Background Therapeutic hypothermia (TH) is an important treatment after cardiac arrest to mitigate cerebral ischemia-reperfusion (I/R) injury, but its underlying mechanism remains unclear. Studies have shown that cold-inducible RNA binding protein (CIRP), as a stress-response protein, plays a key role in improving neurological outcomes following TH treatment in cases of global ischemia. Objective This in vitro study aimed to investigate the role of CIRP in primary hippocampal neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and to explore the underlying mechanisms. Materials and Methods Primary hippocampal neurons were cultured and an OGD/R model was established. After OGD/R injury, neurons were resuscitated in normal or hypothemia (32 °C) condition for 6 h. Adenovirus transfection were used to regulate the expression of CIRP. The ultrastructure of neurons was visualized by transmission electron microscope (TEM). Flow cytometry were use to detect OGD-induced neuronal apoptosis. Reverse transcription polymerase chain reaction (RT-PCR) and western blot were used to detect the expression of CIRP mRNA and protein levels. Meanwhile, the enzyme-linked immunosorbent assay (ELISA) was used to evaluate the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and gutathione (GSH). Results Hypothermia treatment could induce CIRP over-expression in neurons and reverse the down-regulation of CIRP induced by OGD/R. In addition, over-expression of CIRP could reduce the release of reactive oxygen species (ROS) induced by OGD/R through reducing MDA levels and increasing the level of SOD and GSH, and alleviated OGD/R-induced neuronal apoptosis by down regulating Caspase-3 and cleaved Caspase-3 expression and up regulating Bcl-2 expression. Furthermore, CIRP silencing enhanced neuronal OGD/R-induced apoptosis and oxidative stress. Meanwhile, as expected, neurons were seriously damaged and mitochondrial membrane ruptured after OGD/R injury, which were attenuated by CIRP over-expression or TH. Conclusions Our results showed that CIRP at least partially resisted OGD/R-induced neuronal injury by exhibiting anti-apoptotic and anti-oxidative properties. To sum up, targeting CIRP may represent potential therapeutic implications in the treatment of brain I/R injury.

Brain injury after cardiac arrest (CA) is a major cause of death and disability, with neuroinflammation increasingly recognized as a key driver. Although the sphingosine-1-phosphate receptor 3 (S1PR3)-a G protein-coupled receptor-has been linked to neurological disorders, its role in CA-induced brain injury remains unclear. We induced CA in mice via intravenous potassium chloride injection. S1PR3 expression and subcellular localization were assessed in cortex and hippocampus. Mice received intraperitoneal CAY10444 (a selective S1PR3 antagonist) alone or with Colivelin TFA (a Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) agonist). Survival after return of spontaneous circulation (ROSC) was recorded. Neurological function was evaluated using neurological deficit score, rotarod, adhesive removal, and novel object recognition tests. Brain pathology was examined by H&E, Nissl, immunohistochemistry, and Golgi staining. Microglial and astrocyte activation were quantified by immunohistochemistry; IL-1β, TNF-α, and IL-6 mRNA levels were measured; and JAK2/STAT3 pathway activity was assessed by Western blot for p-JAK2 and p-STAT3. CA/CPR upregulated S1PR3 in the brain and increased its co-localization with neurons and glia. CAY10444 improved survival and all behavioral outcomes. It reduced neuronal loss, axonal damage, dendritic spine loss, and suppressed microglial and astrocytic activation in the hippocampus. CAY10444 also lowered IL-1β, TNF-α, and IL-6 expression and decreased CA-induced JAK2/STAT3 phosphorylation. Colivelin TFA partially reversed these benefits. CAY10444 confers neuroprotection after CA/CPR by inhibiting S1PR3 and downstream JAK2/STAT3 signaling, thereby dampening neuroinflammation and neuronal death. S1PR3 is therefore a promising therapeutic target for CA-induced brain injury.

Cardiac arrest (CA) is a global health problem that accounts for more deaths than many other diseases. Global cerebral ischemia-reperfusion injury resulting from CA and resuscitation remains a critical issue that urgently requires further investigation. Neuroinflammation-related cytokines play a central role in exacerbating neuronal injury in conditions involving global cerebral ischemia-reperfusion. As a newly discovered damage-associated molecular pattern (DAMP), cold-inducible RNA-binding protein (CIRP) contributes significantly to various inflammatory diseases. However, the mechanism of CIRP in cardiac arrest and resuscitation associated neuroinflammation remains unclear. This study aims to investigate the role of microglia derived CIRP in neuroinflammation and neuron damage. We established a rat model of CA and hippocampal neuron/BV2 microglia cells oxygen-glucose deprivation/reoxygenation (OGDR) model. In animal experiments, we observed an increase in CIRP expression of hippocampus after CA and resuscitation. Moreover, elevated CIRP level can activate microglia to release more inflammatory factors, thereby damaging neurons. RNA sequencing analysis indicated that the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway may serve as a downstream pro-inflammatory signaling pathway of CIRP. In cell experiments, microglial cells subjected to OGDR secreted numerous exosomes containing CIRP. These exosomes acted on the cells' own inflammatory pathways in an autocrine manner, intensifying the inflammatory response. Moreover, they directly damaged neighboring neurons through paracrine action. Inhibiting the synthesis or secretion of CIRP alleviated neuroinflammation. This study enhances to understand the role of CIRP in the neuroinflammation induced by global cerebral ischemia reperfusion and has identifies potential targets for brain resuscitation therapy following CA.

Cardiac arrest (CA) remains a leading cause of mortality and morbidity worldwide. Cognitive deficits are common neurological sequelae among CA survivors. Preclinical and clinical studies have confirmed that therapeutic hypothermia (TH) is an effective intervention for mitigating brain injury following CA. Hypothermia induces the expression of specific small proteins, including RNA-binding motif protein 3 (RBM3), which provides neuroprotection under stress conditions. However, the role of RBM3 in TH after CA has not been fully elucidated. In this study, we investigated the role of RBM3 in attenuating cognitive deficits following hypothermic brain resuscitation. We constructed a rat model of CA and resuscitation, and used shRNA transfection to interfere with RBM3 expression to explore the underlying mechanisms of TH's effects on cognitive alterations. Rats were randomly assigned to one of five groups: sham group (Sham), CA group (CA), TH group (TH), adeno-associated virus (AAV)-shRNA-RBM3 transfection group (shRNA-RBM3), and AAV-shRNA-negative control transfection group (shRNA-control). Key synaptic regulatory proteins, dendritic spines, and synaptic ultrastructures were examined. The rats exhibited spatial learning and memory impairments in the Morris water maze test and novel object recognition task. Hypothermia increased RBM3 expression in hippocampal neurons, mitigated early brain injury, preserved dendritic spine integrity and synaptic ultrastructure, upregulated key synaptic regulatory proteins, and ameliorated cognitive impairment following resuscitation. When RBM3 expression in the hippocampus was inhibited, the beneficial effects of therapeutic hypothermia were partially reversed. Overall, our findings provide new insights into the mechanisms of hypothermia-induced neuroprotection, demonstrating that neuroplasticity and rehabilitation can be achieved following global cerebral ischemia-reperfusion injury after CA. Therefore, the RBM3-mediated cold shock pathway represents a potential target for enhancing neuroprotection and neurorehabilitation through hypothermia.

Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Background:Postherpetic neuralgia (PHN) remains challenging to treat, with 40%-50% of patients experiencing inadequate pain relief despite comprehensive interventions. Neuromodulation techniques such as pulsed radiofrequency (RF) and traditional methods such as fire acupuncture (FA) are increasingly used for PHN. This study investigated the combined effect of FA and RF on tactile allodynia in a rat model of PHN and explored its underlying mechanisms. Methods:Adult male rats were randomly divided into: Control, PHN, FA, RF, and combined FA_RF groups. PHN was induced by varicella-zoster virus inoculation. FA and/or RF interventions began on Day 15. Pain behavior was assessed via mechanical allodynia and thermal hyperalgesia tests. On Day 37, spinal cord tissues and cerebrospinal fluid were collected to evaluate astrocyte and microglial activation, neuronal apoptosis, expression of Insulin-Like Growth Factor 2 (IGF2), Peripheral Myelin Protein 2 (PMP2), Claudin-19 (CLDN19), Homeobox C8 (HOXC8), and levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α). The role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway was verified using a PI3K/AKT agonist. Results:The results revealed that mechanical allodynia thresholds decreased on Day 8 post-inoculation. Compared to the PHN group, FA_RF combination significantly increased mechanical thresholds and prolonged thermal hyperalgesia latency, with superior effects versus FA or RF alone. The FA_RF group showed increased spinal IGF2, PMP2, and CLDN19 expression, decreased HOXC8, reduced astrocyte activation, and modulated cytokine levels (IL-1β, IL-6, TNF-α, IL-10). The PI3K/AKT agonist reversed the analgesic effects of FA_RF. Conclusion:Combined fire acupuncture and pulsed radiofrequency alleviates tactile allodynia in PHN rats, possibly by inhibiting spinal astrocyte activation, modulating inflammatory responses, and promoting nerve repair via IGF2, PMP2, and CLDN19 expression. The PI3K/AKT pathway may be critically involved in this analgesic mechanism.

Autonomic dysfunction is a risk factor for hypotension after anesthesia induction. Deceleration capacity of heart rate (DC) is a new method to evaluate autonomic function. This prospective observational study was designed to evaluate whether the deceleration capacity of heart rate measured by a 5-min preoperative Electrocardiogram (ECG) can reliably predict post-induction hypotension (PIH). Patients aged 18 to 65 undergoing elective surgery with lower ASA status I or II were included in this study. DC, root mean square density (RMSSD) and low frequency/high frequency ratio (LF/HF) were calculated from 5-min segments of ECG measured in the quiet state before surgery. PIH was defined as mean arterial pressure (MAP) < 65 mmHg or a decrease of > 30

Ciprofol (CIP) for procedural sedation and analgesia (PSA) for painless gastrointestinal endoscopy (GE) can cause respiratory or cardiovascular complications. The literature suggests that intravenous (IV) lidocaine infusion can alleviate visceral pain and enhance humans’ ventilator response to CO2. Therefore, it was hypothesized that IV lidocaine could reduce the CIP dose for painless GE and improve recovery time. This randomized placebo-controlled trial included 40 patients undergoing GE. After CIP titration for unconsciousness, patients in group L were given IV lidocaine (1.5 mg/kg bolus dose, then a 2 mg/kg/h continuous infusion); the same volume saline as placebo was given for N group patients. The primary endpoint was the required CIP dose. Secondary endpoints were: endoscopic examination time, awakening time, post-anesthesia care unit (PACU) discharge time, pain and fatigue after awakening, adverse events, and endoscopist’s and patient’s satisfaction. Both cohorts had comparable demographic characteristics. Group L’s CIP consumption was decreased by 23.0

We sincerely appreciate the valuable comments from the readers, which provide insightful feedback to help us improve our future work. We acknowledge that multiple factors can influence tracheal tube cuff pressure, and we have carefully considered the suggestions provided. Regarding the peritoneal insufflation pressures, these values in different time points had no significant difference as reported in our previous manuscript. Clinical trial number: ChiCTR2100054089. URL: https://www.chictr.org.cn/edit.aspx?pid=142785 htm=4 , Principal investigator: Manlin Duan, Date: 08/12/2021.

Cycloastragenol, a triterpenoid saponin extracted from Astragalus membranaceus, exerts several pharmacological effects. However, its mechanism of action in acute lung injury treatment remains unclear. This study was conducted to test the hypothesis that cycloastragenol can inhibit lipopolysaccharide (LPS)-induced acute lung injury and investigate the underlying molecular mechanisms. This study systematically explored the effects and mechanism of action of cycloastragenol in LPS-induced acute lung injury treatment using network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation. Gene Ontology and Kyoto Encyclopedia of Gene and Genomes enrichment analyses indicated that the effects of cycloastragenol are mediated by inflammation- and apoptosis-related genes. Both in vitro and in vivo experiments were conducted to assess the effectiveness of cycloastragenol in acute lung injury treatment. Lung function was evaluated using a pulmonary function test system with indicators, such as peak expiratory flow, minute ventilation, and lung resistance. The expression of inflammatory factors and apoptosis-related proteins was evaluated using Western blot analysis, quantitative real-time polymerase chain reaction, and immunofluorescence. Apoptosis in lung tissue and mouse primary peritoneal macrophages was assessed using terminal deoxynucleotidyl transferase dUTP nick-end labelling staining and flow cytometry, respectively. Cycloastragenol effectively alleviated pulmonary dysfunction and edema, mitigated histopathological damage, and suppressed the activation of both the NF-κB p65 and Akt signaling pathways induced by LPS, ultimately leading to reduced inflammation and apoptosis. The results suggest that cycloastragenol alleviates acute lung injury by exerting anti-inflammatory and anti-apoptotic effects. These findings suggest that cycloastragenol could be a potential therapeutic candidate for preventing and treating ALI.

Acute postoperative pain is common in surgical patients, and intraoperative noise isolation has been shown to reduce pain for up to 24 h postoperatively. However, acute postoperative pain primarily occurs during the first three days after surgery, and it remains unclear whether intraoperative noise isolation affects the incidence of moderate-to-severe acute postoperative pain during this period. Therefore, this study aimed to investigate whether the use of noise-cancelling earmuffs during laparoscopic surgery reduces the incidence of moderate-to-severe acute postoperative pain. A single-center clinical randomised controlled trial was conducted in Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University. The study included 86 patients aged 18–65 years who underwent elective laparoscopic surgery under general anaesthesia, had an ASA classification I-III, and received patient-controlled intravenous analgesia (PCIA). Participants were randomly assigned to either a noise isolation group or a control group. The noise isolation group wore noise-cancelling earmuffs to attenuate intraoperative noise from induction until the end of surgery, while the control group received conventional anaesthesia management without earmuffs. The primary outcome was the incidence of numeric rating scale (NRS, 0–10) pain scores ≥ 4 at 72 h postoperatively, measured using a 10-point numeric rating scale. Secondary outcomes included the incidence of NRS pain scores ≥ 4 at 24 h and 48 h postoperatively and the proportion of different tiers of NRS pain scores (mild [1–3], moderate [4–6] and severe [7–10]), daily frequency of additional rescue analgesic use over postoperative days 1–3, the maximum resting pain score and the maximum movement-evoked pain score at 24, 48, and 72 h postoperatively and total opioid consumption during the first 72 h postoperatively. The noise isolation group had a significantly lower incidence of moderate-to-severe pain on the third postoperative day (7.1

Laparoscopic surgery is a popular alternative for resection of colorectal neoplasms. Carbon dioxide pneumoperitoneum and Trendelenburg positioning in procedure can significantly increase airway pressure, when endotracheal tube cuff pressure is not monitored. This prospective observational study aimed to evaluate indicators, changes and its correlation factors of endotracheal tube cuff pressure during laparoscopic resection of colorectal neoplasms. 122 patients scheduled for laparoscopic resection of colorectal neoplasms under propofol/remifentanil total intravenous anesthesia with orotracheal intubation were included. Tracheal tube cuff pressure was monitored continuously by calibrated pressure transducers. The ability of several predictors to predict out-of-range tracheal tube cuff pressure at different time points and its correlation factors were assessed. ROC analysis showed that waist-to-hip ratio has the highest AUC for predicting out-of-range tracheal cuff pressure (AUC: 0.86 [95

Background Postoperative sore throat (POST) is an unpleasant outcome that can occur as a result of tracheal intubation in adults. Increased pressure from the endotracheal tube (ETT) cuff often leads to local mucosal injury, resulting in sore throat. The purpose of this study was to compare the effect of two different ETT cuff pressure monitoring systems vs. no cuff pressure monitoring on the incidence and severity of POST in adults. Methods One hundred and fourteen ASA I-III patients of either gender, aged 18–65 years, and undergoing surgery requiring endotracheal intubation were included in this study. Patients were randomized into three groups: control (C), cuff pressure gauge (G), and automated cuff controller (A). The ETT cuff pressure was not monitored intraoperatively in group C but was monitored using a cuff pressure gauge and an automated cuff controller in groups G and A, respectively. Postoperatively, patients were assessed at 2, 24, and 48 h for the presence and severity of POST, hoarseness and cough. Results One hundred and eleven patients completed the study. POST occurred in 40.5% of the patients in group G ( n = 37) ( p = 0.013) and 23.7% of the patients in group A ( n = 38) ( p < 0.001) within 48 h after surgery, compared to 69.4% in group C ( n = 36). There were no significant differences in hoarseness, coughing, and dysphagia across the groups at any time. When comparing groups A and C, individuals in group A exhibited a lower occurrence of significant (grade ≥ 2) POST and hoarseness (10.5% vs. 41.7%, p = 0.002; 26.3% vs. 58.3%, p = 0.005). The incidence of significant cough and dysphagia did not differ substantially across the patient groups within 48 h after surgery. POST scores in group A at 2, 24 h postoperatively were both 0 (0–0), which was significantly lower than those in group C (1 (0–2) at 2 h, p < 0.001 ; 1 (0–1) at 24 h, p = 0.001). POST in group G at 2 h postoperatively was graded as 0 (0–1.5) which was milder than group C ( P = 0.024). The severity of hoarseness in group A with scores of 0 (0–2) was superior to that in group C (2 (0–2), p = 0.006) at 2 h postoperatively. Conclusions In conclusion, the findings of this study indicated that the occurrence of POST can be reduced by using either the cuff pressure gauge approach or the automated cuff controller method. The automated cuff controller monitoring can potentially decrease the severity of POST and hoarseness. Trial registration Chinese Clinical Trial Registry, identifier: ChiCTR2100054089, Date: 08/12/2021.

Acute respiratory distress syndrome (ARDS) is an acute and severe clinical complication lacking effective therapeutic interventions. The disruption of the lung epithelial barrier plays a crucial role in ARDS pathogenesis. Recent studies have proposed the involvement of abnormal mitochondrial dynamics mediated by dynamin-related protein 1 (Drp1) in the mechanism of impaired epithelial barrier in ARDS. Hydrogen is an anti-oxidative stress molecule that regulates mitochondrial function via multiple signaling pathways. Our previous study confirmed that hydrogen modulated oxidative stress and attenuated acute pulmonary edema in ARDS by upregulating thioredoxin 1 (Trx1) expression, but the exact mechanism remains unclear. This study aimed to investigate the effects of hydrogen on mitochondrial dynamics both in vivo and in vitro. Our study revealed that hydrogen inhibited lipopolysaccharide (LPS)-induced phosphorylation of Drp1 (at Ser616), suppressed Drp1-mediated mitochondrial fission, alleviated epithelial tight junction damage and cell apoptosis, and improved the integrity of the epithelial barrier. This process was associated with the upregulation of Trx1 in lung epithelial tissues of ARDS mice by hydrogen. In addition, hydrogen treatment reduced the production of reactive oxygen species in LPS-induced airway epithelial cells (AECs) and increased the mitochondrial membrane potential, indicating that the mitochondrial dysfunction was restored. Then, the expression of tight junction proteins occludin and zonula occludens 1 was upregulated, and apoptosis in AECs was alleviated. Remarkably, the protective effects of hydrogen on the mitochondrial and epithelial barrier were eliminated after applying the Trx1 inhibitor PX-12. The results showed that hydrogen significantly inhibited the cell apoptosis and the disruption of epithelial tight junctions, maintaining the integrity of the epithelial barrier in mice of ARDS. This might be related to the inhibition of Drp1-mediated mitochondrial fission through the Trx1 pathway. The findings of this study provided a new theoretical basis for the application of hydrogen in the clinical treatment of ARDS.

Abstract Background Perioperative hypotension is frequently observed following the initiation of general anesthesia administration, often associated with adverse outcomes. This study assessed the effect of subclavian vein (SCV) diameter combined with perioperative fluid therapy on preventing post-induction hypotension (PIH) in patients with lower ASA status. Methods This two-part study included patients aged 18 to 65 years, classified as ASA physical status I or II, and scheduled for elective surgery. The first part (Part I) included 146 adult patients, where maximum SCV diameter (dSCVmax), minimum SCV diameter (dSCVmin), SCV collapsibility index (SCVCI) and SCV variability (SCVvariability) assessed using ultrasound. PIH was determined by reduction in mean arterial pressure (MAP) exceeding 30% from baseline measurement or any instance of MAP < falling below 65 mmHg for ≥ a duration of at least 1 min during the period from induction to 10 min after intubation. Receiver Operating Characteristic (ROC) curve analysis was employed to determine the predictive values of subclavian vein diameter and other relevant parameters. The second part comprised 124 adult patients, where patients with SCV diameter above the optimal cutoff value, as determined in Part I study, received 6 ml/kg of colloid solution within 20 min before induction. The study evaluated the impact of subclavian vein diameter combined with perioperative fluid therapy by comparing the observed incidence of PIH after induction of anesthesia. Results The areas under the curves (with 95% confidence intervals) for SCVCI and SCVvariability were both 0.819 (0.744–0.893). The optimal cutoff values were determined to be 45.4% and 14.7% (with sensitivity of 76.1% and specificity of 86.7%), respectively. Logistic regression analysis, after adjusting for confounding factors, demonstrated that both SCVCI and SCVvariability were significant predictors of PIH. A threshold of 45.4% for SCVCI was chosen as the grouping criterion. The incidence of PIH in patients receiving fluid therapy was significantly lower in the SCVCI ≥ 45.4% group compared to the SCVCI < 45.4% group. Conclusions Both SCVCI and SCVvariability are noninvasive parameters capable of predicting PIH, and their combination with perioperative fluid therapy can reduce the incidence of PIH.

Inflammation plays a crucial role in the initiation and progression of sepsis and induces alterations in brain neurotransmission, thereby contributing to the development of sepsis-associated encephalopathy (SAE). Parvalbumin (PV) interneurons are pivotal contributors to cognitive processes and have been implicated in various central nervous system dysfunctions, including SAE. Oxytocin, known for its ability to augment the firing rate of gamma-aminobutyric acid (GABA)-ergic interneurons and directly stimulate inhibitory interneurons to enhance the tonic inhibition of pyramidal neurons, has prompted an investigation into its potential therapeutic effects on cognitive dysfunction in SAE. In the current study, we administered intranasal oxytocin to SAE mice induced by lipopolysaccharide. Behavioral assessments, including open field, Y-maze, and fear conditioning, were used to evaluate cognitive performance. Golgi staining revealed hippocampal synaptic deterioration, local field potential recordings showed weakened gamma oscillations, and immunofluorescence staining demonstrated decreased PV expression in the cornu ammonis 1 (CA1) region of the hippocampus following lipopolysaccharide treatment, all of which were alleviated by oxytocin administration. Furthermore, immunofluorescence staining of PV co-localization with vesicular glutamate transporter 1 or vesicular GABA transporter indicated a balanced excitation/inhibition effect of neurotransmitters on PV interneurons after oxytocin administration in the SAE mice, leading to an improved cognitive function. In conclusion, oxytocin treatment improved cognitive function by increasing the number of PV + neurons in the hippocampal CA1 region, restoring the balance of excitatory/inhibitory synaptic transmission on PV interneurons, and enhancing hippocampal CA1 local field potential gamma oscillations. These findings suggest a potential mechanism underlying the beneficial effects of oxytocin in SAE.

Cardiac arrest is a global health issue causing more deaths than many other diseases. Hypothermia therapy is commonly used to treat secondary brain injury resulting from cardiac arrest. Previous studies have shown that CIRP is induced in specific brain regions during hypothermia and inhibits mitochondrial apoptotic factors. However, the specific mechanisms by which hypothermia-induced CIRP exerts its anti-apoptotic effect are still unknown. This study aims to investigate the role of Cold-inducible RNA-binding protein (CIRP) in mitochondrial-associated endoplasmic reticulum membrane (MAM)-mediated Ca2+ transport during hypothermic brain resuscitation.We constructed a rat model of cardiac arrest and resuscitation and hippocampal neuron oxygen-glucose deprivation/reoxygenation model. We utilized shRNA transfection to interfere the expression of CIRP and observe the effect of CIRP on the structure and function of MAM.Hypothermia induced CIRP can reduce the apoptosis of hippocampal neurons, and improve the survival rate of rats. Hypothermia induced CIRP can reduce the expressions of calcium transporters IP3R and VDAC1 in MAM, reduce the concentration of calcium in mitochondria, decrease the expression of ROS, and stabilize the mitochondrial membrane potential. Immunofluorescence and immunocoprecipitation showed that CIRP could directly interact with IP3R-VDAC1 complex, thereby changing the structure of MAM, inhibiting calcium transportation and improving mitochondrial function in vivo and vitro.Both in vivo and in vitro experiments have confirmed that hypothermia induced CIRP can act on the calcium channel IP3R-VDAC1 in MAM, reduce the calcium overload in mitochondria, improve the energy metabolism of mitochondria, and thus play a role in neuron resuscitation. This study contributes to understanding hypothermia therapy and identifies potential targets for brain injury treatment.

Septic lung injury is characterized by uncontrollable inflammatory infiltrations and acute onset bilateral hypoxemia. Evidence has emerged of the beneficial effect of hydrogen in acute lung injury (ALI), but the underlying mechanism is unclear. In this research, the recovery action of hydrogen on lipopolysaccharide (LPS)-induced ALI in mice and A549 cells was investigated. The 7-day survival rate and body weight of mice were measured after intraperitoneal injection of LPS. Lung function was determined by a whole body plethysmography (WBP) system using the indicators respiratory rate and enhanced pause. Hematoxylin and eosin (HE) staining confirmed the signs of pulmonary edema and inflammatory ooze. Reverse transcription-polymerase chain reaction (RT-PCR) quantification was used to detect the expression of inflammatory factors. Western blotting analysis evaluated the expression levels of involved proteins in the AMP-activated protein kinase (AMPK) pathway. The experimental results confirmed that hydrogen provided an essential solution to the dissipative effects of LPS on survival rate, weight loss and lung function. The LPS-stimulated inflammatory factors, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were also suppressed by hydrogen in A549 cells. Western blot analysis showed that hydrogen significantly upregulated the levels of phosphorylated AMPK (p-AMPK) and lowered the LPS-induced increased expression of dynamin-related protein 1 (Drp1) and Caspase3. These findings prove that hydrogen attenuated LPS-treated ALI by activating the AMPK pathway, supporting the feasibility of hydrogen treatment for sepsis.

Abstract Background Tracheal tube cuff pressure will increase after pneumoperitoneum when the cuff is inflated with air, high pressure can cause tracheal mucosal damage. This prospective trial aimed to assess if inflating with normal saline or lidocaine can prevent increase of tracheal tube cuff pressure and tracheal mucosal damage in laparoscopic surgeries with general anesthesia. Whether changes of tracheal tube cuff transverse diameter (CD) can predict changes of tracheal tube cuff pressure. Methods Ninety patients scheduled for laparoscopic resection of colorectal neoplasms under general anesthesia were randomly assigned to groups air (A), saline (S) or lidocaine (L). Endotracheal tube cuff was inflated with room-temperature air in group A (n = 30), normal saline in group S (n = 30), 2% lidocaine hydrochloride injection in group L (n = 30). After intubation, tracheal tube cuff pressure was monitored by a calibrated pressure transducers, cuff pressure was adjusted to 25 cmH2O (T0.5). Tracheal tube cuff pressure at 15 min after pneumoperitoneum (T1) and 15 min after exsufflation (T2) were accessed. CD were measured by ultrasound at T0.5 and T1, the ability of ΔCD (T1-0.5) to predict cuff pressure was accessed. Tracheal mucous injury at the end of surgery were also recorded. Results Tracheal tube cuff pressure had no significant difference among the three groups at T1 and T2. ΔCD had prediction value (AUC: 0.92 [95% CI: 0.81–1.02]; sensitivity: 0.99; specificity: 0.82) for cuff pressure. Tracheal mucous injury at the end of surgery were 0 (0, 1.0) in group A, 0 (0, 1.0) in group S, 0 (0, 0) in group L (p = 0.02, group L was lower than group A and S, p = 0.03 and p = 0.04). Conclusions Compared to inflation with air, normal saline and 2% lidocaine cannot ameliorate the increase of tracheal tube cuff pressure during the pneumoperitoneum period under general anesthesia, but lidocaine can decrease postoperative tracheal mucosa injury. ΔCD measured by ultrasound is a predictor for changes of tracheal tube cuff pressure. Trial registration Chinese Clinical Trial Registry, identifier: ChiCTR2100054089, Date: 08/12/2021.

目的 分析脑膜瘤切除术患者苏醒期高血压的严重程度和持续时间对术后并发症的影响.方法 回顾性分析 2019 年1 月-2021 年6 月于东部战区总医院接受脑膜瘤切除术患者临床资料.以Clavien-Dindo分级法(≥Ⅱ级)评估的术后并发症为研究主要结局.按苏醒期SBP和DBP分层设置血压阈值,以 5 种方法描述血压持续时间.单因素分析比较并发症组和对照组患者的术前、麻醉和手术方面及术后临床特征.筛选出P＜0.1 的变量纳入多因素Logistic回归模型,以调整潜在混杂变量,评估苏醒期高血压的升高幅度和持续时间对脑膜瘤术后并发症和术后住院天数的影响.结果 共 529 例患者纳入分析,脑膜瘤切除术后并发症发生率为 27.2%.多因素Logistic回归分析结果显示,苏醒期SBP≥160 mmHg总累积持续时间延长会增加术后并发症的发生风险[aOR =1.16(1.00～1.34),P=0.049].与无苏醒期高血压组相比,术后并发症风险与SBP≥160 mmHg长持续时间显著相关[aOR =2.78(1.23～6.28),P=0.014],而与SBP较基线血压增加＞30%无关联.苏醒期SBP≥160 mmHg累积持续时间和单次最长持续时间增加会延长患者的术后住院时间.结论 苏醒期高血压特别是SBP≥160 mmHg持续时间大于 15 min可显著增加脑膜瘤患者术后并发症的发生风险.