ObjectiveBased on the established characteristic profiles， quantitative analysis of multiple components， and chemometric analysis of Taraxacum mongolicum， the quality of different T. mongolicum germplasms was evaluated at the chemical level， thereby providing a reference for the screening of high-quality germplasms and the rational utilization of wild resources. MethodsAn ultra-performance liquid chromatography （UPLC） was employed to establish characteristic profiles. Principal component analysis （PCA） and partial least squares-discriminant analysis （PLS-DA） were then adopted to screen and comprehensively rank marker compounds. ResultsThe UPLC fingerprint of T. mongolicum germplasm identified 13 chromatographic peaks corresponding to gallic acid， coumaric acid， neochlorogenic acid， monocaffeoyltartaric acid， chlorogenic acid， cryptochlorogenic acid， caffeic acid， p-coumaric acid， cichoric acid， luteoloside， isochlorogenic acid B， isochlorogenic acid A， and isochlorogenic acid C. Combined with chemometric analysis such as PCA and PLS-DA， eight core markers （cichoric acid， luteoloside， cryptochlorogenic acid， isochlorogenic acid B， chlorogenic acid， caffeic acid， isochlorogenic acid C， and isochlorogenic acid A） were screened for distinguishing wild and cultivated germplasms. Additionally， eight core markers （cichoric acid， caffeic acid， luteoloside， chlorogenic acid， cryptochlorogenic acid， isochlorogenic acid A， monocaffeoyltartaric acid， and neochlorogenic acid） were selected for the evaluation and screening of different T. mongolicum germplasms. ConclusionThis study establishes a UPLC analysis method capable of simultaneously determining 13 characteristic components in T. mongolicum， such as cichoric acid and chlorogenic acid， as well as their precursor compound contents in the biosynthetic pathway. Based on the above methods， three T. mongolicum germplasms （PGY-004， PGY-009， and PGY-010） with promising medicinal potential are selected for subsequent research on variety breeding. The present study provides a reference for quality control of Taraxacum mongolicum， germplasm screening， and the rational development and utilization of wild resources.

ObjectiveTo analyze the current status, hotspot and development trends of rehabilitation technologies for post-stroke dysphagia (PSD). MethodsLiteratures related to rehabilitation technologies for PSD were retrieved from CNKI, VIP and Web of Science Core Collection from inception to July, 2025. Visualization analysis was conducted using CiteSpace 6.3.R1 and VOSviewer 1.2.20. ResultsA total of 1 265 articles were included, consisting of 794 Chinese and 471 English publications. The annual volume of Chinese literature peaked in 2019 (74 articles) and English literature peaked in 2022 (61 articles). Research hotspots included low-frequency surface neuromuscular electrical stimulation, repetitive transcranial magnetic stimulation, surface electromyography biofeedback and transcranial direct current stimulation. Keyword clustering and timeline analysis indicated that researches evolved from early traditional rehabilitation methods to the diversified and integrated application of combined rehabilitation technologies. ConclusionResearch on rehabilitation technologies for PSD is developing rapidly. Future efforts should focus on researches of multi-technology integration, individualized treatment protocols and long-term efficacy assessments.

ObjectiveTo analyze the current status, hotspot and development trends of rehabilitation technologies for post-stroke dysphagia (PSD). MethodsLiteratures related to rehabilitation technologies for PSD were retrieved from CNKI, VIP and Web of Science Core Collection from inception to July, 2025. Visualization analysis was conducted using CiteSpace 6.3.R1 and VOSviewer 1.2.20. ResultsA total of 1 265 articles were included, consisting of 794 Chinese and 471 English publications. The annual volume of Chinese literature peaked in 2019 (74 articles) and English literature peaked in 2022 (61 articles). Research hotspots included low-frequency surface neuromuscular electrical stimulation, repetitive transcranial magnetic stimulation, surface electromyography biofeedback and transcranial direct current stimulation. Keyword clustering and timeline analysis indicated that researches evolved from early traditional rehabilitation methods to the diversified and integrated application of combined rehabilitation technologies. ConclusionResearch on rehabilitation technologies for PSD is developing rapidly. Future efforts should focus on researches of multi-technology integration, individualized treatment protocols and long-term efficacy assessments.

ObjectiveTo analyze the current status, hotspot and development trends of rehabilitation technologies for post-stroke dysphagia (PSD). MethodsLiteratures related to rehabilitation technologies for PSD were retrieved from CNKI, VIP and Web of Science Core Collection from inception to July, 2025. Visualization analysis was conducted using CiteSpace 6.3.R1 and VOSviewer 1.2.20. ResultsA total of 1 265 articles were included, consisting of 794 Chinese and 471 English publications. The annual volume of Chinese literature peaked in 2019 (74 articles) and English literature peaked in 2022 (61 articles). Research hotspots included low-frequency surface neuromuscular electrical stimulation, repetitive transcranial magnetic stimulation, surface electromyography biofeedback and transcranial direct current stimulation. Keyword clustering and timeline analysis indicated that researches evolved from early traditional rehabilitation methods to the diversified and integrated application of combined rehabilitation technologies. ConclusionResearch on rehabilitation technologies for PSD is developing rapidly. Future efforts should focus on researches of multi-technology integration, individualized treatment protocols and long-term efficacy assessments.

ObjectiveTo determine whether Jinshui Huanxian component formula Ⅱ （ECC-JHF Ⅱ） and matrix hardness interfere with the process of epithelial-mesenchymal transition （EMT） during pulmonary fibrosis by regulating integrin β₁ （ITG β₁）， and to elucidate the underlying mechanism. MethodsA pulmonary fibrosis mouse model was established by a single intratracheal instillation of bleomycin （BLM）. To observe the disease progression at various time points， the mice were sacrificed before modeling and on days 7， 14， 21， 28 and 42 after modeling for assessment of relevant indicators. To evaluate the therapeutic effect of drug intervention， the mice were given ECC-JHF Ⅱ and pirfenidone （PFD） by gavage starting on day 29 after modeling for 14 days of treatment， after which the mice were sacrificed. Pulmonary function， pathological changes， collagen deposition， lung tissue hardness and EMT markers were detected. Polyethylene glycol （PEG） composite hydrogels with different hardness were prepared in vitro using biomaterials such as eight-arm polyethylene glycol thiol （PEG-SH） and eight-arm polyethylene glycol maleimide （PEG-MAL）. Human type Ⅱ alveolar epithelial cells cultured in hard matrix culture dishes were treated with low， medium， and high doses of ECC-JHF Ⅱ （15.31， 30.63， 61.25 mg·L^-1） to observe the intervention effect of ECC-JHF Ⅱ on EMT induced by transforming growth factor beta 1 （TGF-β₁）. Human type Ⅱ alveolar epithelial cells cultured on soft （3.8 kPa） and hard （culture dishes， ~ GPa） matrices were treated with ECC-JHF Ⅱ， respectively. The mRNA and fluorescence expression levels of the epithelial marker E-cadherin （CDH1）， the mesenchymal marker N-cadherin （CDH2） and vimentin （VIM）， as well as ITG β₁， were detected by real-time quantitative polymerase chain reaction （Real-time PCR） and immunofluorescence. Western blot was used to detect the protein expression of CDH1， CDH2 and ITG β₁， and the biomechanical mechanism of ECC-JHF Ⅱ on EMT and pulmonary fibrosis was further verified by knocking down and specific activation of ITG β₁. ResultsECC-JHF Ⅱ treatment improved BLM-induced pulmonary fibrosis in mice， as evidenced by significantly increased minute ventilation （MV） and 50% expiratory flow at tidal volume （EF₅₀） （P<0.05）， and significantly increased tidal volume （TV） after treatment （P<0.01） compared with the model group. Immunohistopathological analysis revealed attenuated inflammation and alveolar injury， reduced deposition of type Ⅰ collagen （Col-Ⅰ）， and significantly decreased lung tissue stiffness （P<0.01）， thereby alleviating disease progression. The real-time PCR results showed that， compared with the model group， the ECC-JHF Ⅱ group showed increased CDH1 expression and decreased CDH2 and VIM expression in mouse lung tissues （P<0.05， P<0.01）， indicating that ECC-JHF Ⅱ inhibited the EMT process to ameliorate pulmonary fibrosis. In vitro experimental results showed that both ECC-JHF Ⅱ and matrix softening reversed the EMT phenotype switch. Specifically， compared with the hard matrix group， the cells cultured on the soft matrix exhibited significantly upregulated expression of the epithelial marker CDH1 （P<0.01） and significantly downregulated expression of the mesenchymal markers CDH2 and VIM （P<0.05）. Furthermore， ECC-JHF Ⅱ inhibited the expression of ITG β₁ both in vitro and in vivo. Knockdown and specific activation of ITG β₁ further confirmed that ITG β₁ is involved in the regulatory process by which ECC-JHF Ⅱ inhibits EMT and ameliorates pulmonary fibrosis. ConclusionECC-JHF Ⅱ and matrix softening can block the EMT process and ameliorate pulmonary fibrosis， and the underlying mechanism may be associated with the inhibition of ITG β₁-mediated mechanotransduction. This study reveals a novel mechanism of ECC-JHF Ⅱ intervention in pulmonary fibrosis from a biomechanical perspective.

Acute lung injury （ALI） is a critical respiratory emergency caused by various non-cardiogenic factors， including severe pulmonary and extrapulmonary infections， lung contusion， and sepsis. Its pathological features are centered on alveolar-capillary barrier dysfunction， uncontrolled inflammatory responses， and impaired alveolar fluid clearance， manifesting as refractory hypoxemia and respiratory distress， with a poor clinical prognosis. Modern studies have revealed that mitochondrial dysfunction and glucose metabolic reprogramming in macrophages， characterized by hyperactivated glycolysis， drive pro-inflammatory polarization and represent a key mechanism leading to excessive inflammatory responses and disease progression in ALI. Therefore， targeting macrophage glycolysis may be a potential therapeutic strategy for ALI. The Plain Questions： Special Discussion on Channels and Vessels in Huangdi's Internal Classic states that "The spleen disseminates essence upward to the lungs". When the spleen fails in transport and transformation， the distribution of refined nutrients becomes disordered， resulting in the endogenous generation of turbid pathogens that obstruct the pulmonary collaterals， causing failure of lung dispersion and descent and leading to dyspneic reversal. This forms the dynamic pathological pattern of ''deficiency in the root with excess in the manifestation''， thereby proposing the core pathogenesis of ALI as ''spleen deficiency with transport dysfunction and turbid pathogens obstructing the lungs''. This process is intrinsically associated with the inflammatory cascade triggered by disordered macrophage glucose metabolism. Taking the theory of ''spleen failing to disperse essence'' as the entry point， the present study systematically elucidates the progressive pathological mechanism of "energy metabolism disorder-cytokine storm'' in ALI from the perspectives of the ''spleen deficiency-turbid obstruction'' pathogenesis and macrophage glycolysis-pro-inflammatory polarization. In addition， we summarize Chinese medicine compound formulas and monomeric components that ''restore spleen transport and eliminate turbid pathogens''， and explore their potential mechanisms in the treatment of ALI by regulating macrophage metabolic phenotypes to improve the state of ''spleen failing to disperse essence''. This provides a molecular basis for elucidating the ''spleen-lung'' energy metabolism dialogue， deepens understanding of the multi-target regulatory mechanisms of herbal prescriptions， and promotes the deep integration of classical theory with modern medicine.

Background: This study was performed to characterize the incidence, costs, and risk factors associated with renal and cardiovascular adverse outcomes following primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI). Methods: Patients with STEMI who underwent pPCI using iso-osmolar contrast were enrolled at 39 centers. The incidence of acute kidney injury (AKI) and major adverse renal and cardiovascular events (MARCE) was analyzed, as well as inpatient costs. Logistic regression analysis was performed to identify risk factors. Results: Among 2,293 patients, the incidence of AKI and MARCE within 72 hours post-pPCI was 4.14% (n = 95) and 4.40% (n = 101), respectively. AKI and/or MARCE were associated with systolic blood pressure (AKI: odds ratio [OR], 1.009; 95% confidence interval [CI], 1.000–1.018), hypertension (AKI: OR, 1.815; 95% CI, 1.133–2.906; MARCE: OR, 1.760;95% CI, 1.118–2.769), anterior wall infarction (AKI: OR, 1.895; 95% CI, 1.196–3.004; MARCE:OR, 1.939; 95% CI, 1.240–3.032), Killip class (AKI: OR, 1.465; 95% CI, 1.117–1.922; MARCE:OR, 1.467; 95% CI, 1.131–1.903), and serum creatinine (SCr; MARCE: OR, 1.006; 95% CI, 1.000–1.012). Hospitalization costs for patients with STEMI who developed AKI or MARCE were significantly higher than for those without AKI (9,595 ± 5,795 vs. 8,279 ± 3,872 USD, P = 0.003) or without MARCE (9,890 ± 5,616 vs. 8,255 ± 3,859 USD, P < 0.001). Conclusions In patients with STEMI undergoing pPCI with iso-osmolar contrast, the incidence of AKI and MARCE was associated with higher hospitalization costs. Systolic blood pressure, hypertension, anterior wall infarction, Killip class, and SCr were identified as risk factors for these outcomes.

ObjectiveTo conduct an epidemiological investigation and analysis of a clustered scabies outbreak in a middle school, so as to provide evidence for developing targeted prevention and control strategies. MethodsCase data on a clustered scabies outbreak occurring in a middle school of Shaanxi Province in 2025 were collected. Field epidemiological approaches were adopted to define cases, search for infected individuals, and describe the temporal, spatial, and population distribution. Specimens were collected from individuals and surrounding environments for laboratory testing. ResultsA total of 25 scabies cases were identified in 4 classes and 9 dormitories of the school. All cases were first-year high school students. The overall attack rate was 6.00% (25/414); the attack rate was 10.53% (22/209) among male students and 1.46% (3/205) among female students. The disease course ranged from 10 to 30 days, with a median duration of 14 days, and 3 students (12.00%) continued attending classes with ongoing infection. Skin scrapings collected from lesion sites of 3 patients were examined under microscopy, all of which were positive for Sarcoptes scabiei; no laboratory testing was performed for the remaining cases. This clustered scabies infection outbreak lasted for one month. All affected students recovered completely without severe complications or deaths, and the outbreak was effectively contained. ConclusionThis scabies infection is a clustered school-based scabies outbreak caused by Sarcoptes scabiei. Affected patients present relatively severe symptoms and a prolonged disease course. Scientific and standardized preventive systems should be established to enable timely early warning and emergency response.

Nonalcoholic fatty liver disease（NAFLD） is the most common chronic liver disease in the world. Because of its complex pathogenesis， high clinical prevalence and large population， it poses a great threat and challenge to public health in the world. Therefore， active intervention measures are needed. Currently， western medicine is effective in reducing weight， reducing liver fat content， improving glucose-lipid metabolism and insulin resistance. However， for patients with NAFLD-related fibrosis and cirrhosis， there is still a lack of sufficient histological evidence to support its benefits， and randomized controlled trials are still needed to clarify. Lifestyle intervention is an important cornerstone for the treatment of NAFLD， but there are many problems such as poor implementation and low compliance of patients， and the clinical efficacy is not ideal. Traditional Chinese medicine（TCM） has the significant advantages of multiple pathways and multiple targets. Berberine， the active ingredient of TCM， can interfere with the production of NAFLD from multiple pathways， including increasing energy consumption， weight loss， improving glucose-lipid metabolism， improving insulin resistance， anti-inflammatory， anti-oxidation， regulating intestinal flora， restoring bile acid homeostasis， anti-fibrosis and so on， which can play a positive role in the treatment of NAFLD. At the same time， it was found that the combination of BBR with Chinese and western medicines had significant advantages in promoting drug absorption， improving oral bioavailability， increasing the highest biological distribution in the liver， enhancing the overall therapeutic effect of NAFLD， and reducing adverse drug reactions， which could provide reference for clinical medication.

ObjectiveTo explore the mechanism of the anti-cancer compound formula Feiyanning in inhibiting epithelial-mesenchymal transition （EMT） and invasion and metastasis of non-small cell lung cancer （NSCLC）. MethodsCell proliferation and activity were assessed using the cell counting kit-8（CCK-8） assay to evaluate the effect of Feiyanning on the proliferation of A549 and H1299 cells. Wound healing and Transwell assays were conducted to examine Feiyanning's impact on the metastasis of A549 and H1299 cells. The effects of Feiyanning on EMT and the transforming growth factor-β₁ （TGF-β₁）/Smad signaling pathway proteins in A549 and H1299 cells were detected by Western blot. Exogenous TGF-β₁ was used to induce EMT in A549 and H1299 cells. The effects of Feiyanning on TGF-β₁-induced NSCLC cell metastasis， EMT， and the TGF-β₁/Smad pathway proteins were assessed by wound healing assay， Transwell assay， and Western blot. In vivo， an A549 lung metastasis model was established via tail vein injection in nude mice. A total of 28 SPF male nude mice were randomly divided into four groups： Model （NC） group， Feiyanning low-dose （FYN1） group， Feiyanning high-dose （FYN2） group， and the positive control group （TGF-β receptor kinase inhibitor SB431542 group）. The corresponding interventions were performed. After 40 days， the mice were euthanized， and lung metastases were analyzed. The expression of E-cadherin， N-cadherin， p-Smad2， and p-Smad3 in each group was detected by immunohistochemistry （IHC）. ResultsAfter Feiyanning intervention， compared to the blank group， Feiyanning inhibited the proliferation of A549 and H1299 cells in a concentration-dependent manner （P<0.01）. The metastasis ability of Feiyanning-treated cells was significantly decreased compared to the blank group （P<0.01）. The expression of EMT marker proteins N-cadherin and zinc finger transcription factors （Zeb1， Snail， Slug） was significantly reduced in the Feiyanning groups compared to the blank group （P<0.05， P<0.01）. The expression of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ， key proteins in the TGF-β₁/Smad signaling pathway， was also significantly decreased （P<0.01）. In the TGF-β₁-induced EMT model， compared to the TGF-β₁ group， the cell metastasis ability in the Feiyanning groups was reduced （P<0.01）， and the expression levels of N-cadherin， Zeb1， Snail， and Slug were significantly lower （P<0.01）. The expression levels of p-Smad2/3， Smad2/3， TβRI， and TβRⅡ were also significantly reduced （P<0.01）. In vivo results showed that compared to the model group， the number of lung metastases in the FYN1， FYN2， and SB431542 groups was reduced （P<0.01）， and the range of cell infiltration was narrowed. Immunohistochemical results showed that compared to the model group， the expression of E-cadherin in the FYN1， FYN2， and SB431542 groups was increased （P<0.01）， the expression of N-cadherin decreased （P<0.05， P<0.01）， and the expression of p-Smad2 and p-Smad3， key proteins of the TGF-β₁/Smad pathway， was reduced （P<0.01）. ConclusionFeiyanning inhibits the invasion and metastasis of NSCLC cells and EMT. The mechanism is related to the inhibition of TGF-β₁/Smad signaling pathway.