Chemotherapy-induced myelosuppression (CIM) is a common and serious adverse reaction during chemotherapy in patients with malignant tumors. Kaempferol, an important active component of leukocyte-elevating traditional Chinese medicine, may play a role in its improvement. This study aims to explore the research status and mechanisms of kaempferol in improving CIM and to provide reference evidence for its application in the prevention and treatment of CIM.

Chinese and English literature on kaempferol intervention in CIM was systematically searched in CNKI, WanFang, VIP, PubMed, Web of Science, and Embase databases from database inception to August 8, 2025. Two researchers independently performed literature screening and extracted key information such as study design, intervention measures, and outcome indicators.

A total of 13 eligible studies were included, including 9 animal experimental studies, 1 randomized controlled trial, 2 clinical observational studies, and 1 quasi-experimental study. Existing evidence indicated that kaempferol or compound preparations containing kaempferol increased peripheral blood leukocyte counts to a certain extent and promoted the proliferation of bone marrow nucleated cells. Mechanistic studies suggested that kaempferol exerted bone marrow protective effects through multi-target synergistic actions, including regulation of oxidative stress levels, enhancement of immune function, and inhibition of hematopoietic cell apoptosis.

Kaempferol shows considerable research potential and certain clinical application prospects in improving CIM. However, existing evidence is still mainly based on traditional Chinese medicine compound preparations and predictive analyses, and high-quality basic research and large-scale clinical studies focusing on kaempferol monotherapy remain insufficient. In the future, rigorously designed empirical studies are needed to further clarify its independent efficacy and mechanisms of action, so as to promote standardized translational application in the prevention and treatment of CIM.

Actin filament-associated protein 1 like 1 (AFAP1L1) is an adaptor protein lacking enzymatic and transcriptional activity, but the AFAP1L1 gene functions as an oncogene in colorectal cancer and gastric cancers. This study aims to investigate the role of AFAP1L1 in glioma and to explore changes in AFAP1L1 expression during glioma progression.

Clinical and transcriptomic data of glioma patients were downloaded from The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), and the Gene Expression Omnibus (GEO) databases to analyze the associations between AFAP1L1 expression and glioma prognosis, somatic mutations, immune cell infiltration, and enriched signaling pathways. Western blotting and real-time polymerase chain reaction (PCR) were used to detect AFAP1L1 messenger RNA (mRNA) and protein expression in glioma patients.

Patients with high AFAP1L1 expression had poorer prognosis, and AFAP1L1 was identified as an independent risk factor for glioma. In addition, glioma patients with high AFAP1L1 expression exhibited lower levels of somatic mutations, including amplification of oncogenes such as epidermal growth factor receptor and deletion of tumor suppressor genes such as cyclin-dependent kinase inhibitor 2A (CDKN2A). Estimation of STromal and Immune cells in Malignant Tumours using Expression (ESTIMATE) algorithm analysis showed that AFAP1L1 expression was positively correlated with the immune microenvironment. Tumor immune dysfunction and exclusion (TIDE) analysis indicated that glioma patients with high AFAP1L1 expression responded poorly to immunotherapy. Single cell analysis showed that AFAP1L1 expression was mainly concentrated in glioma cells. Enrichment analysis suggested that AFAP1L1 was potentially associated with small guanosine triphosphatases (GTPases), hypoxia-inducible factor-1 (HIF-1), focal adhesion, and mitogen-activated protein kinase (MAPK) signaling pathways.

AFAP1L1 is a novel biomarker indicating glioma progression and a potential therapeutic target for glioma.

Oral squamous cell carcinoma (OSCC) is a common and aggressive cancer sometimes subsequent to oral potentially malignant disorders (OPMDs). Notwithstanding progress in surgical, radiotherapeutic, and chemotherapeutic interventions, survival rates for OSCC continue to be inadequate and are associated with significant functional impairment, underscoring the necessity for preventive and interceptive therapeutic approaches. Chemoprevention has emerged as a viable strategy to inhibit, postpone, or reverse oral carcinogenesis by targeting the molecular and cellular processes implicated in malignant transformation.

This review synthesizes current evidence on chemopreventive agents investigated in OPMDs and OSCC. Relevant literature was analyzed focusing on natural compounds, synthetic drugs, and targeted biological therapies, as well as emerging delivery approaches. Significant emphasis is placed on bioactive phytochemicals such as retinoids, carotenoids (β-carotene and lycopene), curcumin, resveratrol, black raspberries, and vitamin E, alongside synthetic agents including cyclooxygenase-2 inhibitors and epidermal growth factor receptor (EGFR)-targeted therapies. These drugs demonstrate chemopreventive effects via modulating oxidative stress, inflammation, cell cycle regulation, apoptosis, angiogenesis, epithelial-mesenchymal transition, and immune evasion in the tumor microenvironment. Clinical and experimental investigations examined in this review reveal inconsistent, although promising results, including the regression of dysplasia, decreased rates of malignant transformation, and enhanced molecular risk profiles in OPMDs. Nonetheless, obstacles persist about long-term effectiveness, ideal dose, toxicity, and patient adherence.

Chemopreventive medicines, especially when utilised in combination and through sophisticated delivery systems, signify a prospective adjunct or alternative approach in the care of OPMDs and OSCC, with the capacity to diminish disease burden and enhance patient outcomes.

Cholangiocarcinoma (CHOL) is an aggressive gastrointestinal carcinoma, characterized by its rapid progression and the absence of effective therapeutic biomarkers. Although recent studies have implicated S100A12 in tumor formation, its specific functions in CHOL development have been insufficiently explored. We conducted an integrative multi-omics study combining Mendelian Randomization (MR) and bioinformatics. The MR approach was employed to investigate causal relationships between cytokines, immune cells, and CHOL risk. Bioinformatics analysis utilizing data from TCGA and GTEx database assessed S100A12 expression in CHOL tissues, functional enrichment, and correlations with immune infiltration as well as immune checkpoint molecules. Experimental validation was conducted using siRNA-mediated S100A12 knockdown in CHOL cell lines, followed by functional assays including proliferation, invasion, and migration. S100A12 exhibited a significant causal association with CHOL risk. Bioinformatics analysis further confirmed that S100A12 is significantly upregulated in cholangiocarcinoma and associated with poor prognosis. The high S100A12 expression group displayed a distinct immune cell infiltration pattern characterized by reduced regulatory T cells and increased M0, M2 macrophages, and neutrophils. Furthermore, S100A12 expression correlated with a series of co-stimulatory or co-inhibitory immune checkpoint molecules. In vitro studies validated that S100A12 enhances proliferation, invasion, and migration capabilities in CHOL cell lines RBE and HuccT1 while simultaneously suppressing apoptosis. The study identified S100A12 as a potential biomarker and therapeutic target for CHOL, paving the way for improved management of this aggressive cancer.

Epstein-Barr virus (EBV) is a ubiquitous herpesvirus and a causal factor for Burkitt Lymphoma (BL), Hodgkin Lymphoma (HL), gastric carcinoma (GC) and nasopharyngeal carcinoma (NPC). Whether EBV contributes to a wider spectrum of cancers remains uncertain. We reviewed MEDLINE, Embase and Web of Science on 30^th July 2024 to identify observational studies that examined the association between EBV infection or EBV-infectious mononucleosis (IM) and cancers beyond BL, HL, GC and NPC. Evidence was appraised using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. For cancers meeting minimum thresholds we assessed etiologic fractions (EFs), biological plausibility, epidemiological burden, latency after IM, and predictive biomarkers. Thirty-three eligible studies were identified, yielding 13 hypotheses (i.e., specific potential reported associations between EBV infection or IM and individual cancer types) that advanced through GRADE. Breast cancer and NHL had the greatest weight of biological plausibility, cervical and prostate the least. Despite an array of tests, testicular cancer studies provided limited evidence. EFs ranged between 12.3% (IM-breast) and 85.1% (EBV infection-NHL). Breast and prostate cancers had the highest global incidence. Only one study (for NHL) provided data on time from IM to cancer onset, and prostate-specific antigen was the only biomarker identified. In this review, we highlight eight cancers across six cancer groups (breast, cervical, leukaemia/other haematologic, NHL, prostate, testicular) with some evidence of EBV involvement. These results reinforce the potential long-term value of EBV vaccine development, while emphasising the need for high-quality prospective studies with robust methods of viral detection to establish causality.

Growing evidence suggests an association between SARS-CoV-2 infection and oxidative stress-related genomic damage, primarily from cross-sectional studies. However, longitudinal evaluations remain limited. Here, we assessed DNA damage in peripheral blood mononuclear cells (PBMCs) from hospitalized COVID-19 patients during the first days of hospitalization, using the alkaline comet assay. A longitudinal descriptive study was conducted at a modular COVID-19 hospital in Lima, Peru, throughout October 2020. Blood samples were collected at admission (day 0), day 3, and day 6. DNA damage was assessed by measuring tail length, tail moment, and tail intensity, which were modeled using mixed-effects linear models. Concurrent hematological parameters and acute-phase proteins were also analyzed to characterize their time-course patterns in conjunction with DNA damage. Results from the adjusted mixed-effects model showed a significant temporal increase in DNA damage parameters, particularly tail intensity (β = 0.25 per day, p = 0.003), relative to baseline measurements, with a peak observed on day 3 of hospitalization. These changes aligned with variations in platelet counts and transferrin levels, while lymphocyte and monocyte counts, along with C-reactive protein, showed an inverse trend, reflecting the dynamic interplay of the inflammatory response and DNA damage. No significant differences in comet assay parameters were observed between survivors and non-survivors, likely due to the limited and unbalanced sample. The findings indicate the presence of a measurable DNA damage burden in PBMCs of hospitalized COVID-19 patients, highlighting the need to further studies to clarify the mechanisms underlying DNA damage and its potential long-term biological implications.

Glottal insufficiency can lead to persistent hoarseness and aspiration, and some patients require surgical intervention. Vocal fold injection can improve glottic structure, but the effect of postoperative voice therapy on voice quality remains to be evaluated. This study aims to analyze the clinical efficacy of vocal fold injection with fat and rectus abdominis fascia combined with voice training in the treatment of glottal insufficiency.

Clinical data of 15 patients with glottal insufficiency treated in the Department of Otolaryngology-Head and Neck Surgery of the Second Affiliated Hospital of Nanchang University from August 2018 to December 2024 were retrospectively collected. Patients received injection of fat and rectus abdominis fascia into the middle portion of the paralyzed vocal fold, and voice training was initiated 2 weeks after surgery. Patients were evaluated and followed up before surgery and at 3, 6, and 12 months after surgery. The primary outcome indicator was the change in glottal gap. Secondary outcome indicators included voice acoustic parameters, including maximum phonation time (MPT), normalized noise energy (NNE), shimmer, and jitter, as well as the Grade, Roughness, Breathiness, Asthenia, and Strain (GRBAS) scale score.

In all treated patients, the injected vocal fold was fuller than before surgery, and no leakage of injected material occurred. The injected vocal fold appeared thickened and shifted medially. Hyperemia and edema were observed within 1 week after surgery, and redness and swelling subsided after 2 months. Compared with before treatment, glottal gap, NNE, shimmer, jitter, and GRBAS scores were significantly reduced at 3, 6, and 12 months after treatment, while MPT was significantly prolonged, with statistically significant differences (all P<0.05). With the increase in the number of voice training sessions, the therapeutic effect became more significant. No patient required secondary vocal fold injection during the 12-month follow-up period.

Vocal fold injection with fat and rectus abdominis fascia combined with voice training can improve glottal closure and voice quality in patients with glottal insufficiency during short- and mid-term follow-up, and is a feasible treatment.

Short-term spinal cord stimulation (st-SCS), as a minimally invasive neuromodulation technique for zoster-associated pain (ZAP), can effectively relieve pain and reduce the incidence of postherpetic neuralgia (PHN). This paper reports two elderly male patients with ZAP admitted to the First Affiliated Hospital, Zhejiang University School of Medicine in August 2024, who developed acute pulmonary embolism (APE) 3 days after st-SCS implantation. Both patients had preoperative high-risk factors, including a history of hypertension and elevated D-dimer levels. Close monitoring of D-dimer levels was performed after st-SCS. When further elevation was observed, computed tomography angiography (CTA) was conducted promptly. After APE was confirmed, anticoagulation therapy with low-molecular-weight heparin bridging to direct oral anticoagulants (DOACs) was initiated, followed by electrode removal. At 3-month follow-up after discharge, repeat pulmonary CTA showed no significant embolism. Advanced age, preexisting cardiovascular and cerebrovascular diseases, elevated preoperative D-dimer levels, perioperative stress, and postoperative immobility due to fear of electrode displacement were all high-risk factors for thrombosis. During the perioperative period, a comprehensive prevention strategy should be established, including preoperative Caprini risk assessment, D-dimer evaluation, and lower-extremity vascular ultrasound screening, intraoperative physical prophylaxis, early postoperative mobilization, and dynamic monitoring of D-dimer levels. Multidisciplinary collaboration should be adopted to optimize individualized management. Based on the above experience, no cases of APE occurred among the subsequent 68 patients with ZAP treated with st-SCS in our hospital, suggesting that APE is preventable and controllable.

Pulmonary hypertension (PH) is a progressive disease characterized by elevated pulmonary arterial pressure, and its prognosis is closely associated with right ventricular (RV) function. Echocardiography, as a noninvasive and convenient imaging modality, plays an important role in the diagnosis of PH, etiological screening, assessment of RV function, and risk stratification. In response to the anatomical, physiological, and pathophysiological adaptive changes of the RV caused by PH, echocardiography demonstrates significant value in the detailed evaluation of both systolic and diastolic function. Noninvasive parameters such as the ratio of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP) have also been confirmed to possess important prognostic value in assessing RV-pulmonary arterial (RV-PA) coupling. In addition, the application of artificial intelligence in echocardiographic analysis provides new tools for the early detection of PH and helps overcome limitations of conventional estimation methods. Current evidence indicates that a noninvasive right heart functional assessment system centered on echocardiography plays a central role in the management of PH. Future studies are required to further validate the performance of multiparametric combined models and to promote deeper integration of artificial intelligence technologies with clinical practice, thereby enabling earlier and more precise individualized diagnosis and treatment.

Vascular aging constitutes a significant pathological basis for the aging of various organs and systems within the human body. This study employed a murine model of atherosclerosis (AS) and Transient Receptor Potential Vanilloid 1 (TRPV1)-deficient AS mice to ascertain whether TRPV1 exerts an influence on AS by modulating aortic aging. Furthermore, the study sought to expand upon the molecular mechanisms by which TRPV1 regulates aortic aging. TRPV1 expression was examined in aortic tissue of Apoe^-/- mice, and its expression level was significantly reduced in comparison with that of control mice. Apoe^-/-Trpv1^-/- mice were subjected to a high-fat diet, after which a significant increase in aortic sinus senescent cell area, senescence-associated secretory phenotypes (SASP) and expression of senescence-associated proteins was observed, accompanied by an increase in plaque area and instability. Transcriptome sequencing ascertained that the deletion of TRPV1 led to a substantial augmentation in the expression of ubiquitin-like protein 15 (ISG15) within the aortic tissue. It then demonstrated that TRPV1 deletion promotes ISG15-induced aortic senescence using Apoe^-/-Trpv1^-/- high-fat dietary mice, as well as cellular experiments. Studies utilising PPI analysis and in vitro cultured EA.hy926 cells have demonstrated that ISG15 promotes vascular endothelial cell senescence by facilitating the expression and phosphorylation of p53 and p21, and by impeding the phosphorylation of retinoblastoma (Rb). Aortic TRPV1 deficiency promotes aortic senescence by promoting upregulation of ISG15 expression, which in turn promotes p53 and p21 phosphorylation and inhibits Rb phosphorylation.