Guang’anmen Hospital

Atherosclerosis (AS) severely threatens global health, while current therapies exhibit limitations. Recognized as a 'superior-grade' herb in the Shennong Ben Cao Jing, Salvia miltiorrhiza Bunge (Danshen) has been shown in modern studies to protect against cardiovascular diseases. The aim of this study was to investigate the therapeutic potential and protective mechanism of pharmacological components of Salvia miltiorrhiza against AS. Relevant animal studies were collected from 8 databases, namely, PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang Data, VIP, and SinoMed. Risk of bias of the included studies was evaluated using the SYRCLE's tool. Statistical analysis was performed using R 4.2.0 and Python 3.14.2 software. Machine learning model was trained to predict optimal intervention parameters and was subsequently validated. A total of 64 studies were included. The pharmacological components of Salvia miltiorrhiza ameliorated atherosclerotic plaque formation and stability, and modulated various biomarkers, including lipid profiles, inflammatory cytokines, oxidative stress indicators, endothelial function markers, as well as matrix metalloproteinases. Machine learning identified an optimal Tanshinone IIA regimen against AS, which was defined as a single dose of 33.18mg/kg dose over 84 days and demonstrated predictive robustness in validation. The pharmacological components of Salvia miltiorrhiza attenuate AS by regulating lipid metabolism, anti-inflammatory and antioxidant actions, improving endothelial function, modulating of vascular smooth muscle cells, remodeling extracellular matrix, and regulating programmed cell death. These findings provide translational insights that pave the way for subsequent preclinical and early-clinical studies, pending systematic validation through more rigorous research.

Endometriosis(EMS) symptoms, progression, and onset are all linked to the patient's immune system dysfunction. Research on immune cells and their molecular mechanisms has long been a prime focus of EMS studies. Nonetheless, the immune environments of EMS patients and cells are constantly changing. How to effectively study and treat EMS depends on our ability to comprehend the temporal changes in immunity in EMS patients. Consequently, the immunological time sequence of endometriosis is methodically discussed and summarized in this article as four steps: 1) immune escape, in which Ectopic Endometrial Cells(EECs) evade immune surveillance and growth in the peritoneum; 2) pro-inflammatory immune response, immune killer cells are triggered, and the lesions show signs of inflammation; 3) immunological anti-inflammatory, which converts pro-inflammatory micro-environment to anti-inflammatory micro-environment and helps the body avoid excessive inflammation; 4) Immune exhaustion: Immune killer cells gradually lose their ability to attack EECs as they experience exhaustion and paralysis. In addition to providing a reference for future EMS staging treatments, this study offers a comprehensive understanding of the temporal alterations in EMS. It reveals cellular and molecular processes associated with immune exhaustion.

Thrombosis represents a significant complication in leukemia patients, associated with treatment interruption and reduced survival outcomes. Although multiple risk prediction models have been developed, their methodological quality and applicability remain uncertain. This review aims to evaluate existing risk prediction models for thrombosis in patients with leukemia. We conducted comprehensive literature searches across nine databases from the inception to August 4, 2025. Two reviewers independently performed study selection, data extraction, and quality assessment using the CHARMS checklist and PROBAST tool. Of 1825 initially identified records, 14 studies comprising 16 prediction models were included. Development cohorts ranged from 102 to 1252 participants. Model discrimination measured by AUC/C-index varied between 0.641-0.917. Internal validation was performed in nine studies, while only one conducted external validation. Key predictors included central venous catheter placement, prior history of thrombosis, D-dimer levels, platelet count, white blood cell count, the Eastern Cooperative Oncology Group (ECOG) score, chemotherapy/radiotherapy, comorbidities, type of leukemia, use of hemostatic drugs, and age. All studies were rated high risk of bias, and five raised major concerns regarding applicability. Sensitivity analyses excluding chronic leukemia studies, excluding non-English publications and excluding dissertations yielded consistent overarching conclusions. In summary, current models often report moderate to good apparent discrimination, but are limited by methodological shortcomings and inadequate validation. All models should be considered exploratory and not ready for routine clinical use without prospective external validation. Future research should prioritize prospective, multicenter cohorts with standardized outcome adjudication and rigorous internal/external validation across diverse leukemia subtypes.

Metabolic associated fatty liver disease (MAFLD) is mainly caused by liver cell steatosis or fat storage due to lipid metabolism disorders. It may induce the diseases such as liver cirrhosis and liver cancer. Our study aimed to explore the efficacy and mechanism of polyene phosphatidylcholine (PPC) combined with atorvastatin (ATV) in treating MAFLD. Ninety-two MAFLD patients were divided into control and observation groups which received PPC alone and PPC combined with ATV for six months. The total therapeutic efficiency, liver function indicators, blood lipid indicators, inflammatory factors and liver injury indexes were evaluated and compared between two groups. After treatment, comparing to the control group, in the observation group the total effective rate was significantly increased and the liver function indicators, blood lipid indicators, inflammatory factors and liver injury index transforming growth factor-β (TGF-β) and nuclear transcription factor-κB (NF-κB) levels were significantly improved (all P < 0.05). PPC combined with ATV is superior to PPC alone in improving the liver function, lipid metabolism, inflammation and liver injury without increasing the adverse reactions. It may represent a safe adjunct strategy in MAFLD management.

ABSTRACT This article is to study the existence of multiple solutions for the following degenerate Kirchhoff‐type equation with logarithmic nonlinearity: where is a smooth bounded domain in . By using the variational methods and appropriate hypotheses of and , we get two positive solutions for the case of , a positive ground state solution and a sequence of high energy solutions for . Our results generalize and improve some recent results in the literature.

Atherosclerosis (AS) constitutes a major cardiovascular disorder posing a severe threat to human health, with the rupture of vulnerable plaques marking a critical turning point in the progression of AS. This pathological event can trigger acute myocardial infarction and stroke, thereby exerting a profound adverse impact on patient prognosis. In contrast to normal arterial tissues, vulnerable plaques are characterized by an abundance of neovascularization, which is generated through angiogenic pathways. Although these neovessels serve to alleviate the hypoxic microenvironment within the plaque, they concurrently compromise plaque stability. Notably, angiogenesis engages in crosstalk with AS-associated phenotypic processes, including cellular apoptosis, extracellular matrix remodeling, inflammatory responses, and oxidative stress. This interplay forms a positive feedback loop that further exacerbates the destabilization of vulnerable plaques. The vascular endothelial growth factor (VEGF) pathway plays a central regulatory role in angiogenesis. Targeting the VEGF pathway to inhibit angiogenesis and enhance plaque stability has thus opened a novel therapeutic avenue for AS management. In comparison, this strategy has demonstrated promising efficacy in preclinical studies; however, a lack of safe and reliable pharmaceutical agents remains, hindering their translation into clinical practice for AS treatment. In this review, the authors summarize the underlying mechanisms governing angiogenesis and vulnerable plaque formation, and further explore the phenotypic crosstalk between these processes. The ultimate aim is to provide valuable insights to facilitate future breakthroughs in the development of therapeutic strategies for AS.