Sleep disruption (SD) is increasingly recognized as a systemic stressor that worsens inflammatory disease, yet how it reshapes lung immunity remains poorly defined. To address this, we combined an ovalbumin (OVA)-induced allergic airway inflammation model with sleep disruption paradigms, together with transcriptomic profiling, in vivo pharmacological interventions, and in vitro RAW264.7 macrophage-like cells. In an OVA-induced allergic airway inflammation model, SD markedly increased methacholine responsiveness, aggravated peribronchial inflammation and mucus metaplasia, and promoted a more severe inflammatory airway phenotype. These changes were accompanied by enhanced pulmonary catecholaminergic signaling, reflected by increased tyrosine hydroxylase immunoreactivity and elevated norepinephrine levels. Mechanistically, SD induced mitochondrial dysfunction in the lung, characterized by ultrastructural injury, increased mitochondrial reactive oxygen species, and accumulation of cytosolic mtDNA, together with activation of the cGAS-STING pathway. Cell-type localization analysis showed that activated STING signaling was predominantly associated with F4/80-positive pulmonary macrophages, whereas overlap with Ly6G-positive neutrophils was limited. In vivo, chemical sympathectomy with 6-hydroxydopamine attenuated airway hyperresponsiveness and reduced pulmonary STING pathway activation. In RAW 264.7 cells, norepinephrine (NE) amplified lipopolysaccharide (LPS)-induced inflammatory responses, promoted mitochondrial oxidative stress, increased cytosolic mtDNA accumulation, and enhanced IRF3 activation, effects that were attenuated by adrenergic blockade and STING inhibition. Together, these findings support a model in which sleep disruption increases catecholaminergic exposure in allergic lungs, thereby driving macrophage mitochondrial stress and mtDNA-cGAS-STING dependent inflammatory amplification. This work identifies a brain-to-lung neuroimmune mechanism linking sleep loss to worsened airway disease and highlights sympathetic-macrophage signaling as a potential mechanism-informed therapeutic target. Sleep disruption enhances sympathetic nervous system activity, leading to increased norepinephrine (NE) release to the lung. NE acts on pulmonary macrophages, likely through adrenergic signaling pathways, inducing mitochondrial oxidative stress and structural disruption. This is characterized by elevated mitochondrial ROS, which promotes the release and cytosolic accumulation of mitochondrial DNA (mtDNA). The released mtDNA activates the cGAS-STING signaling pathway, leading to TBK1-IRF3 activation and downstream inflammatory gene expression, ultimately contributing to enhanced airway inflammation, mucus hypersecretion, and airway hyperresponsiveness under allergen challenge. Created in BioRender. Haotian, C. (2026) https://BioRender.com/xywyr61.

Asthma is frequently accompanied by anxiety disorders, yet the mechanisms linking asthma to neuropsychiatric symptoms remain poorly defined. Here, we investigated the contribution of the pulmonary microbiota and its metabolites to anxiety-like behavior in an ovalbumin-induced asthma mouse model. Behavioral testing and resting-state functional magnetic resonance imaging revealed anxiety-like phenotypes and altered hippocampal function in a subset of asthmatic mice that were susceptible to anxiety-like behavior. These mice exhibited hippocampal neuroinflammation and neuronal damage, accompanied by dysbiosis of the pulmonary microbiota. Intratracheal transplantation of lung microbiota from anxiety-susceptible donors induced similar behavioral changes in recipient mice, indicating a causal role of the pulmonary microbiota. Untargeted metabolomics identified formononetin as a candidate metabolite positively correlated with the relative abundance of Acidobacteria. Intratracheal administration of formononetin alleviated anxiety-like behaviors, reduced hippocampal inflammation and injury, and restored hippocampal BDNF/TrkB signaling. However, these effects were abolished by the TrkB antagonist ANA-12. Transcriptomic and immunofluorescence analyses suggested that formononetin acts through modulation of hippocampal microglia. In vitro and small RNA sequencing analyses further demonstrated that formononetin promotes BDNF production by downregulating miR-1912-3p, thereby relieving its translational repression in microglia. Together, these findings reveal a lung-brain axis in which a pulmonary microbiota-associated metabolite modulates microglial function to alleviate asthma-related anxiety.

Airway epithelial dysfunction is a hallmark of asthma, contributing to chronic inflammation and structural remodeling. Recent research suggests the role of post-translational modifications in regulating epithelial immune responses. However, the role of specific deubiquitinating enzymes (DUBs) remains unclear. In this study, we identified OTU deubiquitinase 7a (OTUD7a) as a gene that is significantly downregulated in a murine model of allergic asthma. Transcriptomic analysis of two independent datasets (GSE71822 and GSE9383) consistently revealed the suppression of OTUD7a in asthmatic lungs. Furthermore, immunofluorescence analysis suggested that OTUD7a was detected in CC10-positive bronchiolar epithelial cells, non-ciliated epithelial cells known for their anti-inflammatory functions. To explore the molecular associations of OTUD7a, we established a club cell line overexpressing Flag-tagged OTUD7a and performed co-immunoprecipitation-mass spectrometry (Co-IP/MS). We identified 1135 candidate interacting proteins. In parallel, LC-MS/MS-based ubiquitinome profiling in ovalbumin (OVA)-induced asthmatic lungs revealed widespread changes in protein ubiquitination, with more than 3000 differentially modified ubiquitination sites. These changes were enriched in pathways associated with immune signaling, cytoskeletal dynamics, and epithelial barrier function. Collectively, our findings suggest that OTUD7a, as a DUB detected in CC10-positive bronchiolar epithelial cells, is markedly decreased in asthma and they present a comprehensive landscape of ubiquitination changes in allergic airway inflammation. Therefore, our study offers new insight into post-translational regulation in the pathogenesis of asthma.

Purpose:To observe the effect of ultrasound-guided single right stellate ganglion block (SGB) on postoperative first night sleep in patients undergoing maxillofacial surgery. Methods:This study included 120 participants who underwent maxillofacial surgery under general anesthesia from 11 April 2023 to 31 August 2024. These participants were divided into three groups, namely blank control group, 1% lidocaine group, and 2% lidocaine group, with 40 patients in each group. Their blood pressure, heart rate, blood oxygen saturation, and the visual analog scale (VAS) scores were recorded before the operation (baseline), immediately after awakening, immediately after arrival at the anesthesia intensive care unit (AICU), 1 h after arrival at the AICU, and 2 h after arrival at the AICU. The Richard-Campbell Sleep Questionnaire (RCSQ) was used to evaluate the sleep quality in the three patient groups on the first night after surgery. Complications associated with SGB and the number of sedative analgesic medication doses supplemented on the first postoperative night were recorded. Results:The RCSQ scores of the blank control group, 1% lidocaine group, and 2% lidocaine group were 44.5 (33.3, 62.0), 67.0 (54.0, 87.9), and 96.0 (65.8, 100.0), respectively, and the scores gradually increased (comparison among three groups: P < 0.0001). There was a statistical difference among the three groups in the gradual slowing down of heart rate after extubation and wakefulness, immediately after arrival at the AICU, 1 h after arrival at the AICU, and 2 h after arrival at the AICU. There were no significant complications of SGB in the three groups. The 1% and 2% lidocaine group reduced the number of postoperative sufentanil remedies. Conclusion:Ultrasound-guided single right SGB effectively improved the quality of postoperative first night sleep according to RCSQ and reduced stress reactions within 2 h in patients undergoing maxillofacial surgery. Notably, the efficacy of 4 mL of 2% lidocaine was superior to that of 4 mL of 1% lidocaine, making it a safe and effective method for improving postoperative sleep.

The gut-lung axis, a vital signaling network linking the gastrointestinal and pulmonary systems, regulates immune responses and the progression of respiratory diseases. Nutritional components can modulate the gut microbiome and regulate the synthesis of critical intestinal microbial metabolites, which are essential for maintaining immune homeostasis and supporting respiratory health. Conversely, poor dietary habits exacerbate asthma and other respiratory conditions through the modulation of systemic inflammation and immune responses. Dietary interventions, such as the Mediterranean diet, are reported to restore microbial balance and improve respiratory health by increasing the production of anti-inflammatory metabolites, potentiating immune responses, and preserving epithelial barrier integrity. In contrast, Western dietary patterns, which are characterized by high fat and low fiber intake, disrupt microbial diversity, resulting in increased levels of pro-inflammatory metabolites that aggravate airway inflammation and asthma severity. This review aimed to elucidate the mechanisms underlying the regulatory effects of gut microbes and their metabolites on asthma. Additionally, previous findings related to the gut-lung axis have been summarized, providing insights into potential therapeutic strategies for asthma management.

Patients with microtia undergoing ear reconstruction with costal cartilage harvest often experience significant postoperative chest pain. The efficacy and safety of ultrasound-guided superficial serratus anterior plane block (SSAPB) in pediatric patients remain unclear. In this randomized controlled trial, sixty children were randomized to SSAPB or incision infiltration anesthesia (IA) (30 ml of 0.25

Objective:To explore the feasibility of establishing a mouse stellate ganglion (SG) regulation model through infrared polarized light (IPL) irradiation of the SG, and preliminarily evaluate its effects on SG function and related physiological indicators. Surgery, and IPL groups, with 8 mice in each group. A ZZIR-ID therapeutic device was used to directly irradiate bilateral SG regions of IPL group mice, with wavelength 980 nm, power density 1000 mW/cm2, 10 min per session (5 min per side), every other day for 6 times. The control group received no treatment, while the. Results:Compared with the control and Sham surgery groups, the incidence of Horner's syndrome in the IPL group increased significantly (P < 0.05), manifesting as bilateral ptosis and enophthalmos, lasting about 2 h. Immediately after treatment, eye temperature in the IPL group increased significantly compared to pre-treatment (P < 0.05). Heart rate in the IPL group decreased significantly 30 min post-treatment compared to pre-treatment (P < 0.01), lasting 1-2 h. There was no statistically significant difference in weight changes between groups (P > 0.05). In all treated mice, the characteristic signs of Horner's syndrome developed within minutes of starting IPL exposure, reached their peak intensity between 1.5 and 2.5 h, and resolved completely within 3-4 h of the 10-min irradiation session. Conclusion:IPL irradiation of SG can effectively induce Horner's syndrome in mice, elevate eye temperature, and reduce heart rate. These findings suggest IPL as a potential method for modulating SG activity in preclinical models.

Airway hyperresponsiveness (AHR) is often associated with mood disorders such as anxiety and depression which makes the airway symptoms more complicated and refractory. However, the underlying mechanisms remain unclear. This study investigated whether this was related to the activation of microglia in the hippocampus. Female Balb/c mice were randomly assigned into an AHR model induced by ovalbumin (OVA) and an anxiety model induced by chronic restraint stress (CRS). Anxiety-like behavior was assessed by open field test, elevated plus maze and tail suspension test. Airway resistance following methacholine inhalation was measured by using the FlexiVent apparatus. Hematoxylin and eosin, periodic acid-Schiff as well as Masson trichrome were performed to evaluate inflammatory cell infiltration in the lung tissue. In addition, the status of microglia in the hippocampus was evaluated by immunofluorescence, while the activation of inflammation signaling pathway was assessed by Western blots. Compared with the Control group, mice in OVA and CRS groups exhibited higher airway resistance, spent less time in the center area of the open field and the open arms of the elevated plus maze, and showed increased immobility time in the tail suspension test. Microglia in hippocampus exhibited pronounced morphological alterations, increased expression of activation markers Iba1 and CD86, and upregulation of the NLRP3 inflammasome pathway. Minocycline treatment significantly reduced the airway resistance and anxiety-like behavior in OVA mice, while also inhibiting activation of the NLRP3 inflammasome pathway. This study provides evidence for the comorbidity between AHR and anxiety, potentially mediated by hippocampal microglial activation and the NLRP3/Caspase-1/IL-1β pathway. These findings enhance our understanding of the underlying mechanisms, and offer potential targets for treating AHR-related anxiety.

Airway hyperresponsiveness (AHR) is characterized by excessive contraction of airway smooth muscle, leading to airflow limitation, increasing perioperative airway spasm and even triggering the defense of silent lungs, which can lead to delayed surgery. Stellate ganglion blockade (SGB) has gained attention for its immunomodulatory and anti-inflammatory effects; however, its impact on AHR and the underlying mechanisms remain unexplored. This study aims to evaluate whether SGB reduces AHR and if this effect is related to inflammation. The experimental groups included Control, OVA (ovalbumin-induced AHR), OVA + SGB2, OVA + SGB4, OVA + SGB5, OVA + SGB6, OVA + SGB8, OVA + 4PBA, Tm, and Tm + SGB6. Mice underwent varying numbers of SGB interventions over 17 days. On day 18, lung function tests were performed, followed by ELISA of IL-4, IL-5, and IL-13 levels in alveolar lavage fluid from the right lung, and finally, tissue from the right lung was extracted for transcriptome analysis, and tissue from the left lung (without lavage fluid) was stained with HE staining to assess histopathological changes. Compared to the Control group, the OVA group exhibited increased overall respiratory resistance (Rrs), overall respiratory elasticity (Ers), central airway resistance (Rn), peripheral tissue elasticity (H), and tissue damage (G), alongside decreased overall respiratory compliance (Crs) (P < 0.05). SGB significantly improved lung function parameters, with the OVA + SGB6 group showing the most pronounced improvement (P < 0.05). The Tm group displayed elevated Rrs compared to Control (P < 0.05), while the OVA + 4PBA group demonstrated significant improvement in Rrs (P < 0.05). The Tm + SGB6 group also showed significant improvement in Rrs compared to the Tm group (P < 0.05). The expression of IRE1β-IKK/NF-κB genes was upregulated in the OVA group and downregulated in the OVA + SGB6 group. Furthermore, ER stress inhibitors reduced the expression of these key genes in OVA-induced AHR. Notably, the expression of ER stress-related genes was elevated in the OVA group, with a significant decrease in Agr2 (a promoter of ER stress IRE1β) observed in the OVA + SGB6 group compared to the OVA group (114 vs. 16). SGB effectively reduced AHR while down-regulating the expression of key genes in the IKK/NF-κB/IL-4/IL-5/IL-13 signaling pathway, which may be related to IRE1β-mediated endoplasmic reticulum stress. However, further studies are needed to confirm the exact mechanism.

Asthma is a chronic inflammatory respiratory disease that seriously affects patients’ quality of life. Although various pharmacological treatments are currently available, some patients still have poor responses, highlighting the urgent need for new intervention strategies. In recent years, stellate ganglion irradiation (SGI), as an emerging neuromodulation technique, has shown unique therapeutic advantages in various inflammatory diseases. However, the mechanism by which SGI alleviates asthma remains unclear. Silent information regulator 1 (SIRT1), an NAD+-dependent histone deacetylase, plays a key role in regulating cellular inflammatory responses by inhibiting NF-κB and other inflammatory signaling pathways. Given the involvement of SIRT1 and NF-κB imbalance in the pathogenesis of asthmatic airway inflammation, we hypothesize that SGI may alleviate asthmatic inflammation by activating SIRT1 and inhibiting NF-κB activation. To test this hypothesis, we used an ovalbumin (OVA)-induced mouse model of asthma to comprehensively evaluate the effects of SGI on asthma pathophysiology and explore the mediating role of the SIRT1-NF-κB pathway. We found that compared with the asthma group, SGI treatment significantly improved the general symptoms of mice, reduced airway hyperresponsiveness, alleviated inflammatory cell infiltration and cytokine levels in bronchoalveolar lavage fluid (BALF), and ameliorated lung histopathological changes. Mechanistic studies showed that SIRT1 expression was downregulated and the NF-κB pathway was activated in the lung tissues of asthmatic mice, while SGI treatment upregulated SIRT1 expression and inhibited NF-κB activity. In conclusion, this study reveals for the first time that SGI alleviates asthmatic airway inflammation through the SIRT1-NF-κB pathway, providing a new approach for the adjuvant treatment of asthma.

Serratus anterior plane block (SAPB) and parasternal block (PSB) are used in multimodal analgesia strategies to improve postoperative comfort and recovery. Their combined effectiveness for pediatric auricular reconstruction (AR) patients needs clarification. A study was conducted on 100 children aged 8 to 12 undergoing autologous rib cartilage transplant in AR. Subjects were randomized into two groups: the ultrasound (US)-directed SAPB plus modified PSB group (SAPB+PSB group) and the US-guided SAPB alone group (SAPB group). The primary outcome was the 24 h postoperative Quality of Recovery-15 (QoR-15) score. The secondary endpoints were pain scores, surgical field bleeding scores, sufentanil consumption within 24 h post-surgery, the time to first ambulation, and incidence of complications. The SAPB+PSB group demonstrated significantly higher scores in physical comfort, emotional status, and pain aspects on the QoR-15 scale compared to the SAPB group, the difference was significant (P ≤ 0.001). No significant differences were observed between the groups in terms of psychological support and physical independence (P > 0.05). The total QoR-15 score was augmented among SAPB+PSB versus SAPB participants (P < 0.001). At 12 h, the SAPB+PSB group reported lower NRS scores than the SAPB group during rest (P < 0.001) and cough (P = 0.014). The sufentanil consumption at 24 h was substantially diminished among SAPB+PSB recipients (P < 0.001), and the time to first ambulation was shorter relative to the SAPB recipients, and the different was significant (P < 0.001). US-guided SAPB combined with modified PSB significantly enhances postoperative recovery quality in pediatric patients undergoing AR, effectively improving postoperative comfort and facilitating recovery. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Abstract Background There have been no reports on the successful implementation of stellate ganglion block (SGB) in mice. Objectives This study aims to investigate a new method for implementing SGB in mice by placing them in a supine position with abducted upper limbs and touching the trachea and sternoclavicular joint with the hand. Methods Fifty BABL/C mice, 8–10 weeks, were selected and randomly divided into four groups: control group (n = 5); SGB-R group (n = 15); SGB-L group (n = 15); and SGB-L + R (group n = 15). SGB was administered with 0.15% ropivacaine solution in a volume of 0.1 mL. The control group received equal volumes of saline. Horner's syndrome, heart rate, and complications such as brachial plexus block, vascular injury, pneumothorax, local anesthetic toxicity, and death were observed. Results Horner's syndrome developed in 100% of SGB surviving mice; no difference was seen in the time to onset (100.4 ± 13.4 vs 96.7 ± 12.4, mean ± SD, seconds) and duration (264.1 ± 40.5 vs 296.3 ± 48.0, mean ± SD, min) of Horner's syndrome in the left and right SGB (P > 0.05). Compared with the control group (722 [708–726], median [IQR], bpm), the heart rate was significantly slowed down in the right SGB (475 [451.5–491], median [IQR], bpm) (P < 0.05). While the heart rate was slowed down after performing the left SGB, the difference was not statistically significant (P > 0.05). The overall complication rate was 18.4%, with a brachial plexus block rate of 12.3%, a vascular injury rate of 4.6%, and a mortality rate of 1.5%, as well as no local anesthetic toxicity (includes bilateral implementation of SGB) or pneumothorax manifestations were found. Conclusions This method allows for the successful implementation of SGB in a mouse model.

Severe COVID-19 cases often progress to life-threatening conditions such as acute respiratory distress syndrome (ARDS), sepsis, and multiple organ dysfunction syndrome (MODS). Gelsolin (GSN), an actin-binding protein with anti-inflammatory and immunomodulatory properties, is a promising therapeutic target for severe COVID-19. Plasma GSN levels are significantly decreased in critical illnesses, including COVID-19, correlating with dysregulated immune responses and poor outcomes. GSN supplementation may mitigate acute lung injury, ARDS, and sepsis, which share pathophysiological features with severe COVID-19, by scavenging actin, modulating cytokine production, enhancing macrophage phagocytosis, and stabilizing the alveolar-capillary barrier. Preliminary data indicate that recombinant human plasma GSN improves oxygenation and lung function in severe COVID-19 patients with ARDS. Although further research is needed to optimize GSN therapy, current evidence supports its potential to mitigate severe consequences of COVID-19 and improve patient outcomes. This review provides a comprehensive analysis of the biological characteristics, mechanisms, and therapeutic value of GSN in severe COVID-19.

Background According to the Chinese Society of Anesthesiology, it is recommended that patients with difficult airways be documented and notified, which will provide healthcare professionals with a direct reference when managing airways. However, compliance with this initiative remains unclear. This study was conducted to investigate the current status and need for difficult airway notification at Plastic Surgery Hospital and to explore the factors contributing to noncompliance. Methods Anesthesiologists, surgeons, and patients in Plastic Surgery Hospital were administered separate questionnaires regarding notification of difficult airway management. Participants were surveyed regarding their attitudes and current practices regarding difficult airway notification. In addition, questions were asked regarding the barriers that contribute to noncompliance. Results A total of 632 valid responses were obtained and analyzed, giving a response rate of 99.21%. 399 patients (89.46%) felt it was very important for anesthesiologists to inform them about their difficult airway, and 91.03% felt it was very important for them to receive a letter of their airway assessment. However, twenty-two anesthesiologists (64.7%) reported verbally informing less than 50% of patients about their difficult airway after surgery, and only four anesthesiologists informed all patients they encountered. Most surgeons (91.22%) and anesthesiologists (91.18%) believe that it is vital to inform patients verbally, while 114 surgeons (77.03%) and 31 anesthesiologists (91.18%) believe that it is essential to complete a difficult airway notification alert. Among the factors causing noncompliance, 17 (34.69%) believed that absence of mandatory rules, 9 (18.37%) believed that increased workload, and 8 (16.33%) believed that notification methods were lacking. Conclusions The compliance to difficult airway notification remains low in Plastic Surgery Hospital despite the high incidence of difficult airways. Although anesthesiologists, surgeons, and patients are strongly in favor of it. Among the barriers to compliance were the absence of a well-developed notification system and a means of notification such as an alert form for difficult airways. This may spur the anesthesiology society to publish the notification system.

Objective To explore the feasibility of establishing a mouse stellate ganglion (SG) regulation model through infrared polarized light (IPL) irradiation of the SG, and preliminarily evaluate its effects on SG function and related physiological indicators. Methods BALB/c mice were randomly divided into control, Sham surgery, and IPL groups, with 8 mice in each group. A ZZIR-ID therapeutic device was used to directly irradiate bilateral SG regions of IPL group mice, with wavelength 980 nm, power density 1000 mW/cm2, 15 minutes each time, every other day for 6 times. The control group received no treatment, while the Sham surgery group received IPL irradiation on the top of the head. Horner's syndrome manifestations were observed and eye temperature was measured before and immediately after treatment. Heart rate changes were continuously recorded. Results Compared with the control and Sham surgery groups, the incidence of Horner's syndrome in the IPL group increased significantly (P < 0.05), manifesting as bilateral ptosis and enophthalmos, lasting about 2 hours. Immediately after treatment, eye temperature in the IPL group increased significantly compared to pre-treatment (P < 0.05). Heart rate in the IPL group decreased significantly 30 minutes post-treatment compared to pre-treatment (P < 0.01), lasting 1–2 hours. There was no statistically significant difference in weight changes between groups (P > 0.05). Conclusion IPL irradiation of SG can effectively induce Horner's syndrome in mice, elevate eye temperature, reduce heart rate, and exert certain anti-inflammatory immunomodulatory effects. This provides experimental evidence for IPL as a novel method to establish SG regulation models.

Silent information regulator two homolog 1 (SIRT1), an NAD + -dependent histone deacetylase, plays a pivotal regulatory role in a myriad of physiological processes. A growing body of evidence suggests that SIRT1 can exert protective effects in metabolic disorders and neurodegenerative diseases by inhibiting endoplasmic reticulum (ER) stress and the nuclear factor-κB (NF-κB) inflammatory signaling pathway. This review systematically elucidates the molecular mechanisms and biological significance of SIRT1 in regulating ER stress and the NF-κB pathway. On one hand, SIRT1 can deacetylate key molecules in the ER stress pathway, such as glucose-regulated protein 78 (GRP78), X-box binding protein 1 (XBP1), PKR-like ER kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6 (ATF6), thereby alleviating ER stress. On the other hand, SIRT1 can directly or indirectly remove the acetylation modification of the NF-κB p65 subunit, inhibiting its transcriptional activity and thus attenuating inflammatory responses. Through these mechanisms, SIRT1 can ameliorate insulin resistance in metabolic diseases, exert cardioprotective effects in ischemia-reperfusion injury, and reduce neuronal damage in neurodegenerative diseases. However, it is important to note that while these findings are promising, the complex nature of the biological systems involved warrants further investigation to fully unravel the intricacies of SIRT1’s regulatory mechanisms. Nevertheless, understanding the regulatory mechanisms of SIRT1 on ER stress and the NF-κB pathway is of great significance for expanding our knowledge of the pathogenesis of related diseases and exploring new preventive and therapeutic strategies targeting SIRT1.

BACKGROUND:Dexmedetomidine (Dex) as a local anesthesia adjuvant for nerve block procedures can improve the quality of patient recovery. However, the impact of using Dex as a local anesthetic adjuvant for serratus anterior plane block (SAPB) procedures on recovery quality for children undergoing ear reconstruction remains unclear. METHODS:Eighty-four patients who underwent ear reconstruction with autogenous costal cartilage (ACC) were randomized into two groups (n = 42/group) in which SAPB was performed with ropivacaine alone (R group) and with Dex and ropivacaine (DR group). Primary outcomes were patient 15-item quality of recovery (QoR-15) scale scores on days 1 and 2 post-surgery. Secondary outcomes included postoperative rest and coughing numerical rating scale (NRS) chest pain scores, duration of analgesia, oral rescue analgesic usage, and opioid-related side effects. RESULTS:Forty patients per group completed the study. QoR-15 scores on days 1 and 2 post-surgery in the DR group were significantly increased relative to the R group (126.35 ± 9.81 vs. 115.53 ± 8.58 and 131.78 ± 8.67 vs. 122.80 ± 8.59, all P < 0.001). Rest and coughing NRS chest pain scores at 2, 4, 8, 12, and 24 h postoperatively in the DR group were all significantly lower relative to the R group (all P < 0.05). The DR group also exhibited significantly longer analgesic duration (P < 0.001) and significantly reduced incidences of oral rescue analgesic usage and opioid-related side effect (all P < 0.05). CONCLUSION:Combining Dex and ropivacaine for SAPB in children undergoing ear reconstruction with ACC can significantly improve the quality of recovery, quality of analgesia, and analgesic duration.

OBJECTIVE:To study the efficacy of ultrasound-guided parasternal block (US-PSI) in pediatric patients undergoing auricular reconstruction surgery.METHODS:For this study, the authors recruited 60 children between the ages of 5 and 12 years who underwent auricular reconstruction with autologous costal cartilage (ACC) to correct microtia. They were randomized to receive either ultrasound-guided modified parasternal block or periprostatic local infiltration anesthesia (PLIA), with 30 cases in each group. Ultrasound-guided parasternal block was administered following anesthesia induction, whereas PLIA was administered after ACC harvest. Lastly, following surgery, all children were provided with patient-controlled intravenous analgesia with sufentanil, and the numeric pain rating scale (NRS) was used to assess the intensity of pain. Our primary outcomes were the resting NRS pain scores and the NRS scores upon coughing at 1, 6, 12, 24, and 48 hours postsurgery. Sufentanil consumption within the first 24 hours of surgery, the mean duration to first ambulation, and the usage of rescue analgesics were our secondary outcomes. The authors also recorded the occurrence of undesirable side effects as well as more serious side effects like pneumothorax.RESULTS:Pediatric patients who were administered US-PSI showed significantly reduced NRS chest pain scores at 6 and 12 hours postsurgery compared to those who received PLIA (P<0.05). In addition, sufentanil consumption within the first 24 hours postsurgery, duration to first ambulation, and use of rescue analgesics were significantly lower among patients in the US-PSI group when compared to those in the PLIA group (P<0.05).CONCLUSIONS:This study found that US-PSI was a highly efficacious and safe technique for postsurgical analgesia following auricular reconstruction with ACC in pediatric patients.LEVEL OF EVIDENCE:Level II, therapeutic study.

Abstract Background Cricothyrotomy is a lifesaving surgical technique in critical airway events. However, a large proportion of anesthesiologists have little experience with cricothyrotomy due to its low incidence. This study aimed to develop a multisensory, readily available training curriculum for learning cricothyrotomy and evaluate its training effectiveness. Methods Seventy board-certificated anesthesiologists were recruited into the study. Participants first viewed an instructional video and observed an expert performing the bougie-assisted cricothyrotomy on a self-made simulator. They were tested before and after a one-hour practice on their cricothyrotomy skills and evaluated by a checklist and a global rating scale (GRS). Additionally, a questionnaire survey regarding participants’ confidence in performing cricothyrotomy was conducted during the training session. Results The duration to complete cricothyrotomy was decreased from the pretest (median = 85.0 s, IQR = 72.5–103.0 s) to the posttest (median = 59.0 s, IQR = 49.0–69.0 s). Furthermore, the median checklist score was increased significantly from the pretest (median = 30.0, IQR = 27.0-33.5) to the posttest (median = 37.0, IQR = 35.5–39.0), as well as the GRS score (pretest median = 22.5, IQR = 18.0–25.0, posttest median = 32.0, IQR = 31.0-33.5). Participants’ confidence levels in performing cricothyrotomy also improved after the curriculum. Conclusion The simulation-based training with a self-made simulator is effective for teaching anesthesiologists to perform cricothyrotomy.

Blood‑oxygenation-level-dependent (BOLD) functional MRI (fMRI) has provided a wealth of information about brain function and neural networks. However, the BOLD signal is based on vascular responses secondary to neural activity. Therefore, alterations in the vascular function could confound the task-evoked fMRI findings, and also affect functional connectivity mapping in resting-state fMRI. Cerebrovascular reactivity (CVR), referring to the ability of the cerebral blood vessels to dilate or constrict in response to stimulus, is an important indicator of cerebrovascular health. Conventional CVR mapping techniques require breathing maneuvers or drug challenges, which could be cumbersome in clinical settings and impractical in some patient cohorts. Recently, CVR mapping techniques using resting-state fMRI data have been developed. This chapter describes current evidence and literature on how CVR influences resting-state fMRI measurements, and how CVR can be extracted from resting-state fMRI data and utilized in clinical patients.