Introduction Postoperative impaired sleep quality and pain are associated with adverse outcomes. Stellate ganglion block (SGB) has shown promising results in enhancing sleep quality and alleviating neuropathic pain. This study aimed to investigate the effects of ultrasound-guided SGB on postoperative sleep quality and pain in patients undergoing breast cancer surgery. Methods This study is a parallel-group randomized controlled clinical trial with two groups: SGB and control. Fifty female patients undergoing breast cancer surgery were randomized in a 1:1 ratio to receive preoperative ultrasound-guided single-injection SGB (SGB group) or just an ultrasound scan (control group). All participants were blinded to the group assignment. The primary outcome was postoperative sleep quality, assessed by the St. Mary’s Hospital Sleep Questionnaire and actigraphy 2 days postoperatively. The secondary outcome was postoperative pain, measured by the visual analog scale. Results A total of 48 patients completed the study, with 23 patients in the control group and 25 in the SGB group. The postoperative St. Mary’s Hospital Sleep Questionnaire scores were significantly higher in the SGB group than in the control group on 1 day postoperative (30.88 ± 2.44 versus 27.35 ± 4.12 points, P = 0.001). The SGB also increased the total sleep time and sleep efficiency (main actigraphy indicators) during the first two postoperative nights. Compared with the control group, preoperative SGB reduced postoperative pain and the incidence of breast cancer-related lymphedema (20% versus 52.2%, P = 0.02, odds ratio 0.229, 95% confidence interval 0.064–0.821). There were no adverse events related to SGB. Conclusion Preoperative ultrasound-guided SGB improves postoperative sleep quality and analgesia in patients undergoing breast cancer surgery. SGB may be a safe and practical treatment to enhance the postoperative quality of life in patients with breast cancer. Trial Registration The study was registered in the Chinese Clinical Trial Registry (ChiCTR2100046620, principal investigator: Kai Zeng, date of registration: 23 May 2021).

To explore effect of goal-directed fluid therapy (GDFT) on early cognitive function in elderly patients with spinal stenosis. 83 elderly patients with spinal stenosis were randomly classified into two groups: control group (n = 40) and GDFT group (n = 43). The Montreal Cognitive Assessment (MoCA) score, IL-6 and S100β levels, hemodynamic parameters, cerebral oxygen saturation (rSO2), arterial lactic acid values, output of surgery, operation time and cases of hypotension, intraoperative complications within 7 days were recorded for all patients. The incidence of postoperative cognitive dysfunction (POCD) was about 21.67% in this study. The MoCA scores, inflammatory mediators, perfusion indexes (rSO2 and lactic acid)and intraoperative hemodynamics(HR, MAP, and CI)were not all the same at different time points (P < 0.05). The levels of inflammatory mediators (IL-6 and S100β) in GDFT group were lower than those in the control group (P < 0.05). Total intake, amount of lactated Ringer's solution and cases of hypotension in GDFT group were significantly lower than control group (P < 0.05), but amount of voluven was higher than control group(P < 0.05). Compared with control group, the incidence of postoperative delirium, nausea and vomiting, and hypotension in GDFT group was lower (P < 0.05). GDFT can maintain the stability of perioperative hemodynamics in the prone position of elderly patients with spinal stenosis, improve the balance between perfusion of tissue and organ and supply and demand of oxygen, reduce the inflammatory response, and reduce the incidence of early POCD in this type of surgery.

Background: Sepsis is characterized by high morbidity and mortality rates, alongside limited therapeutic efficacy. Atrial fibrillation (AF), the most common arrhythmia, has been closely linked to sepsis in prior research. However, the specific mechanisms through which sepsis leads to new-onset AF remain poorly understood. This study focuses on identifying critical genes that are dysregulated in the development of new-onset AF within the context of sepsis, with the goal of uncovering new potential targets for its diagnosis and prevention.Material and methods: Our study began by applying Mendelian Randomization (MR) to assess the causal link between sepsis and AF. We then sourced sepsis and AF datasets from the Gene expression Omnibus (GEO) database. Using Weighted Gene Co-expression Network Analysis (WGCNA), we pinpointed key modules and genes associated with both sepsis and AF conditions. Protein-protein interaction (PPI) network was constructed. The Transcriptional Regulatory Relationships Unravelled by Sentence-based Text-mining (TRRUST) database helped build the transcription factor (TF) interaction network. Key genes were scrutinized through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) to delve into their roles in new-onset AF's pathophysiology during sepsis. We employed the CIBERSORT algorithm to evaluate immune infiltration and the association between key genes and immune cells. The Connectivity Map (CMap) database facilitated the prediction of potential small molecule compounds targeting key genes. To culminate, an acute sepsis mouse model was developed to validate the implicated mechanisms of key genes involved in new-onset AF during sepsis, and to assess the prophylactic effectiveness of identified drug candidates.Results: MR revealed potential independent risk factors for new-onset AF in sepsis. S100A12 was identified as a core interaction gene with elevated levels in sepsis and AF, underscoring its diagnostic and predictive significance. S100A12, along with associated genes, was mainly linked to immune and inflammatory response signaling pathways, correlating with immune cell levels. Targeting S100A12 identifies five potential small molecule therapeutics: amlexanox, balsalazide, methandriol, olopatadine, and tiboloe. In animal studies, acute sepsis increased S100A12 expression in serum and atrial tissues, correlating positively with inflammatory markers (IL-1β, IL-6, TNF-α) and negatively with heart rate, indicating a predisposition to AF. Early amlexanox administration can reduced S100A12 expression, dampened inflammation, and lessened new-onset AF risk in sepsis.Conclusion: This study demonstrates that sepsis may independently increase the risk of new-onset AF. We identified S100A12 as a key gene influencing the new-onset AF in sepsis through immune regulation, presenting considerable diagnostic and predictive value. Notably, amlexanox, by targeting S100A12 emerges as the most clinical relevant intervention for managing new-onset AF in sepsis patients.

Background: Sleep deprivation (SD)-induced cognitive impairment is highly prevalent worldwide and has attracted widespread attention. The temporal and spatial oscillations of circadian genes are severely disturbed after SD, leading to a progressive loss of their physiological rhythms, which in turn affects memory function. However, there is a lack of research on the role of circadian genes and memory function after SD. Therefore, the present study aims to investigate the relationship between circadian genes and memory function and provide potential therapeutic insights into the mechanism of SD-induced memory impairment. Methods: Gene expression profiles of GSE33302 and GSE9442 from the Gene Expression Omnibus (GEO) were applied to identify differentially expressed genes (DEGs). Subsequently, both datasets were subjected to Gene Set Enrichment Analysis (GSEA) to determine the overall gene changes in the hippocampus and brain after SD. A Gene Oncology (GO) analysis and Protein-Protein Interaction (PPI) analysis were employed to explore the genes related to circadian rhythm, with their relationship and importance determined through a correlation analysis and a receiver operating characteristic curve (ROC), respectively. The water maze experiments detected behavioral changes related to memory function in SD rats. The expression of circadian genes in several critical organs such as the brain, heart, liver, and lungs and their correlation with memory function was investigated using several microarrays. Finally, changes in the hippocampal immune environment after SD were analyzed using the CIBERSORT in R software. Results: The quality of the two datasets was very good. After SD, changes were seen primarily in genes related to memory impairment and immune function. Genes related to circadian rhythm were highly correlated with engagement in muscle structure development and circadian rhythm. Seven circadian genes showed their potential therapeutic value in SD. Water maze experiments confirmed that SD exacerbates memory impairment-related behaviors, including prolonged escape latencies and reduced numbers of rats crossing the platform. The expression of circadian genes was verified, while some genes were also significant in the heart, liver, and lungs. All seven circadian genes were also associated with memory markers in SD. The contents of four immune cells in the hippocampal immune environment changed after SD. Seven circadian genes were related to multiple immune cells. Conclusions: In the present study, we found that SD leads to memory impairment accompanied by changes in circadian rhythm-related genes. Seven circadian genes play crucial roles in memory impairment after SD. Naïve B cells and follicular helper T cells are closely related to SD. These findings provide new insights into the treatment of memory impairment caused by SD.

Background: A novel protocol for accurate stellate ganglion block under ultrasound guidance was designed in rats. This technique raises the success rate of stellate ganglion block and reduces the incidence of brachial plexus and vagus nerve block.Methods: Fifty-six Sprague-Dawley were randomly divided into an ultrasound-guided group (n = 28) and a blind technique group (n = 28). The rats in the blind technique group were injected with 1.5% lidocaine mixed with methylene blue after signs of brachial plexus stimulation were elicited. The lateral side of the cephalic brachial vein was located under the first rib, where lidocaine was injected into the rats in the ultrasound-guided group. The up-and-down sequential method of Dixon was used to determine the minimum effective volume for stellate ganglion block in rats. Furthermore, we calculated the required operative duration of the two methods and observed the difference in the lidocaine diffusion range between the two groups.Results: The minimum effective volume for stellate ganglion block in the ultrasound-guided group was 0.040 ml, and the 95% CI was 0.026–0.052 ml. In the blind technique group, the minimum effective volume was 0.639 ml, and the 95% CI was 0.490–0.733 ml. Within the 95% CI of the lowest effective volume, the incidence of brachial plexus block as a complication of stellate ganglion block under ultrasound guidance was 10.00%.Conclusion: Stellate ganglion block under ultrasound guidance is more accurate than blind detection, which the incidence of complications of stellate ganglion block under ultrasound guidance was significantly lower than under blind detection; the rate of methylene blue staining in the vagus nerve was significantly lower under ultrasound guidance.