To explore the therapeutic effect of Huangqi Guizhi Wuwu decoction on oxaliplatin-related peripheral neurotoxicity in patients with colorectal cancer receiving adjuvant chemotherapy.

A total of 42 colorectal cancer patients who received mFOLFOX6 adjuvant chemotherapy in a hospital from March 2022 to December 2024 were enrolled in this study. They were randomly divided into two groups (n=21 each). The control group was treated with chemotherapy alone, while the experimental group received Huangqi Guizhi Wuwu decoction for 4 cycles concurrently with chemotherapy. The CTCAE V4.0 standard was used to evaluate oxaliplatin-related peripheral neurotoxicity, and the primary study endpoint was the incidence of grade 3 and above peripheral neurotoxicity.

The incidences of grade 3 or higher peripheral paresthesia in the experimental group and the control group were 23.8% vs. 57.1% (P=0.03). The incidences of grade 3 and above peripheral sensory neuropathy were 19.1% vs. 47.6% (P=0.04), with statistically significant differences observed between the two groups.

Taking Huangqi Guizhi Wuwu decoction simultaneously during chemotherapy can effectively prevent and treat oxaliplatin-induced peripheral paresthesia and peripheral sensory neuropathy.

To systematically elucidate the multidimensional mechanisms of vitamin D in wound healing, thereby providing scientific evidence for clinical treatment and offering new directions for wound repair research.

The regulatory effects of vitamin D were analyzed on pathways including VDR, calcium signalling, anti-inflammation, TGF-β/Smad, Hippo, skin barrier-related signaling pathways, PI3K/AKT/HIF-1α, and Notch during different stages of wound healing.

Vitamin D exerted its effects on key aspects of wound healing-including cell proliferation, migration, differentiation, extracellular matrix synthesis and remodelling, inflammatory response, immune regulation, and angiogenesis-by regulating the aforementioned pathways. These pathways intertwined to form a regulatory network that promoted wound healing.

Vitamin D demonstrates significant potential in research into wound healing mechanisms, with its multi-pathway regulatory mechanisms providing multidimensional support for wound repair. Future research should further explore interactions between pathways, carry out clinical trials in humans, and investigate other relevant pathways to advance clinical applications.

To evaluate the analgesic and anti-inflammatory effects of gout pills using animal experiments.

The mice were randomly divided into low-medium and high-dose gout pill groups, the model control group and positive control group. The analgesic and anti-inflammatory effects of gout pills were initially evaluated through the acetic acid-induced writhing test, ear swelling test, capillary permeability test and measurement of certain inflammatory factors.

Gout pills significantly reduce the number of writhes, auricular swelling degree and capillary permeability, serum levels of IL-6 and TH1 levels in mice, and elevated the levels of TH2 and IgG.

Gout pills have good anti-inflammatory and analgesic effects.

To explore the potential molecular mechanism by which saffron exerts its antidepressant effect by regulating the expression of angiotensinogen (Agt) in the nucleus accumbens (NAc) and regulating synaptic remodeling.

Fifty mice were randomly divided into five groups: blank control group, model group, fluoxetine group, low-dose saffron group, and high-dose saffron group. The chronic unpredictable stress (CUMS) model was established in mice (except the blank control group), and continuous intragastric administration was performed for 7 days after modeling.. Depressive-like behaviors of mice were evaluated using the forced swimming test (FST), sucrose preference test (SPT), and tail suspension test (TST). The mRNA and protein expression levels of Agt in the NAc were detected. The mRNA levels of angiotensin II (Ang-Ⅱ), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in mouse brain tissues were measured. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in mouse brain tissues were assayed. Additionally, the protein expression levels of synaptophysin (Syp), postsynaptic density protein 95 (Psd-95), and brain-derived neurotrophic factor (Bdnf) in mouse brain tissues were determined.

Compared with the model group, the fluoxetine group, low-dose saffron group, and high-dose saffron group showed improved depressive-like behaviors, with a significant increase in SPT and a significant decrease in immobility time in FST and TST (P<0.05). Compared with the model group, the high-dose saffron group exhibited significantly reduced mRNA levels of Agt, Ang-Ⅱ, IL-6, and TNF-α (P<0.05), decreased MDA content, and significantly increased SOD activity in brain tissues (P<0.05). The protein expression of Syp, Psd-95, and Bdnf in brain tissues was significantly upregulated in the high-dose saffron group (P<0.05).

Crocetin exerts its antidepressant effect by inhibiting the expression of Agt in the NAc, regulating the renin-angiotensin system (RAS), alleviating neuroinflammation and oxidative stress, and promoting synaptic remodeling mediated by Syp, Psd-95, and Bdnf.

To systematically analyze the polymorphic characteristics of the ITGA2 gene and the impact of the rs1126643 F253L mutation on the biological function of the ITGA2 protein and the antiplatelet effect of aspirin, thereby providing a theoretical foundation and potential genetic biomarkers for the individualized diagnosis and treatment of aspirin resistance (AR).

The ITGA2 gene and encoded protein sequences were obtained from NCBI and UniProt databases. Physicochemical properties and hydrophobicity profiles of the encoded protein were analyzed using ProtParam and Protscale, respectively. Protein-protein interaction networks were constructed via STRING, secondary structure elements were predicted using SOPMA and DNAStar, and tertiary structural models were generated using SWISS-MODEL, with detailed analysis of conformational differences at the mutation site. Functional and pathogenicity impacts of wild-type versus mutant proteins were assessed in silico, followed by validation through molecular docking and molecular dynamics simulations.

The ITGA2 gene spans 105 428 base pairs and encodes a 1 181 amino-acid protein, classifying it as an acidic, hydrophilic protein. Secondary structure analysis revealed that α-helices constitute 14.39%, extended strands 27.35%, and random coils 58.26% of the protein structure. Although the F253L substitution does not significantly alter the fundamental physicochemical properties of the protein, stability prediction tools including DUET and MUpro consistently indicated reduced structural stability. Six out of seven pathogenicity prediction algorithms classified the variant as highly pathogenic. MutPred2 analysis suggested that the mutation may disrupt protein function by decreasing relative solvent accessibility and altering ordered interfacial regions. The ITGA2 protein is involved in critical biological processes such as cell-matrix adhesion, and the F253L mutation may contribute to pathological mechanisms through structural and functional perturbations. These findings were further substantiated by molecular docking and molecular dynamics simulations.

The ITGA2 F253L mutation represents a core molecular mechanism underlying aspirin resistance, acting through destabilization of the ITGA2 protein structure, reduction in solvent accessibility, reduced binding affinity to aspirin, and thereby attenuating the antiplatelet effect of aspirin. This study highlights the pivotal role of the ITGA2 F253L polymorphism in modulating aspirin responsiveness and provides potential biomarkers and mechanistic insights for genetic profiling and personalized antiplatelet therapy in patients with AR.

This study aimed to identify novel ligands targeting Site C of Nur77-LBD (ligand binding domain), a critical regulatory binding site of inflammation, using computational approaches.

A structure-based virtual screening of 9 371 DrugBank compounds was conducted against the Nur77 ligand-binding domain (PDB ID:4JGV) using molecular docking. Top-scoring hits were subjected to 500-ns molecular dynamics (MD) simulations using Schrödinger Desmond module. Binding stability was assessed by root mean square deviation (RMSD), root mean square fluctuation (RMSF), Protein-ligand interaction analysis, and MM-GBSA calculations.

Five candidate compounds were identified to potentially bind to Nur77-LBD. Among them, compounds 1, 2, and 3 demonstrated stable binding, with low RMSD fluctuations and persistent protein-ligand interactions comparable to reference ligands 13 and 29.

These findings highlight compound 1 as the most promising candidate, showing comprehensive binding stability and interaction strength, and provide new chemical scaffolds for further optimization of Nur77 modulators.

Based on the US FDA Adverse Event Reporting System (FAERS), this study comprehensively evaluated the adverse reaction characteristics of cephalosporins on the gastrointestinal system, and analyzed the risk heterogeneity among different drug varieties and the influence of patients' baseline characteristics.

The data from the FAERS database from 1994 to 2024 were extracted, and disproportionality analysis combined with Bayesian method was used to mine the correlation signals between cephalosporins and gastrointestinal adverse events.

A total of 54.249 6 million adverse event reports were included, and 793 gastrointestinal system adverse events related to signal-positive cephalosporins were screened out.The signal intensity of cefdinir [ROR=2.69 (2.52-2.88)] was significantly higher than that of other drugs. The Bayesian method verified the association of high-risk events, such as the megacolon signal of cefixime [EBGM=75.21 (95%CI:23.54)]. The risk of signal-negative cephalosporin was low, and very few had a certain intensity of PT signal values.

This study analyzed the risk of gastrointestinal adverse reactions associated with the use of different types of cephalosporins. Among them, cefdinir had the highest risk of gastrointestinal-related adverse events (AEs), while non-oral signal-negative ceped drugs.

To explore the characteristics and development trends of asthma drug clinical trials in China, and to provide references for promoting the research of new asthma drugs.

Using "asthma" as the keyword, we searched the Chinese Clinical Trial Registry and Information Disclosure Platform. Data regarding clinical trials of asthma drugs registered from January 2013 to December 2025 were collected, and statistical analyses were performed on registration time, geographic information, investigational drugs and other relevant information.

A total of 663 clinical trials of asthma drugs were included in this study. Over the past decade, the number of clinical trials of asthma drugs has shown an upward trend. In terms of trial phases, bioequivalence trials accounted for the largest proportion (n=398, 60.03%). Regarding the categories of investigational drugs, there were 527 chemical drugs, 110 biological agents, and 26 traditional Chinese medicines/natural medicines. The geographical distribution of clinical trial sites was generally characterized by a concentration in eastern China and a scarcity in central and western regions. Regarding pharmacological mechanisms, glucocorticoids were the most widely studied drug category (n=131, 19.76%), while there were 105 biotargeted drugs (15.84%). Among them, domestic innovative drugs have been growing rapidly in recent years.

Significant progress has been made in clinical trials of asthma drugs in China, particularly with the rapid development of biotargeted drugs. However, problems such as uneven regional distribution of clinical trials and low proportion of innovative drugs still exist. It is necessary to strengthen policy support, optimize the allocation of regional medical and pharmaceutical resources, and continuously promote the research and development of asthma drugs and the advancement of related clinical trials.