Based on spleen deficiency-phlegm dampness as the core pathogenesis of obesity， and integrating recent advances in modern medicine regarding the key role of immune inflammation in obesity， this paper proposes a multidimensional pathogenic network of "obesity-spleen deficiency-phlegm dampness-immune imbalance". Various traditional Chinese medicine （TCM） herbs that strengthen the spleen， regulate qi， and resolve phlegm and dampness can treat obesity by improving spleen-stomach transport and transformation， promoting water-damp metabolism， and regulating immune homeostasis. This highlights immune inflammation as an important entry point to elucidate the TCM concepts of "spleen deficiency-phlegm dampness" and the therapeutic principle of "strengthening the spleen and eliminating dampness to treat obesity". By systematically analyzing the intrinsic connection between "spleen deficiency generating dampness， internal accumulation of phlegm dampness" and immune dysregulation in obesity， this paper aims to provide theoretical support for TCM treatment of obesity based on dampness.

Objective: To analyze the epidemiological characteristics of pulmonary tuberculosis (PTB) among college students in Yangzhou from 2020 to 2024, so as to provide a scientific basis for developing prevention and control strategies. Methods: An epidemiological investigation was conducted among 162 college students with PTB, and 7 134 of their contacts were screened. Data were obtained from the tuberculosis information management system and on campus screening records. Using descriptive epidemiological methods, trends in incidence, seasonal distribution, and bacteriological characteristics were analyzed. Results: From 2020 to 2024, the annual average incidence of pulmonary tuberculosis among college students in Yangzhou was 29.42 per 100 000, showing an overall fluctuating downward trend ( χ 2=12.36, P <0.01). Cases were mainly concentrated in summer and autumn, with the highest proportion in autumn (41.36%, 67/162), followed by summer (23.46%, 38/162). The proportion of etiologically positive cases increased from 37.21% in 2020 to 71.43% in 2024; among positive cases, the proportion of latent tuberculosis infection (LTBI) decreased from 66.67% (10/15) to 26.67% (4/15). The etiological positive rate was higher in females than in males ( χ 2= 11.76 , P <0.01). Comparison of screening methods showed that among index cases, the LTBI detection rate of the recombinant Mycobacterium tuberculosis fusion protein skin test (C-TST) was higher than that of the tuberculin skin test (TST), but the difference was not statistically significant ( χ 2=0.65, P =0.42); among close contacts, the detection rate of TST was higher than that of C-TST (15.1%,10.1%; χ 2=5.23, P <0.05). Conclusion From 2020 to 2024, the annual average incidence of pulmonary tuberculosis among college students in Yangzhou showed an overall fluctuating downward trend, with differences in TB infection screening methods and gender.

High-throughput sequencing-based high-throughput screening （HTS²） technology， as a new advancement in the field of high-throughput biotechnology， is the world's first technology to integrate high-throughput sequencing into large-scale drug screening and target discovery. The artificially designed DNA probes were bound to the undetermined mRNAs of thousands of genes in cell lysates， and then the probes were ligated with ligases. The large-scale simultaneous detection of gene expression changes in thousands of drug-treated cell samples was performed using barcoding， automated operating platforms， and high-throughput sequencers. This technology enables high-throughput identification of drugs that significantly perturb the gene expression profiles characteristic of diseases. It can also take gene expression signature as the readout and exert great high-throughput advantages in the screening of multi-drug， multi-component， and multi-target drugs， as well as the research on complex mechanisms. Therefore， it is particularly suitable for elucidating the multi-target mechanisms of traditional Chinese medicine and identifying its multi-effective components. Its main technical advantages include high throughput， automation， and low cost. In recent years， HTS² technology has yielded important achievements in the elucidation of the mechanism of action of traditional Chinese medicine formulas， the scientific connotation analysis of the regional characteristics of traditional Chinese medicine， the targeted isolation of active compounds of traditional Chinese medicine， and the discovery of novel pharmacological functions of monomeric compounds of traditional Chinese medicine. In the era of artificial intelligence， HTS² technology will serve as a powerful tool for generating high-quality， original big data of traditional Chinese medicine， providing core data support and promoting AI-driven traditional Chinese medicine research. Ultimately， HTS² technology offers new strategies and critical data support for deeply analyzing the scientific connotation of traditional Chinese medicine and discovering novel traditional Chinese medicine-based drugs， thereby accelerating the modernization and internationalization of traditional Chinese medicine in China.

ObjectiveTo explore the mechanism by which Qijia Rougan decoction ameliorates liver fibrosis through amino acid/fatty acid metabolic reprogramming and phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） pathway， based on the miRNA-mRNA regulatory network and the interaction between metabolism and signaling pathways. MethodsSprague-Dawley （SD） rats were randomized into four groups （n=8）： control， model， and low-dose and high-dose （7.0， 28.0 g·kg^-1·d^-1， respectively） Qijia Rougan decoction. Liver fibrosis was induced by subcutaneous injection of carbon tetrachloride （CCl₄）. From week 9， drug intervention was implemented for 7 weeks. After the final administration， the pathological changes in the liver were evaluated through hematoxylin-eosin （HE） and picrosirius red （PSR） staining. An automated biochemical analyzer was used to measure the serum levels of biochemical indicators， including alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， alkaline phosphatase （ALP）， total bile acid （TBA）， albumin （ALB）， and cholesterol （TC）. High-throughput miRNA sequencing was performed to identify differentially expressed miRNAs （DemiRs） during liver fibrosis. A miRNA-mRNA interaction network was constructed to identify key targets， which were then subjected to GO and KEGG enrichment analyses. The expression levels of selected DemiRs were validated by Real-time PCR. ResultsCompared with the control group， the model group showed marked hepatic lobular necrosis， increased collagen deposition， significant fibrosis， elevated serum levels of ALT， AST， ALP， and TBA （P<0.01）， and declined levels of ALB and TC （P<0.01）. Compared with the model group， Qijia Rougan decoction treatment reduced hepatic necrosis， collagen accumulation， and fibrosis， lowered the serum levels of ALT， AST， ALP， and TBA （P<0.01）， and raised the levels of ALB and TC （P<0.01）. Integrated miRNA-seq and RNA-seq analysis identified 31 DemiRs （6 upregulated and 25 downregulated） and 498 targets. The expression trends of four selected DemiRs， including rno-miRNA-376b-3p， were consistent with sequencing results （R²=0.93）. Functional annotation revealed that top 20 upregulated targets were enriched in amino acid and fatty acid metabolism， while top 20 downregulated targets were significantly associated with the PI3K/Akt signaling pathway and cancer progression. ConclusionQijia Rougan decoction alleviates liver fibrosis by reconstructing the miRNA-mRNA regulatory network， promoting metabolic reprogramming， and inhibiting the PI3K/Akt signaling pathway. These findings provide mechanism evidence supporting the multi-targeted antifibrotic effects of traditional Chinese medicine compound formulas.

Objective: To evaluate the methodological quality and reporting quality of clinical practice guidelines or expert consensus on blood transfusion and blood use (BTBU) in China (hereinafter referred to as "guidelines/consensus"), providing reference for the development and updating of future BTBU guidelines/consensus. Methods: A systematic search was conducted in Chinese databases such as China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP Data-base, relevant guideline release platforms, and professional association websites. BTBU-related guidelines/consensus published between January 2006 and December 2025 were included. According to the inclusion and exclusion criteria, after completing literature screening and data extraction, three evaluators independently assessed the quality of the included literature using the Scientificity, Transparency, and Applicability of Guidelines Rating Tool (STAR), the Appraisal of Guidelines for Research and Evaluation Ⅱ (AGREE Ⅱ), and the International Practice Guideline Reporting Standards (RIGHT). Results: A total of 29 documents were included, including 5 guidelines, 22 consensus statements, and 2 protocols. The results of the STAR assessment showed that the total score was (21.7±8.8)%. The domain score ratios for registration, research protocol, funding, working group, conflict of interest, clinical question, evidence, consensus method, recommendation, accessibility and other domains were (2.2±12.1)%, 0, (36.7±25.1)%, (18.3±7.6)%, (19.2±15.3)%, (16.6±23.1)%, (15.1±6.3)%, (9.6±21.2)%, (54.3±18.4)%, (31.7±10.4)% and (10.3±31.0)%, respectively. For the AGREE Ⅱ assessment, the methodological quality of 26 articles was rated Grade B and 3 articles Grade C. The results of the RIGHT assessment indicated that the overall reporting rate of all guidelines/consensuses was (65.3±4.0)%. Conclusion: The methodological and reporting quality of current expert guidelines/consensus on BTBU in China still need improvement, and guidelines and consensus should be strictly formulated and standardized according to the standards of STAR, AGREE II and RIGHT.

Utilizing CiteSpace and VOSviewer， a bibliometric analysis was conducted on 1，496 articles from the China National Knowledge Infrastructure， Chinese Science and Technology periodical database， Wanfang data， and the Web of Science database spanning 2006 to 2025， systematically revealing the evolutionary patterns of knowledge regarding doctor‐patient shared decision‐making （SDM） in the field of chronic disease management. The research indicated that the number of publications at home and abroad displayed an overall upward trend， yet their development paths differed significantly. International research has formed a “core-periphery” cooperation network， with research hotspots focusing on the improvement of decision-making quality， optimization of decision-making aids， application in primary care settings， and ethical issues in decision-making. Domestic research， driven by policies， developed rapidly and paid more attention to coverage improvement and cultural adaptation， but notable gaps remained in cross-institutional cooperation and tool localization. Currently， China’s practice still encountered multiple challenges， including restricted patients’ participation willingness due to “family-oriented” cultural values， inadequate localization of decision-making aids， and imperfect decision-making support systems in primary healthcare institutions. On this basis， this paper put forward localized suggestions from three dimensions， including cultural adaptation， technological innovation， and institutional coordination. Through multi-dimensional strategies such as advocating for constructing a family-empowered decision-making model， developing decision-making aids integrated with the dialectical logic of traditional Chinese medicine， and promoting the linkage between SDM implementation and the reform of medical insurance payment methods， it was expected to connect international experience with China’s practice. This aimed to provide references for building a chronic disease decision-making model with Chinese characteristics and contribute to the “patient-centered” medical transformation.

ObjectiveTo investigate the mechanism of Hei Xiaoyaosan （HXS） in ameliorating cognitive impairment in the rat model of Alzheimer's disease （AD） by regulating the adenosine 5'-monophosphate-activated protein kinase （AMPK）/sterol regulatory element-binding protein 2 （SREBP2）/proprotein convertase subtilisin/kexin type 9 （PCSK9）/low-density lipoprotein receptor-related protein 1 （LRP-1） signaling pathway to clear amyloid-β （Aβ） from the peripheral circulation. MethodsNinety 8-week-old specific pathogen-free （SPF）-grade male Sprague-Dawley （SD） rats were acclimatized for 1 week. After acclimatization， 10 rats were randomly selected as the blank control group， and the remaining 80 rats were prepared for surgical modeling. Among the 80 rats for modeling， 70 were anesthetized and injected with 1 μL of amyloid-β_1-42 （Aβ_1-42） solution into the bilateral hippocampal CA1 region for the modeling of AD， and the remaining 10 were assigned to the sham operation group， which received an injection of 1 μL normal saline at the same anatomical site. The successfully modeled rats were randomly assigned into 6 groups （n=10 per group）： a model group， a donepezil hydrochloride group， an acadesine （AICAR， an AMPK agonist） group， and high-， medium-， and low-dose HXS groups. After 42 consecutive days of administration intervention， the Morris water maze test and T-maze test were performed to evaluate the learning and memory abilities of rats. Fluoro-Jade B （FJB） staining was conducted to observe pathological changes of neurons in the rat hippocampus， and thioflavin S staining to quantify the area of Aβ deposition in the hippocampal region. Immunofluorescence double staining （IF-DS） was performed to detect the expression of LRP-1 and Aβ signals in the liver tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of Aβ_1-42 and soluble LRP-1 （sLRP-1） in the serum. Western blot was performed to determine the protein levels of AMPK， phosphorylated AMPK （p-AMPK）， SREBP2， PCSK9， and LRP-1 in the liver tissue. Real time polymerase chain reaction（Real-time PCR） was adopted to assess the mRNA levels of AMPK， SREBP2， PCSK9， and LRP-1 in the liver tissue. ResultsCompared with the blank control group， the model group showed increased total swimming distance on day 6 and path length in the target quadrant on day 7 （P<0.01）， a decreased correct alternation rate in the T-maze test （P<0.01）， disarrangement of hippocampal neurons， increased FJB-positive cells （P<0.01）， enlarged area of Aβ deposition （P<0.01）. reduced LRP-1 fluorescence signals and enhanced Aβ fluorescence signals in the liver tissue （P<0.01）， elevated serum level of Aβ_1-42， declined serum level of sLRP-1 （P<0.01）， downregulated protein levels of p-AMPK and LRP-1 as well as mRNA levels of AMPK and LRP-1， and upregulated protein and mRNA levels of SREBP2 and PCSK9 in the liver tissue （P<0.01）. Compared with the model group， the high-dose HXS group， donepezil hydrochloride group， and AICAR group exhibited reduced total swimming distance and target quadrant path length （P<0.05， P<0.01）， an increased correct alternation rate in the T-maze test （P<0.05）， decreased FJB-positive cells （P<0.01）， reduced Aβ deposition （P<0.01） in the hippocampal tissue， enhanced LRP-1 signals and weakened Aβ signals in the liver tissue （P<0.01）， a declined serum level of Aβ_1-42 and an elevated serum level of sLRP-1 （P<0.01）， upregulated protein levels of p-AMPK and LRP-1 as well as mRNA levels of AMPK and LRP-1， and downregulated protein and mRNA levels of SREBP2 and PCSK9 in the liver tissue （P<0.01）. ConclusionHei Xiaoyaosan can regulate the AMPK/SREBP2/PCSK9/LRP-1 signaling pathway to enhance the clearance of peripheral Aβ by the liver tissue and reduce Aβ deposition in the brain， thereby improving the learning and memory abilities of AD rats.

ObjectiveTo investigate the role and mechanism of Hei Xiaoyaosan in regulating asparaginyl endopeptidase （AEP） to inhibit tau protein （tau） phosphorylation， amyloid-beta protein （Aβ） deposition， and neuroinflammation in the prevention and treatment of Alzheimer's disease （AD）. MethodsNinety SPF-grade SD male rats of 8 weeks old were selected and randomly grouped as follows： 10 rats in the blank group， 10 rats in the sham group （bilateral hippocampus injected with 1 μL normal saline）， and 70 rats in the modeling group （bilateral hippocampus injected with 1 μL Aβ_1-42 solution for the modeling of AD）. Fifty successfully modeled rats were selected and randomly assigned into the model， donepezil hydrochloride （positive control， 0.45 mg·kg^-1）， and high-， medium-， and low-dose （15.30， 7.65， and 3.82 g·kg^-1， respectively） Hei Xiaoyaosan groups. Rats were administrated with corresponding agents by gavage once a day for 42 days. Morris water maze and Y maze tests were carried out to assess the cognitive abilities of rats. Hematoxylin-eosin （HE） staining was employed to observe morphological changes in hippocampal neurons， and immunohistochemistry （IHC） was employed to assess phosphorylation （p）-tau and Aβ expression in the hippocampal tissue of rats. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of interleukin-1 beta （IL-1β）， interleukin-18 （IL-18）， and Aβ_1-42 in the hippocampal tissue. Western blot was employed to determine the protein levels of AEP， tau， phosphorylated tau （p-tau）， α-Syn （α-Syn）， phosphorylated α-Syn （p-α-Syn）， Toll-like receptor 2 （TLR2）， and NOD-like receptor thermal protein domain associated protein 3 （NLRP3）. Real time polymerase chain reaction （Real-time PCR） was employed to determine the mRNA levels of AEP， tau， α-Syn， TLR2， and NLRP3. ResultsCompared with the blank group， the model group showed prolonged escape latency， a decreased percentage of time spent in the platform quadrant， and a decreased alternation rate （P<0.01）， a reduced number， shrinkage， and increased vacuoles of hippocampal neurons， increased expression of p-tau and Aβ in the hippocampus （P<0.01）， elevated levels of IL-1β， IL-18， and Aβ_1-42， up-regulated protein and mRNA levels of AEP， tau， α-Syn， TLR2， and NLRP3， and up-regulated protein levels of p-tau and p-α-Syn （P<0.01）. Compared with the model group， the positive control group and the high-dose Hei Xiaoyaosan group exhibited shortened escape latency （P<0.01）， an increased percentage of retention time in the target quadrant， an increased alternation response rate （P<0.05， P<0.01）， alleviated neuronal shrinkage， regular morphology and arrangement of neurons in the hippocampal tissue， lowered levels of p-tau and Aβ in the hippocampal tissue （P<0.05， P<0.01）， declined levels of IL-1β， IL-18， and Aβ_1-42， downregulated mRNA and protein levels of AEP， tau， α-Syn， TLR2， and NLRP3， and downregulated protein levels of p-tau and p-α-Syn （P<0.05， P<0.01）. ConclusionHei Xiaoyaosan can protect hippocampal neurons and ameliorate cognitive impairment in the rat model of AD. Specifically， it may inhibit AEP to regulate tau phosphorylation， Aβ deposition， and neuroinflammation.

ObjectiveTo investigate the effects of Hei Xiaoyaosan on neuroinflammation in APP/PS1 mice and decipher the mechanism based on the C-X3-C chemokine ligand 1 （CX3CL1）-CX3CL1 receptor 1 （CX3CR1） signaling axis. MethodsSixty 16-week-old male APP/PS1 mice were selected and acclimatized for one week， and they were then randomly allocated into a model group， a CX3CL1 group （bilateral hippocampal injection of CX3CL1 at 0.5 g·L^-1）， and high-， medium-， and low-dose （22.10， 11.05， and 5.53 g·kg^-1， respectively） Hei Xiaoyaosan groups， with 12 mice in each group. Twelve age-matched male C57BL/6J mice served as the blank group （bilateral hippocampal injection of an equal volume of PBS）. The high-， medium-， and low-dose Hei Xiaoyaosan groups received corresponding drugs via gavage， while the blank group received an equal volume of normal saline， with an intervention period of 90 days. Morris water maze was used to assess learning and memory abilities. Nissl staining was performed to observe the pathological changes in neurons of the hippocampal CA1 region. Immunohistochemistry was adopted to detect amyloid-β_1-42 （Aβ_1-42） deposition in the hippocampal CA1 region. The immunofluorescence assay was employed to detect the expression of M1 and M2 microglial markers， including cluster of differentiation 86 （CD86）/ionized calcium-binding adapter molecule 1 （Iba-1） and arginase-1 （Arg1）/Iba1. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of interleukin-8 （IL-8） and interleukin-13 （IL-13） in the hippocampal tissue. Western blot was employed to determine the protein levels of CX3CL1， CX3CR1， CREB-binding protein （CBP）， cyclic AMP response element-binding protein （CREB）， phosphorylated （p）-CREB， and brain-derived neurotrophic factor （BDNF） in the hippocampal tissue. ResultsCompared with the blank group， the model group exhibited prolonged escape latency on day 5 and a reduced swimming distance in the target quadrant （P<0.01）， disarrangement of hippocampal neurons， with a reduced number of cells and uneven Nissl body staining， increased CD86/Iba1 expression， decreased Arg1/Iba1 expression （P<0.01）， enhanced Aβ expression （P<0.01）， an elevated IL-8 level and a declined IL-13 level （P<0.01）， and downregulated protein levels of CX3CL1， CX3CR1， CBP， p-CREB， and BDNF （P<0.01）. Compared with the model group， all treatment groups showed shortened escape latency on day 5 and an increased swimming distance in the target quadrant （P<0.05， P<0.01）， regular arrangement of neurons with an increased number and increased Nissl bodies， reduced CD86/Iba1 expression， increased Arg1/Iba1 and decreased Aβ expression （P<0.01）， and a declined IL-8 level and an elevated IL-13 level （P<0.05， P<0.01）. In the CX3CL1 group and the high- and medium-dose Hei Xiaoyaosan groups， the relative expression levels of CX3CL1， CX3CR1， CBP， and p-CREB were upregulated （P<0.01）. In the low-dose Hei Xiaoyaosan group， the relative expression levels of CX3CL1， CX3CR1， CBP， p-CREB/CREB， and BDNF were upregulated （P<0.05， P<0.01）. ConclusionHei Xiaoyaosan can improve learning and cognitive abilities in APP/PS1 mice. Specifically， it may regulate the CX3CL1/CX3CR1 signaling axis to activate the CREB/BDNF signaling pathway for the subsequent release of BDNF， modulation of microglial polarization， reduction of inflammatory cytokine levels， and attenuation of Aβ deposition.

ObjectiveTo investigate the effect and mechanism of Hei Xiaoyaosan in preventing and treating Alzheimer's disease （AD） by activating autophagy through regulating the adenosine monophosphate-activated protein kinase （AMPK）/UNC-51 like autophagy activating kinase 1 （ULK1） signaling pathway. MethodsNinety 8-week-old male SPF-grade SD rats were selected and randomized into two groups： a blank control group （n=10） and a modeling group （n=80）. From the modeling group， 10 rats were randomly assigned as a sham group （bilateral hippocampal injection of 1 μL normal saline）， while the remaining 70 rats were injected with 1 μL Aβ_1-42 solution bilaterally into the hippocampus to replicate the AD model. The Morris water maze test was conducted to screen the successfully modeled rats， which were then randomly allocated to the model， donepezil hydrochloride， 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside （AICAR， an AMPK agonist）， and high-， medium-， and low-dose Hei Xiaoyaosan groups， with 10 rats per group. After 42 days of drug intervention， the Morris water maze and open field tests were conducted to assess learning and memory abilities and motor function. Pathological changes in the hippocampal tissue were observed by Nissl staining， and autophagy-related pathological damage was examined via transmission electron microscopy （TEM）. The expression of LC3 in the hippocampus was observed by immunofluorescence staining. The protein levels of AMPK， phosphorylate （p）-AMPK， ULK1， p-ULK1， p62， and autophagy related 7 （Atg7） were determined by Western blot， while the mRNA levels of AMPK and ULK1 were measured by Real-time polymerase chain reaction （Real-time PCR）. ResultsCompared with the blank control group， the model group showed increased escape latency （P<0.01） and decreased platform crossings （P<0.01） on day 6 in the water maze test， reduced total distance traveled and average speed in the open field test （P<0.01）， disarranged neurons with Nissl body loss and evident autophagic damage， weakened LC3 fluorescence signal （P<0.01）， downregulated protein levels of p-AMPK， p-ULK1， and Atg7 and mRNA levels of AMPK and ULK1 in the hippocampus （P<0.01）， and upregulated protein level of p62 （P<0.01）. Compared with the model group， the positive drug group， high-dose Hei Xiaoyaosan group， and AICAR group showed decreased escape latency （P<0.05， P<0.01） and increased platform crossings （P<0.01） on day 6， and increased total distance traveled and average speed in the open field test （P<0.05）. The positive drug group， high- and medium-dose Hei Xiaoyaosan groups， and the AICAR group showed alleviated cellular structural damage， regular neuronal arrangement， increased Nissl bodies， and orderly distribution of autophagosomes. Furthermore， the LC3 fluorescence intensity was enhanced in the positive drug group， high- and medium-dose Hei Xiaoyaosan groups， and the AICAR group （P<0.01）. The positive drug group， high-dose Hei Xiaoyaosan group， and the AICAR group exhibited upregulated protein and mRNA levels of p-AMPK and p-ULK1 （P<0.05， P<0.01）， upregulated protein level of Atg7 （P<0.05， P<0.01）， and downregulated protein level of p62 （P<0.01）. ConclusionHei Xiaoyaosan can improve learning and memory abilities and alleviate pathological status in the rat model of AD by regulating the AMPK/ULK1 signaling pathway， enhancing cellular autophagy， and repairing damaged nerve cells.