Introduction: Recent evidence increasingly supports a potential role of Perivascular Macrophages (PVMs), a unique subpopulation of brain immune cells, in the pathogenesis of Alzheimer’s disease (AD). Strategically positioned at the brain-vasculature interface, PVMs sense the redox status, modulate immunity, and potentially influence ferroptosis—an iron-dependent form of regulated cell death increasingly implicated in AD. However, whether the involvement of PVMs in AD pathology specifically entails mechanisms related to the crosstalk between immunometabolism and ferroptosis, and the precise molecular pathways linking PVMs, immunometabolism, and ferroptosis to AD, remains unclear. Methods: We first obtained single-cell RNA sequencing data of PVMs from AD patients and control subjects via the GEO database, identified Differentially Expressed Genes (DEGs), and applied Mendelian Randomization (MR), with robustness validated via leave-one-out analysis to pinpoint key genes among the DEGs with causal relevance to AD. Next, we identified ferroptosis-related genes within these key genes and examined their associations with immune cell infiltration and immunometabolic signaling pathways, while also predicting their regulatory transcription factors to inform potential therapeutic strategies. Results and Discussion: We identified 149 DEGs in PVMs between AD and control groups, which were primarily enriched in immune and metabolic pathways. MR analysis established eight genes (ACSL1, SPATA6, RAB31, NIBAN1, HDAC4, GRAMD1B, GCC2, and DENND3) as causally and negatively associated with AD risk (IVW analysis identified all P < 0.05, with robustness confirmed by leave-one-out analysis), with ACSL1 being recognized as a known ferroptosis driver. Immune cell infiltration analysis revealed significant differences in monocyte and neutrophil proportions in AD, with DENND3 identified as the sole gene significantly correlated with monocyte abundance. The Key genes demonstrated distinct associations with immunometabolic pathways: GRAMD1B expression was positively associated with PI3K/AKT/mTOR signaling, whereas both NIBAN1 and SPATA6 showed enrichment in cells with high Notch signaling activity. ACSL1 exhibited robust associations with multiple pathways implicated in ferroptosis, including the IL-6/JAK/STAT3, interferon-γ, TGF-β, bile acid metabolism, and cholesterol homeostasis pathways, suggesting potential mechanisms that mediate the crosstalk between immunometabolism and ferroptosis. Transcription factor analysis highlighted shared regulation by CEBPD and the SP1/2/3/4 family, indicating convergent transcriptional control of these genes. Conclusion: This study identifies eight key genes in PVMs that may protect against AD through mechanisms involving the interplay between immunometabolism and ferroptosis. Our findings provide novel insights into the function of PVMs in AD pathophysiology and suggest potential therapeutic targets for this devastating neurodegenerative disease.

Background Bone cancer pain (BCP) is one of the most severe complications faced by cancer patients, with complex physiological and pathological mechanisms and unclear molecular characteristics.Methods The BCP model was established by inoculating Lewis lung cancer cells into the femur to induce hyperalgesia and spontaneous pain. Single-cell RNA sequencing technology was used to characterize the cell composition and molecular features of the L2-L4 spinal cord after BCP modelling.Results Our research results identified a total of 10 cell types, namely excitatory neurons, inhibitory neurons, oligodendrocytes, oligodendrocyte precursor cells, Schwann cells, astrocytes, microglia, endothelial cells, fibroblasts, and pericytes. RNA sequencing analysis of the BCP model showed that the proportion of cells in the L2-L4 spinal cord changed significantly, with microglia increased by 45% and oligodendrocytes increased by 43%. Then, data were extracted from microglia, oligodendrocytes, blood-spinal cord barrier component cells (endothelial cells, pericytes, astrocytes), excitatory neurons, and inhibitory neurons, and differential genes were analysed and further enriched. The results suggest that the signalling pathways related to pain perception and transmission and promoting inflammation in the above cells have changed significantly. Finally, this study revealed the interaction between L2-L4 spinal cord cells in BCP.Conclusions These data help to understand the molecular mechanism changes caused by BCP and contribute to the development of new treatment methods.

Vascular invasion is associated with metastasis and poor prognosis in patients with lung adenocarcinoma (LUAD). Recent studies have highlighted the role of intercellular mitochondrial transfer, mediated by both contact-dependent and contact-independent mechanisms, in tumor progression. Here, we reveal an abnormal accumulation of mitochondria in vascular endothelial cells invaded by tumor cells. Further in vivo and in vitro experiments demonstrated that tumor cells can transfer mitochondria with highly expressed mitochondrial tRNA-derived small RNAs (tsRNAs), mt-5'tiRNA-34-GlnTTG, to endothelial cells. Mechanistic investigations indicated that mt-5'tiRNA-34-GlnTTG binds to FUBP3 and facilitates its translocation, ultimately enhancing ribosomal assembly efficiency and translation rates in endothelial cells. This molecular cascade leads to increased endothelial cell proliferation and migration, thereby promoting LUAD metastasis. Moreover, we demonstrated the potential clinical translational value of lipid nanoparticles(LNPs) encapsulating mt-5'tiRNA-34-GlnTTG inhibitors in animal experiments. Utilizing LNPs encapsulating mt-5'tiRNA-34-GlnTTG inhibitors effectively suppressed lung cancer metastasis in in vivo models. These findings reveal a novel mechanism of LUAD progression mediated by mitochondrial tsRNA transfer and highlight a promising therapeutic strategy for limiting metastatic spread.

Cancer is a widespread disease that often causes severe pain, significantly reducing patients’ quality of life and increasing the overall burden of the illness. Managing cancer pain effectively remains a major clinical challenge. Metabolism is a fundamental biological process that involves both the breaking down of substances to produce energy (catabolism) and the building of complex molecules (anabolism). Cancer cells exhibit altered energy metabolism, including glycolysis, oxidative phosphorylation, glutamine metabolism, and lipid metabolism. Emerging research suggests that these metabolic changes can amplify cancer pain through specific signalling pathways, such as AMPK and PI3K/AKT. Targeting these metabolic pathways offers a promising approach for pain relief. This review explores the link between cancer pain and energy metabolism, highlighting potential new therapeutic strategies aimed at metabolic targets.

ObjectivesThe purpose of this study is to explore the clinical value and molecular role of the peroxiredoxins (PRDXs) family in prostate cancer (PCa).MethodsWe first analyzed the differentially expressed genes (DEGs) in Prostatic Adenocarcinoma (PRAD) using the Cancer Genome Atlas (TCGA) database, and then demonstrated the expression of six members of the PRDXs family in PRAD. Subsequently, we evaluated the expression of the PRDXs family using PCa cells and tissues. we also analyzed the diagnosis and overall survival (OS) of the PRDXs family in PCa. We used online tools to analyze the expression of PRDX4 in pan-cancer, the proteins interacting with it, as well as the amino acid regions and sites to pathogenicity. We used CCK8 and transwell assay to detect the proliferation and invasion of PCa cells after silencing PRDX4. Finally, we predicted traditional Chinese medicine drugs targeting PCa with PRDX4.ResultsWe found that PRDX2 and PRDX4 were highly expressed in PRAD through the TCGA database. Compared with prostate epithelial cells, PRDX2, PRDX3, PRDX4, and PRDX6 were expressed higher in PCa cells. In PCa tissues, the PRDXs family is widely expressed positively (P<0.05). The PRDXs family has relatively low diagnostic value in PCa, except for PRDX4. Based on the above results, we selected PRDX4 for molecular role detection. We found that the expression of PRDX4 in PCa was higher than that in more than half of the cancer types in pan-cancer. We found that there are eight proteins interacting with PRDX4. The pathogenic amino acid regions and sites of PRDX4 protein mutation that are prone to disease were mainly concentrated in the area after the 50th amino acid. We found that silencing PRDX4 slowed down the proliferation and invasion of PCa cells. Finally, we found that there are 14 traditional Chinese medicines targeting PCa with PRDX4, among which 5 have statistical differences, and Shi Liu Zi may be the best targeted traditional Chinese medicine drug.ConclusionThis study found that PRDX4 is highly expressed in PCa, which may promote the phenotypic progression of PCa cells and has high clinical value.

Despite being the leading cause of lung cancer-related deaths, the underlying molecular mechanisms driving metastasis progression are still not fully understood. Transfer RNA-derived fragments (tRFs) have been implicated in various biological processes in cancer. However, the role of tRFs in lung adenocarcinoma (LUAD) remains unclear. Our study identified a tRF, tRF-Val-CAC-024, associated with the high-risk component of LUAD, through validation using 3 cohorts. Our findings demonstrated that tRF-Val-CAC-024 acts as an oncogene in LUAD. Mechanistically, tRF-Val-CAC-024 was revealed to bind to aldolase A (ALDOA) dependent on Q125/E224 and promote the oligomerization of ALDOA, resulting in increased enzyme activity and enhanced aerobic glycolysis in LUAD cells. Additionally, we provide preliminary evidence of its potential clinical value by investigating the therapeutic effects of tRF-Val-CAC-024 antagomir-loaded lipid nanoparticles (LNPs) in cell-line-derived xenograft models. These results could enhance our understanding of the regulatory mechanisms of tRFs in LUAD and provide a potential therapeutic target.

Background: To identify the potential key genes of ferroptosis in the pathogenesis of lung cancer with bone metastasis (LCBM) by bioinformatics analysis to provide new targets for treating LCBM and an indicator for early monitoring.Methods: We first obtained differentially expressed genes (DEGs) associated with ferroptosis from the Gene Expression Omnibus (GEO) database. MiRWalk 2.0 was used to predict the key microRNAs (miRNAs) and construct related gene-miRNA interaction networks. The functional enrichment analysis of key miRNAs was performed using the miEAA database. Finally, the clinical data of 105 lung cancer patients were retrospectively analyzed, and logistic regression analysis was conducted to assess the relationship between serum alkaline phosphatase (ALP), neuron-specific enolase (NSE), and bone metastasis in lung cancer patients, and a receiver operating characteristic (ROC) curve was drawn.Results: We identified 15 ferroptosis-related genes that were differentially expressed in lung cancer bone metastasis. GO and KEGG enrichment analyses suggested that these genes may affect the oxidative stress response, hypoxia response, rough endoplasmic reticulum, mitochondrial outer membrane, iron-sulfur cluster binding, virus receptor activity, central carbon metabolism in cancer, the interleukin-17 (IL-17) signaling pathway, and other aspects to participate in the occurrence and development of lung cancer bone metastasis. Among the 105 lung cancer patients included in the study, 39 cases had bone metastasis, and the incidence rate was 37.14%. A high Eastern Cooperative Oncology Group (ECOG) score and serum ALP and NSE overexpression were associated with bone metastasis in patients with lung cancer. By assessing the risk of bone metastasis in patients with lung cancer, we found that the Area Under Curves (AUCs) of serum ALP and NSE alone and combined were >0.70.Conclusions: The differentially expressed ferroptosis-related genes and predicted miRNA regulatory network in lung cancer bone metastasis and the related functional enrichment analysis provide new targets for the treatment of lung cancer bone metastasis. At the same time, from a serological perspective, it was found that early monitoring of serum ALP and NSE expression in patients with lung cancer could be considered to assess the risk of bone metastasis in the future.

目的 观察超声引导低位前锯肌平面阻滞(SSPB)对胃癌根治术后炎症及康复的影响.方法 采用随机数字表法将2018年5月至2019年12月该院收治的80例择期行胃癌根治术患者分为C组(单纯全身静脉麻醉)和SSPB组(全身麻醉复合SSPB),每组40例.SSBP组在麻醉诱导后行超声引导双侧腋中线第8肋水平型前锯肌平面阻滞,分别注入0.25％罗哌卡因,每侧各30 mL.两组均采用全身麻醉气管插管,术毕均给予患者自控静脉镇痛.记录两组患者术中芬太尼、瑞芬太尼用量;测定两组患者术前,术后1、3 d C反应蛋白(CRP)水平及中性粒细胞计数;记录两组患者术后24、48 h视觉模拟疼痛量表(VAS)评分,恶心、呕吐发生次数,术后镇痛泵有效按压次数及补救镇痛例数;记录两组患者首次排气时间、住院时间及术后不良反应发生情况;记录两组患者术前、术后3 d恢复质量.结果 SSBP组患者术中瑞芬太尼用量明显低于C组,差异有统计学意义(P<0.05);两组患者术后1、3 d CRP水平及中性粒细胞计数均明显升高,但SSBP组患者术后1、3 d CRP水平及中性粒细胞计数明显低于C组,差异均有统计学意义(P<0.05);与C组比较,SSPB组患者术后24 h VAS评分明显降低,术后24、48 h内有效按压次数、术后48 h内镇痛补救发生率均明显减少,术后首次排气时间明显缩短,差异均有统计学意义(P<0.05);但两组患者术后48 h VAS评分、住院时间、术后不良反应发生率比较,差异均无统计学意义(P>0.05).SSBP组患者术后3 d术后恢复质量QoR-40量表总分及各系项目评分均明显高于C组.结论 超声引导SSPB可降低胃癌根治术患者术后CRP水平及中性粒细胞计数,改善机体的炎性反应及术后疼痛,提高患者术后早期恢复质量.

Bone cancer pain (BCP) severely compromises the life quality of patients with advanced cancer or bone metastases. This study investigates the analgesic effect of sodium aescinate (SA) on BCP, and the underlying mechanisms within the spinal cord (SC) and dorsal root ganglion (DRG). Walker 256 cells were intratibially inoculated into rats to establish a BCP model. 10, 20, and 40 g/L of SA was intrathecally injected, respectively, and then, hyperalgesia and allodynia were evaluated by measuring the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). The effect of SA on neuroinflammation was observed by detecting the production of the pro-inflammatory cytokines based on RT-qPCR and ELISA. The NF-κB and p38 MAPK/c-Fos signaling was detected by WB analysis. Furthermore, RT-qPCR and WB analyses of Iba-1and CD206 were performed to assess microglial activation. The development of hyperalgesia and allodynia, and an increase of pro-inflammatory cytokines production, as well as microglial activation, were observed in the BCP rats. SA (40 g/L) not only relieved the pain-related behaviors induced by BCP but also suppressed the release of pro-inflammatory cytokines and the activation of microglia in the SC and DRG. SA could also inhibit p38 MAPK/c-Fos signaling in both the SC and DRG, which might contribute to the suppression of microglial activation. Our findings suggest that SA plays a promising analgesic role in the BCP rats by suppressing inflammation and microglial activation, and these effects may be associated with the suppression of p38 MAPK/c-Fos signaling.

Background Dorsal root ganglia (DRG) plays an important role in mediating the peripheral sensation transduction through the primary afferent neurons in pain research. Neuropathic pain (NP) is a syndrome of hyperalgesia, spontaneous pain and allodynia caused by central or peripheral nerve injury. Recent trends of study are turning towards the development of therapies for the management of NP. Activation of autophagy in glial cells in the spinal cord has been reported to be associated with attenuation of NP, but the autophagic process in DRG is rarely studied. Methods The analgesic effect of electroacupuncture (EA) was evaluated in NP-induced rats developed using spared nerve injury (SNI). Acupuncture or EA was performed after 7 days of SNI at Zusanli (ST36) and Huantiao (GB30) acupoints. Then, the activation status of autophagy process in DRGs of rats treated with SNI and EA were investigated, and the possible mechanism of the analgesic effect of EA were explored. Results Application of EA has been found to reduce mechanical hyperalgesia. Autophagy indicator p62 was colocalized with the marker proteins for macrophages (CD11b), but not with NeuN (marker protein for neurons) or GFAP (marker protein for satellite glial cells), as shown by immunofluorescence. Western blots results indicate that the expression levels of p62, Beclin-1 and LC3-II in the L4-L6 DRG of rats in the SNI group were increased, compared with that in the control group. EA treatment resulted in decreased expression of p62 and increased expression of Beclin-1 and LC3-II/LC3-I. Furthermore, we explored the causal relationship between EA-induced suppression of NP and increased levels of autophagy in DRG using electron microscopy and the AMPK (AMP-activated protein kinase) inhibitor compound C. Conclusions SNI achieved a significant upregulation of autophagy levels in DRG macrophages. Furthermore, EA attenuated NP, which may contribute to the promotion of AMPK/mTOR (mammalian target of rapamycin)-mediated autophagy in DRG macrophages. Therefore, this strategy provides a new target for therapeutic intervention of NP.

Objective:To observe the effects of ultrasound-guided transverse abdominal muscle plane block (TABP) on neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) in the peripheral blood of patients undergoing radical gastrectomy.Methods:A total of 100 patients who were scheduled for radical gastrectomy were selected. According to the random number table method, they were randomly divided into two groups ( n=50): a TAPB combined with general anesthesia group (group TAP+GA) and a general anesthesia group (group GA). Group TAP+GA and group GA underwent ultrasound-guided TABP assisted with general anesthesia, and routine general anesthesia, respectively. Both groups were compared for operation time, anesthesia time, blood loss, and the dosages of fentanyl and remifentanil. Their counts of neutrophils, platelets and lymphocytes, NLR and PLR in the peripheral blood were recorded before and 24 h and 72 h after surgery. Their Visual Analogue Scale (VAS) scores 24 h and 48 h after operation, adverse reactions and the length of hospitalization stay were recorded. Results:There were no significant differences in operation time, anesthesia time, blood loss and fentanyl dosage between the two groups. Compared with group GA, the dosage of remifentanil in group TAP+ GA was significantly reduced ( P<0.05). There were no statistical differences in the counts of neutrophils, platelets and lymphocytes, PLR and NLR in the peripheral blood between the two groups ( P>0.05). Compared with group GA, group TAP+GA presented remarkably reduced counts of neutrophils in the peripheral blood 24 h and 72 h after operation ( P<0.05). There were no statistical differences in the counts of lymphocytes and platelets and PLR between the two groups 24 h and 72 h after operation ( P>0.05). No statistical difference was found in the value of NLR between the two groups 24 h after operation ( P<0.05). The value of NLR in the peripheral blood of group TAP+GA was significantly lower than that in group GA 72 h after operation ( P>0.05). The VAS score 24 h and 48 h after operation in group TAP+GA were lower than that in group GA ( P<0.05). Postoperative nausea and vomiting were significantly reduced in group TAP+GA, compared with group GA ( P<0.05). There were no statistical differences in the length of hospitalization stay, postoperative pulmonary infection, anastomotic fistula, and postoperative intestinal obstruction between the two groups ( P>0.05). Conclusions:Ultrasound-guided TABP assisted general anesthesia is useful for reducing the counts of neutrophils and NLR in patients. It also improves postoperative pain, and reduces the occurrence of postoperative nausea and vomiting.

目的 探讨通气侧肺前列腺素E1(PGE1)雾化吸入预给药对食管癌患者FiO250％单肺通气(OLV)期间机体氧合的影响.方法 选择拟行左剖胸食管癌根治术的患者113例,男92例,女21例,年龄18～79岁,BMI<30 kg/m2,ASAⅡ或Ⅲ级.采用随机数字表法将患者分为四组:PGE10.1μg/kg组(P1组,n=29)、PGE10.2μg/kg组(P2组,n=29)、PGE10.3μg/kg组(P3组,n=30)和生理盐水对照组(C组,n=25).麻醉平稳改右侧卧位后,P1组、P2组和P3组分别给予右侧肺PGE10.1、0.2和0.3μg/kg(以生理盐水稀释至10 ml)雾化吸入,C组给予右侧肺生理盐水10 ml雾化吸入,雾化吸入时间均为10 min.记录术前PaO2、手术时间、OLV时间、术中出血量、尿量、输液量.分别于全麻后右侧卧位时(T0)、OLV 10 min(T1)、OLV 15 min(T2)、OLV 30 min(T3)、OLV 60 min(T4)、OLV 120 min(T5)抽取桡动脉血和右颈内静脉血各2 ml,采样后立刻行血气分析,计算肺内分流率(Qs/Qt),记录T0—T5时PaO2、PaCO2、PETCO2、MAP、HR、Ppeak.于T0、T4、OLV结束恢复双肺通气30 min(T6)及术后24 h(T7)抽取中心静脉血,采用ELISA法检测血清白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)浓度.记录术后第2天临床肺部感染评分(CPIS),记录术后7 d内肺不张、吻合口瘘等肺部并发症的发生情况以及ICU停留时间、总住院时间.结果 四组术前PaO2、手术时间、OLV时间、术中出血量、尿量、输液量差异无统计学意义.T1—T3时P3组Qs/Qt明显低于其余三组,PaO2明显高于其余三组(P<0.05);P2组Qs/Qt明显低于P1组和C组,PaO2明显高于P1组和C组(P<0.05);P1组Qs/Qt明显低于C组,PaO2明显高于C组(P<0.05).T4时P1组、P2组和P3组Qs/Qt明显低于C组,PaO2明显高于C组(P<0.05);P3组Qs/Qt明显低于P1组,PaO2明显高于P1组(P<0.05).T1、T2时P3组MAP明显低于C组(P<0.05).T4、T6、T7时P1组、P2组和P3组血清IL-6、TNF-α浓度明显低于C组(P<0.05).P1组、P2组和P3组CPIS评分明显低于C组(P<0.05).四组术后肺不张、吻合口瘘发生率、ICU停留时间、总住院时间差异无统计学意义.结论 在FiO250％的条件下,于双肺通气期间预先给予OLV期间的通气侧肺雾化吸入PGE1,可以通过降低肺内分流率而改善氧合,以保证机体氧供(该效应在OLV 10、15、30 min时呈明显的剂量依赖性),同时降低患者围术期血清IL-6和TNF-α浓度.

目的:探讨PDCA循环在手术室外周静脉留置针输液安全管理中的应用效果.方法:收集2021年7至9月在南京某三甲医院手术室内进行外周静脉留置针输液患者的输液情况,于2021年10月至12月实施PDCA循环管理并收集相关资料.比较PDCA循环管理前后,手术室外周静脉留置针输液过程中不安全现象的发生情况、相关人员对输液管理的满意度以及手术室护士的焦虑自评量表(SAS)评分.结果:通过鱼骨图分析发现,引起输液不安全问题发生的决定性因素为输液安全意识不强,缺乏精细化管理流程,管路护理知识缺乏.应用PDCA循环后,引起输液不安全问题的3个决定性因素发生例次均降低,差异均有统计学意义(2X值分别为28.59、25.53、26.26,均P＜0.01);输液不安全问题(外周输液渗出、输液器滑脱、静脉留置针滑脱、静脉留置针堵管、穿刺部位皮肤红肿)发生率也均降低,差异均有统计学意义(2X值分别为58.33、25.77、12.56、7.60、14.03,均P＜0.05);患者、麻醉医生对输液管理满意度均提高,手术室护士因输液不安全引起的SAS评分降低,差异均有统计学意义(P＜0.05).结论:PDCA循环管理可有效地减少手术室外周留置针输液过程中不安全问题的发生,提高患者、麻醉师对输液管理的满意度,减少手术室护士的焦虑,可应用于手术室外周静脉留置针输液的安全管理.

Posttraumatic stress disorder (PTSD) is a prevalent psychiatric disorder and sometimes deadly consequence of exposure to severe psychological trauma. However, there has been little known about the definitive molecular changes involved in determining vulnerability to PTSD. In the current study, we used proteomics to quantify protein changes in the hippocampus of foot shocks rats. A total of 6151 proteins were quantified and 97 proteins were significantly differentially expressed. The protein-protein interaction (PPI) analysis showed that oxidation-reduction process and glutathione homeostasis may be the potential key progress of being vulnerable to PTSD. The Gene Ontology analysis revealed enriched GO terms in the protein groups of Susceptible group vs Control group rats for glutathione binding,oligopeptide binding,modified amino acid binding,and glutathione transferase activity for their molecular functions (MF) and in the process of cellular response to toxic substance,xenobiotic metabolic process, urea metabolic process, and response to drug for the biological process (BP).SIGNIFICANCE:In recent years, there has been a growing interest in mental illness associated with trauma exposure. We found that stress susceptibility was associated with increased expression of arginase 1 indicated as a potential treatment target. Our results also proposed that carbonic anhydrases 3 could be a biomarker for the development of PTSD. This research helps to explain the potential molecular mechanism in PTSD and supply a new method for ameliorating PTSD.

目的 探讨血清中性粒细胞/淋巴细胞比值(NLR)预测老年胃癌根治术患者术后认知功能障碍(POCD)的价值.方法 选择择期行胃癌根治术患者100例,男67例,女33例,年龄≥65岁,ASA Ⅱ或Ⅲ级.患者手术均在气管插管全麻下进行,在术前及术后第7天通过Z计分法评估患者认知功能,根据评分结果将患者分为两组:POCD组和NPOCD组.记录术前1 d、术后1、3 d血清中NLR的变化.应用受试者工作特征(ROC)曲线,分析各时点血清NLR对老年胃癌根治术患者发生POCD的预测价值.结果 术后7 d发生POCD患者22例(22％).与术前1 d比较,术后1、3 d两组NLR明显升高(P＜0.05).术后1、3d POCD组血清NLR明显高于NPOCD组(P＜0.05).术后3 d血清中NLR预测老年胃癌根治术患者发生POCD的最佳界值为6.986,预测POCD发生的AUC为0.818(95％CI 0.728～0.888),敏感性和特异性分别为88.5％和68.2％,高于术后1 d NLR的AUC为0.799(95％CI 0.707～0.872).结论 老年胃癌根治术患者术后3 d NLR对术后7 d POCD发生的预测价值较高,血清中NLR的升高可能与术后POCD的发生相关,术后NLR升高是发生POCD的危险因素.

目的 比较老年结直肠癌患者手术后使用切口局部持续镇痛系统与使用静脉自控镇痛泵的镇痛效果及镇痛相关的不良反应情况.方法 选择2017年3月至2018年8月南京医科大学附属肿瘤医院普外科老年结直肠癌开腹手术患者46例,按照随机数字表法分为成两组.静脉自控镇痛组(n=23):手术结束后常规配制使用静脉自控镇痛泵;切口镇痛组(n=23):手术关腹时切口皮下放置多孔给药导管,接镇痛泵持续输注罗哌卡因.术后随访并记录疼痛评分、患者恶心、呕吐发生情况、Ramsay评分、呼吸抑制发生率以及皮肤瘙痒情况;吗啡补救使用剂量、切口感染情况、切口愈合情况以及肠功能恢复时间.结果 与静脉自控镇痛组相比,切口镇痛组术后6 h及12 h疼痛评分更低(P<0.05),且切口镇痛组术后恶心、呕吐发生率更低,吗啡补救使用剂量更少,术后肠功能恢复时间更短(P<0.05);两组患者Ramsay评分、呼吸抑制发生率、皮肤瘙痒情况、切口感染情况及切口愈合情况无差异.结论 老年患者腹部手术后使用切口镇痛系统进行术后镇痛效果更好,且副作用较低,加速患者术后康复,值得推广使用.

Objective To evaluate the efficacy of different doses of oxycodone for prevention of fen-tanyl-induced cough during induction of general anesthesia. Methods A total of 250 American Society of Anesthesiologists physical statusⅠor Ⅱ patients of both sexes, aged 22-62 yr, weighing 47-81 kg, un-dergoing elective surgery, were divided into 5 groups (n＝50 each) using a random number table method:different doses of oxycodone groups (O1-4groups) and control group (group C). Oxycodone 0. 025, 0. 050, 0. 075 and 0. 100 mg∕kg were intravenously injected in O1-4groups, respectively, while the equal volume of normal saline was given instead of oxycodone in group C. Five minutes later fentanyl 3 μg∕kg was intrave-nously injected within 5 s, and then 2 min later the other drugs were administered for induction. The occur-rence and severity of cough were observed within 2 min after fentanyl injection. The development of respira-tory depression and hypotension and severe bradycardia during induction of anesthesia were recorded within 5 min after oxycodone injection. Results The incidence of cough was significantly lower in O1-4groups than in group C (P＜0. 05). There was no significant difference in the incidence of cough among O1-4groups (P＞0. 05). No respiratory depression was found in C and O1-3groups. The incidence of respiratory depression was significantly higher in group O4than in C and O1-3groups (P＜0. 05). There were no significant differ-ences in the incidence of hypotension or severe bradycardia during induction of anesthesia among the five groups (P＞0. 05). Conclusion Oxycodone 0. 025 mg∕kg provides better efficacy in preventing fentanyl-induced cough during induction of general anesthesia.

Objective To evaluate the changes in expression of cold-inducible RNA-binding protein (CIRP) in hippocampus during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.Methods Seventv-two clean-grade healthy male Sprague-Dawley rats,weighing 280-350 g,aged 8-10 weeks,were divided into 2 groups using a random number table:sham operation group (S group,n=18) and ischemia-reperfusion group (I/R group,n=54).Tracheal intubation was performed and artery and veins were punctured in group S.Ventricular fibrillation was induced by transoesophageal cardiac pacing to establish the model of cardiac arrest in group I/R.Rats were sacrificed at 12,24 and 48 h after resuscitation and the hippocampus was harvested for determination of CIRP,tumor necrosis factor-alpha (TNF-α) and interleukin-lbeta (IL-1β) protein and mRNA expression (by quantitative polymerase chain reaction or Western blot) and for determination of pathological changes of hippocampi (with a light microscope).Results Compared with group S,the expression of CIRP mRNA in hippocampus was up-regulated at 24 and 48 h after resuscitation,the expression of TNF-α mRNA was up-regulated at 12,24 and 48 h after resuscitation,the expression of IL-1β mRNA was up-regulated at 12 and 24 h after resuscitation,and the expression of CIRP,TNF-α and IL-1β was up-regulated at 12,24 and 48 h after resuscitation in group I/R (P＜0.05).Pathological changes in hippocampal CA1 region were found in group I/R.Conclusion The expression of CIRP in hippocampus is up-regulated,which promotes central inflammatory responses during brain injury in a rat model of cardiac arrest-cardiopulmonary resuscitation.

Purpose: To investigate the role of chemokine in the anterior cingulate cortex (ACC) in a rat model of chronic neuropathic pain. Methods: 80 male Sprague-Dawley rats were randomly assigned into 4 groups (n = 20): the sham group, the control group, the PBS treatment group and the anti-CX3CL1 treatment group. In the sham group, the unilateral infraorbital nerve was only exposed, but not ligated; in the control group, the unilateral infraorbital nerve was exposed and ligated. In the sham and the control group, the behavioral test was undertaken and the protein expression of CX3CL1 and CD11b was compared. Results: Compared with the sham group, there was a significant reduction in the feeling threshold in the ipsilateral ION territory from 3 d to 14 d after CCI-ION in the control group (P<0.05). Rats given antibody in the anti-CX3CL1 treatment group showed an evident increase of the feeling threshold compared with the PBS group (P<0.05). Conclusion: The ACC may take part in the chronic neuropathic pain via associating with the activated microglial cells and increased expression of CX3CL1.

患者,女,62岁,体重54 kg,ASA Ⅲ级。因“胰腺癌伴肝转移化疗介入治疗后半月余”入院,拟在全麻下行“胰腺肿瘤纳米刀消融术”。既往无传染病病史,无高血压、心脏病、糖尿病等慢性病史。确诊胰腺恶性肿瘤后经八个周期的化疗后病情稳定,各项指标除 CA12556.73 U/ml,CA199181.3 U/ml之外无明显异常。术前 MRI 示：肝右前叶病灶合并治疗后改变较前相似,余肝内多发转移灶较前增大。患者于2016年4月21日转入介入科行肝动脉化疗栓塞术,控制肝内转移灶。