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.

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.

Objective: To establish a rapid, accurate, and decentralized workflow for bacterial whole-genome sequencing (WGS) and risk profiling within the shelf-life of platelet concentrates, and to characterize the species, virulence, antimicrobial resistance (AMR), and immune evasion mechanisms of co-existing bacteria in qualified platelet products, thereby providing a scientific basis for transfusion safety assessment. Methods: Three units of platelet concentrates, which tested negative by routine bacterial screening, were collected from the Chengdu Blood Center between May and June 2025. Samples were enriched at 37℃under six aerobic and nine anaerobic conditions for 7 days. Using a culturomics strategy, aliquots were plated for isolation on days 1, 3, 5, and 7 to obtain cultivable isolates, with negative culture controls included to exclude contamination. High-molecular-weight genomic DNA was extracted via mechanical grinding, purified, and size-selected. Sequencing libraries were constructed and sequenced on the G-seq500 single-molecule nanopore sequencing platform. Genomes were assembled using Flye and polished with NextPolish, with quality evaluated by BUSCO and CheckM. Taxonomic identification was performed using GTDB-Tk. Functional annotation and database comparisons were conducted to analyze virulence factors, AMR genes, and genes related to immune evasion and environmental adaptation. Results: Viable bacteria were successfully isolated from all three qualified platelet units within their shelf life. The isolates were identified as Bacillus albus, Niallia taxi, and Staphylococcus warneri. Nanopore sequencing generated 92 227-109 813 reads (totaling 680-758 Mb) with an N50 of 7 625-8 584 bp and Q20/Q30 scores of 97%/93%, respectively. All three genomes were assembled into complete circular chromosomes with 1-3 plasmids, achieving >93% completeness. Functional analysis revealed that B. albus carried multiple hemolysins, metalloproteases, and multidrug resistance genes, indicating the highest potential pathogenicity and AMR risk. S. warneri exhibited a typical multidrug resistance profile and regulatory network characteristic of coagulase-negative staphylococci, suggesting intermediate virulence. N. taxi harbored few canonical virulence factors and lacked functional AMR determinants, presenting a "low-virulence, low-resistance" profile. Notably, all three strains were enriched in genes encoding antimicrobial peptide resistance systems (e.g., dltABCD, mprF, GraRS, BceAB) and antioxidant enzymes, suggesting a strong capacity to withstand immune stress in the blood environment. Conclusion: Viable bacteria can be recovered from qualified platelet concentrates that test negative by routine screening. Nanopore WGS enables rapid strain-level identification and comprehensive risk profiling of virulence, resistance, and immune adaptation traits. The functional repertoires of these "co-existing" isolates range from environmental adaptation to potential pathogenicity, representing an underappreciated risk for transfusion-transmitted infections in susceptible recipients.

Objective To determine the molecular mechanism of Yuchang granule (YCG) against ulcerative colitis （UC） by network pharmacology-based approach combined with molecular docking. Methods TCMSP and HIT database were utilized to search the active components and potential targets of YCG. The effective targets of UC were obtained by GeneCards, CTD, and DisGeNET databases. Venn Diagram was exploited to receive common targets of YCG and UC. Network maps of the TCM of YCG-active component-common targets were constructed by the Cytoscape software to gain key active components. Protein-protein interaction （PPI） of common targets was constructed by the STRING database obtaining core common targets. The mechanism and therapeutic effects of YCG on UC were explored via gene ontology （GO） and the biological pathway （KEGG） enrichment analyses. Molecular docking technology was carried out to verify the combination of core active components with key common targets. Results 98 active components and 237 potential targets were sieved from YCG, and 1061 effective targets were screened from UC. 94 common targets of YCG and UC were regarded as potential therapeutic targets. Bioinformatics analysis revealed that quercetin, luteolin, β-quebrachol, stigmasterol, and kaempferol may be the potential candidate agents. Tumor necrosis factor （TNF）, serine/threonine-protein kinase （AKT1）, tumor protein p53 （TP53）, interleukin-6 （IL-6） and IL-1β could become potential therapeutic targets. KEGG showed pathways in cancer, AGE-RAGE signaling pathway in diabetic complications, TNF signaling pathway, and IL-17 signaling pathway might play an important role in YCG against UC. Molecular docking results showed that quercetin combined well with TNF, AKT1, and TP53. And stigmasterol did well with AKT1. Conclusion This study comprehensively illustrated the potential candidate agents, potential therapeutic targets, and pathways of YCG against UC. It also illustrated that YCG could act on multiple targets through multi-pathway treating UC.

ObjectiveThis study aims to investigate the effect of Liuwei Dihuangwan on the autophagy function in the hippocampus of senescence-accelerated mouse prone 8 （SAMP8） by regulating the expression of glycoprotein non-metastatic melanoma protein B （GPNMB）. Furthermore， it is designed to explore the mechanism of the method of tonifying the kidneys and replenishing essence in the treatment of Alzheimer's disease （AD）. MethodsIn experiment 1， 24 5-month-old SAMP8 mice were randomly and equally divided into the model group， and the low-， middle- and high-dose（0.59，1.18，2.36 g·kg^-1） Liuwei Dihuangwan groups. At the same time， six 5-month-old senescence accelerated mouse resistant 1 （SAMR1） mice were used as the control group. The learning and memory ability was evaluated through novel object recognition experiment. Serum cortisol （Cort）， adrenocorticotropic hormone （ACTH） and urine 17-hydroxycorticosteroid （17-OHCS） levels were detected by enzyme-linked immunosorbent assay （ELISA）. The ultrastructure of hippocampal neurons was observed by transmission electron microscope （TEM）， and the expression levels of hippocampal GPNMB， a disintegrin and metalloproteinase 10 （ADAM10） and autophagy-related proteins were detected by Western blot. In experiment 2， 18 SAMP8 mice were randomly and equally divided into the model group， vector control group （Vector）， and GPNMB overexpression group （GPNMB^OE）. Lentiviral vectors were stereotactically injected into the brain （2 μL per side in the GPNMB^OE group）. Western blot was used to detect the expression of the above target proteins in the hippocampus； In Experiment 3， 24 SAMP8 mice were randomly and equally divided into the model group， Liuwei Dihuangwan group， Liuwei Dihuangwan+negative control （NC） group， and Liuwei Dihuangwan+GPNMB silencing group （shGPNMB）. Before drug treatment， the Liuwei Dihuangwan+NC group and the Liuwei Dihuangwan+shGPNMB group were injected with negative control and GPNMB silencing lentivirus， respectively. Western blot was used to detect the expression of the above target proteins in the hippocampus. ResultsThe novel object discrimination index of mice in the model group was significantly lower than that of mice in the control group （P<0.01）. The novel object discrimination index of mice in the medium- and high-dose Liuwei Dihuangwan groups was significantly higher than that of mice in the model group （P<0.01）. Aggregated autolysosomes were observed in the normal hippocampus tissue by TEM. In the model group， mitochondria were dominant， and no typical characteristic autophagosomes were observed. In the low- and medium-dose Liuwei Dihuangwan groups， a small number of autolysosomes and autophagosomes with double-membrane structures were observed. In the high-dose Liuwei Dihuangwan group， the number of autophagosomes and autolysosomes was greater than that in the low- and medium-dose groups. The results of ELISA and Western blot showed that compared with the control group， the levels of serum Cort， ACTH， and urine 17-OHCS in the model group were substantially increased， while the expression of hippocampal ADAM10， Beclin1， and microtubule associated-protein light chain 3-Ⅱ/Ⅰ （LC3 Ⅱ/Ⅰ） was significantly decreased. The expression of GPNMB and ubiquitin binding protein p62 was significantly increased （P<0.05， P<0.01）. Compared with the model group， the serum Cort and ACTH levels in the low-， medium-， and high-dose Liuwei Dihuangwan groups were significantly reduced， while only the urine 17-OHCS level in the high-dose group was significantly reduced. The hippocampal GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ expression levels in the medium-， and high-dose groups of Liuwei Dihuangwan were significantly increased compared to the model group， whereas the expression of p62 was significantly reduced （P<0.01）. The above indicators showed a progressive trend among the three groups. Compared with the model group， the GPNMB^OE group showed a significant increase in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ expression， and a significant decrease in p62 expression （P<0.01）. Compared with the model group， the expression of GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ in the hippocampus of the Liuwei Dihuangwan group significantly increased， while the expression of p62 significantly decreased （P<0.01）. Compared with the Liuwei Dihuangwan group， the Liuwei Dihuangwan+shGPNMB group showed a significant decrease in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ， and a significant increase in p62 expression （P<0.01）. ConclusionLiuwei Dihuangwan can enhance hippocampal autophagy function and improve AD by upregulating GPNMB expression.

Objective To investigate the effects of crocetin on radiosensitivity of lung adenocarcinoma and its potential mechanisms using a nude mouse xenograft model established with A549 lung adenocarcinoma cells. Methods Forty mice bearing lung adenocarcinoma were randomly divided into four groups: control group, crocetin group, radiotherapy group, and crocetin combined with radiotherapy group, and received the corresponding interventions. After 14 days of treatment, all mice were sacrificed and tumor tissues were excised. Tumor weight was measured in each group and the tumor inhibition rate was calculated. Apoptosis of tumor cells was analyzed by flow cytometry. Immunohistochemistry and RT-qPCR were used to detect and compare the expression of genes encoding hypoxia-inducible factor (HIF-1α) and B-cell lymphoma-2 (BCL-2). Results The mean tumor weight of mice in the crocetin combined with radiotherapy group was significantly lower than that in the radiotherapy group (P < 0.05), and the tumor inhibition rate of the crocetin combined with radiotherapy group was 34.07%. The mean tumor cell apoptosis rate in the crocetin combined with radiotherapy group was significantly higher than that in the radiotherapy group (P < 0.05). HIF-1α expression was significantly lower in the crocetin combined with radiotherapy group than in the radiotherapy group (P = 0.001). Although BCL-2 expression in the crocetin combined with radiotherapy group was lower than that in the radiotherapy group, the difference was not statistically significant (P = 0.894). The expression levels of mRNAs of genes encoding HIF-1α and BCL-2 in the crocetin combined with radiotherapy group were significantly lower than those in the radiotherapy group (P < 0.05). Conclusion Crocetin in combination with radiotherapy significantly enhanced the inhibitory effect of radiotherapy on tumor growth in mice bearing lung adenocarcinoma and increased the tumor inhibition rate. The mechanisms may involve the alleviation of radiotherapy-induced overexpression of HIF-1α, thereby improving hypoxic conditions in tumor tissues, as well as suppression of the anti-apoptotic gene BCL-2 to enhance radiotherapy-induced apoptosis of lung adenocarcinoma cells.

Artificial intelligence （AI） health monitoring devices use AI technology and non-invasive sensors to collect individual data， compare it with big data， and provide real-time monitoring and data analysis of users’ physiological and psychological health， so as to provide personalized health recommendations and health risk warnings. AI health monitoring devices greatly enhance individuals’ self-health management abilities and improve their quality of life through round-the-clock uninterrupted monitoring and tracking. However， they also harbor a series of ethical risks， such as user privacy breaches， the digitization of physical sensations， and potential impacts on human subjectivity. Therefore， under the guidance of the principles of privacy and data protection， inclusiveness and fairness， transparency， and explainability， relevant departments should protect personal privacy with perfect laws and regulations， reduce algorithmic bias， ensure disclosure and transparency to promote user understanding， while adhering to the people-oriented principle approach and conducting responsible research and development of interpretable algorithm models for AI health monitoring devices.

Objective To analyze the trend of global cellulitis disease burden from 1990 to 2019, and to provide a theoretical basis for the prevention and control of cellulitis disease. Methods The Global Burden of Disease 2021 (GBD2021) data were collected, and data on the incidence, mortality, and disability-adjusted life year (DALY) of cellulitis were analyzed for each country worldwide. The estimated annual percentage change (EAPC) and age-standardized rate (ASR) were used to estimate the trend change of cellulitis from 1990 to 2021. Results The global burden of cellulitis increased significantly in 2021, with 55.96 million cases, 28.9 million deaths and 876.1 million DALYs, respectively. Incidence and mortality rates were generally higher in males than in females. The incidence and DALYs were higher in high SDI regions, with the highest burden observed in South Asia. In contrast, East Asia exhibited the lowest burden and demonstrated a declining trend. There were significant differences between countries, with India having the highest prevalence, the United States having the highest incidence, and Bahrain having the fastest growing rate.In 2021, China had the lowest age-standardised incidence of cellulitis in the world and the fastest declining age-standardised incidence and age-standardised DALYs. Conclusion The global disease burden of cellulitis is increasing from 1990-2021, and cellulitis remains an an important global public health problem. Targeted preventive meausres should be taken in areas with different economical levels. Men, middle-aged and elderly people, and newborns are the key groups in need of attention and health education.

Objective: To investigate the status and influencing factors of platelet bacterial contamination in China, and to provide theoretical support for relevant policies in blood collection and transfusion institutions. Methods: A meta-analysis by systematically searching studies on platelet bacterial contamination in China published between 1998 and 2023 was conducted. Data analysis was performed using R4.4 software to combine studies that met the inclusion criteria. Results: Twenty-three studies were included after screening. The combined analysis showed that the overall contamination rate of platelets in China was 0.18% (95% CI: 0.12%-0.24%). The contamination rate of manually condensed platelets was significantly higher than that of apheresis platelet concentrates (0.28% vs 0.17%, P<0.01). No significant difference in platelet contamination rates was found between eastern and central regions (0.21% vs 0.15%, P>0.01). The contamination rate of aerobic bacteria was higher than that of anaerobic bacteria (0.11% vs 0.06%, P<0.01). Publication bias analysis indicated robust results, and sensitivity analysis showed minimal impact of excluding individual studies on the overall conclusion. Conclusion: Although the platelet contamination rate in China is generally low, significant differences exist across collection methods and regions.

Primary ciliary dyskinesia (PCD) is a genetically heterogeneous disease characterized by structural or functional abnormalities of motile cilia. It often presents clinically with recurrent respiratory infections, situs inversus, hydrocephalus, and infertility. Currently, there is no clinical treatment to directly restore ciliary motility in PCD patients.In recent years, researchers have explored gene therapy methods such as gene replacement, gene editing, and RNA replacement in vitro and in mouse models, offering potential new strategies for PCD treatment. This paper comprehensively reviews the current status of PCD gene therapy research, evaluates the potential of different gene therapies, and provides an outlook on the future treatment directions for this disease.