicine but also offers a theoretical foundation for the integrated treatment of chronic， complex age-related diseases.

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.

According to the Qi-blood-body fluid theory and the association between the spleen in visceral manifestation theory of traditional Chinese medicine （TCM） and mitochondria in modern cellular biology， it is proposed that the role of the spleen in generating and transforming Qi and blood is analogous to the energy-producing function of mitochondria—both serving as fundamental power sources for vital activities of the human body. The spleen governs transportation and transformation， playing a critical role in energy metabolism and the digestion and absorption of nutrients. Similarly， mitochondria are vital for maintaining physiological functions such as cellular energy supply， cell survival， and overall human metabolism. Furthermore， spleen deficiency is closely linked to mitochondrial dysfunction. Accordingly， mitochondrial energy conversion and substance metabolism are regarded as the microscopic essence of the spleen's function in transportation and transformation. Spleen deficiency and mitochondrial dysfunction contribute to the formation of pathological products such as phlegm-turbidity and blood stasis. This aligns with the pathogenesis of chronic obstructive pulmonary disease （COPD）， with Qi deficiency as the root cause and phlegm-turbidity and blood stasis as the manifestations. Therefore， the integrative treatment of COPD should follow the therapeutic principle of invigorating the spleen and reinforcing healthy Qi， while also resolving phlegm and removing blood stasis to address both root cause and manifestations. This approach can improve the mitochondrial function， regulate energy metabolism， and reduce oxidative stress levels to alleviate COPD symptoms， slow down disease progression， and improve prognosis. By integrating the holistic concept of TCM with molecular mechanisms of modern medicine， this paper explores the pathogenesis and therapeutic principles of COPD from the spleen-mitochondria correlation. It not only provides a new direction for the modern development of TCM and the integration of Chinese and Western medicine but also offers a theoretical foundation for the integrated treatment of chronic， complex age-related diseases.

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.

Community-acquired pneumonia （CAP） refers to an infectious inflammation of the lung parenchyma （including the alveolar wall，that is，the broad pulmonary interstitium） acquired outside the hospital. Its common pathogens include streptococcus pneumoniae，respiratory viruses， mycoplasma pneumoniae， and so on. The related factors for the occurrence and development of CAP include patient characteristics （immune function，mucus production and clearance function，coagulation function，physical condition， and comorbidity） and pathogen characteristics （susceptibility，virulence，and antibiotic resistance）. The pathogenesis of CAP lies in immune deficiency，pathogen invasion，inflammatory response disorder，mucus production and clearance disorder， coagulation disorder， and so on. The pathogenesis of CAP in traditional Chinese medicine can be described as "vital Qi deficiency and toxic stasis". Vital Qi deficiency （lack of immunity） is the potential pathogenesis of the disease and easy to be invaded by external pathogens （respiratory pathogens）. Toxic stasis （inflammatory disorder，mucus production and clearance disorder，and coagulation dysfunction） is the key pathogenic factor. Vital Qi deficiency and toxic stasis are intermingled in a state of deficiency and excess，which suggests that the treatment of CAP lies in strengthening vital Qi and eliminating pathogenic factors. This involves strengthening vital Qi in the whole process to consolidate body resistance and nourish promordial Qi. It also involves clearing heat，eliminating phlegm，removing dampness，and dispelling stasis to dispel pathogenic toxins based on the syndrome differentiation. Its action mechanism is to regulate immune and inflammatory responses，resist pathogens，and improve mucus production and clearance， as well as coagulation disorders. Starting from the key pathogenesis of CAP，"vital Qi deficiency and toxic stasis"， this paper discussed the pathogenesis of CAP and summarized the action mechanism of vital Qi strengthening for detoxification in its treatment. It is intended to complement the theoretical system by identifying "vital Qi deficiency and toxic stasis" as the key pathogenesis underlying CAP and the scientific connotation of treating CAP with vital Qi strengthening for detoxification，thereby providing insights for its clinical application.

ObjectiveTo explore the effects of hypoxia on the migration ability of human oligodendrocyte precursor cells （hOPCs） and its regulatory mechanisms. MethodsBased on the variations in oxygen concentration within the culture system， three experimental groups were set up： the 21%O₂ group （normoxic control group）， the 5%O₂ group， and the 2%O₂ group. The migration ability of hOPCs under normoxia （21%O₂）， 5%O₂， and 2%O₂ conditions was detected through the Transwell migration assay. RT-qPCR， transcriptome sequencing， and flow cytometry were used to detect the expression changes of genes and proteins such as hypoxia-inducible factor 1 alpha （HIF-1α） and chemokine （C-X-C Motif） receptor 4 （CXCR4）. Bioinformatics analysis was combined to analyze the KEGG pathways related to migration， so as to explore the effects of different oxygen concentrations on the migration ability of hOPCs and their possible mechanisms. ResultsHypoxia treatments at concentrations of 5%O₂ and 2%O₂ could both promote the in vitro migration of hOPCs， and the promoting effect of migration was more significant at the 2%O₂ concentration （P<0.001）. After hypoxia treatment， the mRNA expression levels of HIF-1α， CXCR4， etc. in hOPCs significantly increased （P<0.001）. Compared with the 5%O₂ concentration， the expression of CXCR4 in cells was higher at the 2%O₂ concentration （P<0.000 1）. Flow cytometry analysis detection showed that the expression of CXCR4 increased significantly after hypoxia treatment （P<0.01）， and with the decrease of oxygen concentration， its expression level further increased （P<0.000 1）. Ordinary transcriptome sequencing analysis indicated that hypoxia treatment could activate the PI3K-Akt signaling pathway and the Axon guidance pathway. ConclusionHypoxia treatment can enhance the in vitro migration ability of hOPCs， and this effect is negatively correlated with the oxygen concentration. Its mechanism may be related to the up-regulation of the expression of genes such as HIF-1α and CXCR4， and the activation of the migration related signaling pathway including PI3K-Akt signaling pathway and axon guidance pathway.

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.

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.

Objective: To compare the changes in the concentration of relevant growth factors released from platelet-rich plasma (PRP) stored at -80℃ by cryopreservation and at 4℃ by refrigerated lyophilization over 2 years, aiming to provide a theoretical basis for prolonging PRP storage duration. Methods: PRP (n=15) was separated using a blood cell separator and stored under -80℃ cryopreservation (F-PRP group) and 4℃ refrigerated freeze-drying conditions (FD-PRP group). The contents of growth factors (PDGF-AA, PDGF-BB, EGF, TGF-β1, and VEGF) in both groups were measured by ELISA at 1, 3, 6, 9, 12 and 24 months. Results: PDGF-AA and VEGF maintained good stability in both groups for up to 24 months. PDGF-BB and TGF-β1 showed high stability in the first 12 months but their stability decreased gradually from 12th to 24th months. EGF demonstrated good stability in the first 6 months, and its stability gradually decreased from the 9th to 24th months. Comparing the F-PRP and FD-PRP groups, the concentrations of the five growth factors in the FD-PRP group were either not statistically different or higher than those in the F-PRP group at all time points. Specifically, the concentrations of EGF were significantly higher in the FD-PRP group at all time points. Conclusion: Both -80℃ freezing and 4℃ freeze-drying enable long-term preservation of PRP. Freeze-drying imposes less stringent storage requirements and facilitates growth factor compared to frozen storage.

With the increasing utilization of cancer therapy, the incidence of lung injury associated with these treatments continues to rise. The recognition of pulmonary toxicity related to cancer therapy has become increasingly critical, for which interstitial lung disease (ILD) is a common cause of mortality. Cancer therapy-related ILD (CT-ILD) can result from a variety of treatments including chemotherapy, targeted therapy, immune checkpoint inhibitors, antibody-drug conjugates, and radiotherapy. CT-ILD may progress rapidly and even be life-threatening; therefore, prompt diagnosis and timely treatment are crucial for effective management. This review aims to provide valuable information on the risk factors associated with CT-ILD; elucidate its underlying mechanisms; discuss its clinical features, imaging, and histological manifestations; and emphasize the clinical-related views of its diagnosis. In addition, this review provides an overview of grading, typing, and staging treatment strategies used for the management of CT-ILD.
Humans ; Lung Diseases, Interstitial/diagnosis* ; Neoplasms/therapy* ; Risk Factors ; Immune Checkpoint Inhibitors/adverse effects* ; Antineoplastic Agents/therapeutic use*