To investigate the effect and mechanism of gastrodin regulating synaptopodin 2 (SYNPO2) on hypoxic-ischemic brain damage (HIBD) in neonatal rats.

The left common carotid artery of neonatal rats was ligated, and the rats were placed in a hypoxic chamber for 40 minutes to establish the HIBD model. Rats were randomly divided into sham operation group (no common carotid artery ligation or hypoxia treatment), model group (HIBD model established), gastrodin group (intraperitoneal injection of gastrodin 100 mg·kg^-1 1 hour before common carotid artery ligation, 1 hour after hypoxia, and 12 hours after hypoxia), gastrodin+oe-NC group (3 days before modeling, 3 microliters oe-NC was transplanted intracerebroventricularly in rats, subsequent treatment same as the gastrodin group) and gastrodin+oe-SYNPO2 group (3 days before modeling, 3 microliters oe-SYNPO2 was transplanted intracerebroventricularly in rats, subsequent treatment same as the gastrodin group), with 10 rats in each group. Western blot was used to detect the levels of SYNPO2 and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway-related proteins; short-term behavioral tests were used to detect neurological function in each group; the dry-wet weight method was used to detect brain water content; TdT-mediated dUTP nick end labeling was used to detect the apoptosis rate of brain tissue cells in each group; immunofluorescence was used to detect the levels of lysosomal associated membrane protein 1 (LAMP1) and microtubule associated protein 1 light chain 3 beta (LC3B) proteins in brain tissue of each group.

The relative expression levels of SYNPO2 protein in the sham operation group, model group, gastrodin group, gastrodin+oe-NC group and gastrodin+oe-SYNPO2 group were 1.00±0.16, 2.05±0.34, 1.38±0.18, 1.35±0.17 and 1.68±0.22, respectively; the relative expression levels of phosphorylated PI3K (p-PI3K)/PI3K protein were 1.00±0.19, 0.25±0.04, 0.65±0.08, 0.68±0.07 and 0.35±0.05, respectively; the relative expression levels of phosphorylated Akt (p-Akt)/Akt protein were 1.00±0.13, 0.28±0.04, 0.49±0.06, 0.51±0.07 and 0.31±0.04, respectively; the relative levels of phosphorylated mTOR (p-mTOR)/mTOR protein were 1.00±0.16, 0.22±0.04, 0.52±0.06, 0.54±0.07 and 0.29±0.05, respectively; the righting reflex latency periods were (2.56±0.33), (14.86±2.12), (5.66±0.75), (5.23±0.79) and (10.33±1.56) s, respectively; the negative geotaxis latency periods were (17.86±2.44), (56.33±8.22), (22.12±3.56), (23.05±3.22) and (40.22±5.66) s, respectively; the cliff avoidance reflex latency periods were (7.11±0.85), (16.55±2.32), (7.22±0.85), (7.83±0.96) and (13.55±2.45) s, respectively; the water contents were (51.56±6.47)%, (62.16±6.22)%, (55.02±6.25)%, (54.63±7.22)% and (61.98±5.17)%, respectively; the apoptosis rates were (5.17±0.65)%, (75.32±9.65)%, (25.65±3.89)%, (23.85±2.98)% and (50.56±6.89)%, respectively; the relative fluorescence intensity of LAMP1 were 1.00±0.15, 3.85±0.44, 1.14±0.15, 1.18±0.19 and 3.22±0.39, respectively; the relative fluorescence intensity of LC3B were 1.00±0.18, 3.45±0.52, 1.25±0.16, 1.21±0.15 and 1.68±0.19, respectively; the above indicators of the model group were statistically significant compared with the sham operation group, the above indicators of the gastrodin group were statistically significant compared with the model group, and the above indicators of the gastrodin+oe-SYNPO2 group were statistically significant compared with the gastrodin+oe-NC group (P<0.05, P<0.01, P<0.001).

Gastrodin inhibits SYNPO2, alleviates brain edema and neurological dysfunction in HIBD rats, protects neuronal structural integrity, reduces neuronal apoptosis, and alleviates excessive autophagy, which may be achieved by activating the PI3K/Akt/mTOR pathway.

To evaluate and analyze quality assessment tools for informed consent and provide a reference for selecting appropriate tools.

A systematic search was conducted in Chinese and English databases, including CNKI, VIP, Wanfang, PubMed, Web of Science, and Embase, covering the period from database inception to July 23, 2025. Basic information on the included studies and assessment tools was extracted, and the dimensions covered by the tools as well as their reliability and validity were summarized.

A total of 23 articles and 18 informed consent quality assessment tools were included. The evaluations primarily focused on levels of understanding, information provision, and therapeutic misconception. The information content commonly addressed study objectives, study duration, procedural steps, risks and inconveniences, and potential benefits.

Although numerous quality assessment tools for informed consent are available, many lack sufficient validation in terms of reliability and validity. Future research should prioritize the validation and refinement of existing tools while developing or introducing culturally adapted assessment instruments.

To establish a radiation injury model using primary human lung fibroblasts and screen for key genes driving radiation-induced pulmonary fibrosis through transcriptome sequencing, thereby elucidating their potential mechanisms and providing new therapeutic targets and strategies for the clinical prevention and treatment of radiotherapy-induced lung injury.

Primary human lung fibroblasts were isolated by collagenase digestion and serially passaged. Cell purity was confirmed by flow cytometry prior to establishing an in vitro radiation model. Transcriptome analysis was performed based on qualified sequencing data. DESeq2 was used for differential expression analysis to identify upregulated genes, which were subsequently validated. Protein-protein interactions (PPI) among the differentially expressed gene sets were predicted using the String database and visualized using the igraph package. Finally, functional and pathway enrichment analyses of the core genes were performed via gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) using the clusterProfiler software.

All samples met the quality control standards. Transcriptome analysis identified three significantly upregulated key differentially expressed genes: sulfatase 1 (SULF1), sulfatase 2 (SULF2), and oligodendrocyte myelin glycoprotein (OMG). These findings were consistently validated in a public dataset. PPI network analysis constructed with Cytoscape revealed that SULF1 occupied a central hub position within the network, exhibiting a strong connection with SULF2, and both directly interacted with OMG. GSEA indicated that SULF1/2 and OMG were significantly enriched in pathways related to DNA function, glutathione transferase activity, and neuroimmune regulation. These results suggested that SULF1/2 and OMG may function in radiation-induced lung injury by participating in processes such as DNA damage response, oxidative stress, and neuroimmune interactions.

SULF1, SULF2 and OMG are key molecules in human lung fibroblasts responding to radiation injury and may drive the progression of radiation-induced lung injury through multiple pathways. As potential therapeutic targets, they provide a novel theoretical basis for the clinical prevention and treatment of radiotherapy-induced lung injury.

To investigate the distribution patterns of pharmacogenomic characteristics in hypertensive patients treated and to evaluate the differential benefits of genotype-guided therapy in calcium channel blocker (CCB) strategy versus beta-blocker strategy.

In the first phase, pharmacogenomic data of patients with primary hypertension treated at our hospital were analyzed. In the second phase, treatment-naive hypertensive patients were enrolled and randomly assigned in a 1∶1∶1∶1 ratio to four groups: genotype-guided CCB strategy, standard CCB strategy, genotype-guided beta-blocker strategy, and standard beta-blocker strategy. Seven key pharmacogenomic loci, including adrenergic beta-1 receptor (ADRB1) rs1801253 (1165G>C) and cytochrome P450 3A5 (CYP3A5) rs776746, were genotyped using polymerase chain reaction (PCR)-melting curve method. Primary outcomes included time to blood pressure control, incidence of treatment-related adverse events (TRAEs), and length of hospital stay.

In the retrospective phase, 2 783 patients were enrolled. The C allele frequency of ADRB1 rs1801253 was 76.02% (4 231 cases/5 566 cases), and the G allele frequency of CYP3A5*3 was 72.97% (4 062 cases/5 566 cases). In the prospective phase, 300 patients were enrolled. The genotype-guided therapy significantly shortened time to blood pressure control (mean difference: -2.10 days, 95% confidence interval (CI): -2.80 to -1.40, P<0.001), with a significant interaction between therapy approach and treatment strategy (P<0.05). Specifically, in the CCB strategy, genotype-guided therapy reduced control time by 3.20 days (95% CI: -4.10 to -2.30) versus standard therapy, whereas in the beta-blocker strategy, the reduction was only 0.90 days (95% CI: -1.70 to -0.10). Genotype-guided therapy also significantly lowered TRAEs incidence [12.67% (19 cases/150 cases) vs. 25.33% (38 cases/150 cases), P<0.001].

Hypertensive patients at our hospital exhibited a distinct pharmacogenomic profile. Genotype-guided therapy demonstrates substantially greater clinical benefits when applied to CCB strategy than to beta-blocker strategy, providing robust evidence for precision hypertension management within this single-center clinical setting.

To investigate the effect and safety of subanesthetic-dose esketamine combined with subcostal transversus abdominis plane block (STAPB) on postoperative delirium in patients undergoing radical resection for colorectal cancer (CRC).

Patients scheduled for radical CRC resection were divided into control group and treatment group according to the anesthetic regimen. The control group received conventional anesthesia, while the treatment group was intravenously administered 0.2 mg·kg^-1 esketamine hydrochloride injection before endotracheal intubation on the basis of the conventional anesthesia protocol. Both groups underwent STAPB after intubation and before skin incision. The excellent and good rate of anesthesia, surgical parameters, hemodynamic indices, postoperative recovery quality-related indicators, incidence of delirium, analgesic efficacy parameters, and adverse reactions were compared between the two groups.

A total of 52 patients were enrolled in the control group and 48 in the treatment group. The excellent/good rates of anesthesia of treatment group and control group were 91.67% (44 cases/48 cases) and 88.46% (46 cases/52 cases), respectively (P>0.05). The fluid infusion volume of treatment group and control group were (1 412.69±38.27) and (1 428.63±35.47) mL, respectively; the heart rates at T3 were (76.19±8.56) and (80.69±9.14)beats·min^-1, respectively; systolic blood pressure at T3 were (131.08±10.39) and (138.52±13.78) mmHg, respectively; diastolic blood pressure at T3 were (79.94±7.27) and (82.35±8.25) mmHg, respectively; the extubation time were (16.75±2.71) and (15.54±2.42) min, respectively; the recovery time were (18.63±2.81) and (20.40±2.86) min, respectively; the Quality of Recovery-40 (QoR-40) scores on postoperative day 2 were (160.79±18.70) and (154.35±20.56) points, respectively; the lower Hospital Anxiety and Depression Scale-Anxiety subscale (HADS-A) on postoperative day 7 were (6.25±1.76) and (7.10±2.05) points, respectively; the Depression subscale (HADS-D) on postoperative day were (6.13±1.82) and (7.15±1.95) points, respectively; the total incidences of delirium were 10.42% (5 cases/48 cases) and 26.92% (14 cases/52 cases), respectively; the Numerical Rating Scale (NRS) scores for resting pain were (2.00±0.41) and (2.17±0.47), respectively; the dynamic pain at 48 h postoperatively were 2.60±0.54 and 2.81±0.60), respectively; the differences of above indicators between two groups were all statistically significant (P<0.05, P<0.01, P<0.001). The main adverse drug reactions included dizziness, tachycardia, bucking, nausea and vomiting in the control group, and dizziness, tachycardia, hypertension, nausea and vomiting in the treatment group. The total incidence of adverse drug reactions was 9.62% (6 cases/52 cases) in the control group and 12.50% (6 cases/48 cases) in the treatment group, with no statistically significant difference (P>0.05).

Subanesthetic-dose esketamine combined with STAPB for patients undergoing radical CRC resection can reduce intraoperative fluid requirements, stabilize perioperative blood pressure and heart rate fluctuations, improve postoperative recovery quality, alleviate postoperative anxiety and depression, and decrease the incidence of postoperative delirium. This combined regimen also yields definite postoperative analgesic effects and does not increase the risk of adverse reactions, thus exhibiting favorable clinical safety and tolerability.