Objective:To evaluate the relationship between prognostic nutritional index (PNI) and myocardial injury after non-cardiac surgery (MINS).Methods:This was a retrospective cohort study. The clinical data of adult patients ( n=2 203) who underwent liver resection surgery with general anesthesia at our center from January 2016 to August 2019 were retrospectively collected. The predictive value of preoperative PNI for MINS and the optimal cut-off value of PNI were evaluated and determined according to the receiver operating characteristic curve, and the patients were divided into 2 groups based on the cut-off value: high PNI group and low PNI group. Logistic regression analyses were applied to investigate the relationship between preoperative PNI and MINS. According to the same inclusion and exclusion criteria, the clinical data of patients at our center from January 2022 to December 2023 were collected as the validation set ( n=2 525), and they were grouped using the same PNI cutoff value. Logistic regression analyses were used to verify the relationship between PNI and MINS. Results:The receiver operating characteristic curve analysis showed that the area under the curve of preoperative PNI for predicting MINS was 0.651 (95% confidence interval [ CI] 0.602-0.699), with an optimal cut-off value of 46.193, and the specificity and sensitivity were 0.729 and 0.519 respectively. The integer 46 was considered as the optimal cutoff value for PNI, and the patients were divided into low PNI group (PNI<46, n=606) and high PNI group (PNI≥46, n=1 597). Both univariate and multivariate logistic regression analyses showed that preoperative low PNI was an independent risk factor for the occurrence of MINS (univariate: OR=2.873, 95% CI 2.063-4.003, P<0.001; multivariate: OR=1.844, 95% CI 1.241-2.600, P=0.003). The results in the validation set were still robust (univariate: OR=2.694, 95% CI 1.890-3.833, P<0.001; multivariate: OR=1.602, 95% CI 1.071-2.385, P=0.021). Conclusions:Preoperative low-level PNI is an independent risk factor for MINS, with a certain predictive value.

Background::Renal ischemia-reperfusion (R-I/R) injury is the most prevalent cause of acute kidney injury, with high mortality and poor prognosis. However, the underlying pathological mechanisms are not yet fully understood. Therefore, this study aimed to investigate the role of N-myc downstream-regulated gene 2 ( Ndrg2) in R-I/R injury. Methods::We examined the expression of Ndrg2 in the kidney under normal physiological conditions and after R-I/R injury by immunofluorescence staining, real-time polymerase chain reaction, and western blotting. We then detected R-I/R injury in Ndrg2-deficient ( Ndrg2-/-) mice and wild type ( Ndrg2+/+) littermates in vivo, and detected oxygen and glucose deprivation and reperfusion (OGD-R) injury in HK-2 cells. We further conducted transcriptomic sequencing to investigate the role of Ndrg2 in R-I/R injury and detected levels of oxidative stress and mitochondrial damage by dihydroethidium staining, biochemical assays, and western blot. Finally, we measured the levels of mitophagy in Ndrg2+/+ and Ndrg2-/- mice after R-I/R injury or HK-2 cells in OGD-R injury. Results::Ndrg2 was primarily expressed in renal proximal tubules and its expression was significantly decreased 24 h after R-I/R injury. Ndrg2-/- mice exhibited significantly attenuated R-I/R injury compared to Ndrg2+/+ mice. Transcriptomics profiling showed that Ndrg2 deficiency induced perturbations of multiple signaling pathways, downregulated inflammatory responses and oxidative stress, and increased autophagy following R-I/R injury. Further studies revealed that Ndrg2 deficiency reduced oxidative stress and mitochondrial damage. Notably, Ndrg2 deficiency significantly activated phosphatase and tensin homologue on chromosome ten-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy. The downregulation of NDRG2 expression significantly increased cell viability after OGD-R injury, increased the expression of heme oxygenase-1, decreased the expression of nicotinamide adenine dinucleotide phosphate oxidase 4, and increased the expression of the PINK1/Parkin pathway. Conclusion::Ndrg2 deficiency might become a therapy target for R-I/R injury by decreasing oxidative stress, maintaining mitochondrial homeostasis, and activating PINK1/Parkin-mediated mitophagy.

OBJECTIVE: To explore the regulatory effects of GABAergic neurons in the zona incerta (ZI) on sevoflurane and propofol anesthesia. METHODS: Forty-eight male C57BL/6J mice divided into 8 groups (n=6) were used in this study. In the study of sevoflurane anesthesia, chemogenetic experiment was performed in 2 groups of mice with injection of either adeno-associated virus carrying hM3Dq (hM3Dq group) or a virus carrying only mCherry (mCherry group). The optogenetic experiment was performed in another two groups of mice injected with an adeno-associated virus carrying ChR2 (ChR2 group) or GFP only (GFP group). The same experiments were also performed in mice for studying propofol anesthesia. Chemogenetics or optogenetics were used to induce the activation of GABAergic neurons in the ZI, and their regulatory effects on anesthesia induction and arousal with sevoflurane and propofol were observed; EEG monitoring was used to observe the changes in sevoflurane anesthesia maintenance after activation of the GABAergic neurons. RESULTS: In sevoflurane anesthesia, the induction time of anesthesia was significantly shorter in hM3Dq group than in mCherry group (P < 0.05), and also shorter in ChR2 group than in GFP group (P < 0.01), but no significant difference was found in the awakening time between the two groups in either chemogenetic or optogenetic tests. Similar results were observed in chemogenetic and optogenetic experiments with propofol (P < 0.05 or 0.01). Photogenetic activation of the GABAergic neurons in the ZI did not cause significant changes in EEG spectrum during sevoflurane anesthesia maintenance. CONCLUSION Activation of the GABAergic neurons in the ZI promotes anesthesia induction of sevoflurane and propofol but does not affect anesthesia maintenance or awakening.
Male ; Animals ; Mice ; Mice, Inbred C57BL ; Propofol/pharmacology* ; Sevoflurane/pharmacology* ; Zona Incerta ; Anesthesia, General ; GABAergic Neurons

Objective:To retrospectively review the efficacy of enhanced epidural anesthesia in the patients undergoing cesarean section.Methods:The data from patients who underwent cesarean section in our hospital from August 2008 to December 2021 were retrospectively collected. The method of epidural anesthesia, drug dosage, onset time, blocking level, anesthesia effect, remedial medication, and complications related to the method were recorded. The main points of enhanced epidural anesthesia included: ① test negative pressure by rotating the epidural puncture needle in situ to determine the position of the needle tip; ② catheterization after administering local anesthetic through epidural puncture needle to assess the clinical application of this technique. A questionnaire survey was conducted in 134 anesthesiologists with qualifications for epidural procedures. The questionnaire addressed whether to perform routine needle rotation during epidural procedures, direction of needle rotation, and the percentage of the dosage of local anesthetic administered through puncture needle. Results:A total of 10 054 patients received epidural anesthesia (10 016 cases) and switched to general anesthesia because of poor epidural effect or intraoperative emergencies (38 cases) were enrolled. The consumption of local anesthetics for epidural anesthesia was 18 (15, 20) ml.There were 7 287 cases with block plane records, of which the ratio of the block level reached T 6-8 was 86.84%. The time from the beginning of anesthesia to skin incision was 25 (20, 30) min. Sixteen patients (0.159%) switched to general anesthesia because of poor epidural effect.Among 10 016 patients underwent epidural anesthesia, 925 patients (9.235%) received intravenous adjunctive drugs.No patients experienced total spinal anesthesia, 25 patients (0.248%) had epidural perforation due to puncture or needle rotation, and 4 cases (0.039%) local anesthetic intoxication, 3 cases (0.030%) postoperative nerve injury, and 142 patients (1.412%) requiring intervention with vasoactive drugs due to hemodynamic instability within 30 min after epidural administration. Questionnaire survey: The proportion of anesthesiologists rotating epidural puncture needles was 85.1%, and the proportion of anesthesiologists using epidural puncture needles to inject local anesthesia drugs with a dose greater than 50% of the total dose before catheterization was 84.2%. Conclusions:Enhanced epidural anesthesia can provide effective anesthesia for the patients undergoing cesarean section without increasing the risk of complications related to epidural procedures.

Objective:To explore the effect of desflurane on activity of neurons in 2/3 layer cortex of mice by using high-resolution light-field intelligent imaging system.Methods:Six SPF healthy male Rasgrf/Ai148d mice, aged 8-12 weeks, weighing 25-30 g, were selected. The 6 mice were subjected to skull replacement surgery and then recovered for 2 weeks before experiment.The mice were first fixed under the high-resolution light-field intelligent imaging system for 5 min before calcium signals in 2/3 layer cortex were recorded. The 7.5% desflurane was inhaled for anesthesia starting from 100 s of recording and inhalation was stopped at 700 s, and then the recording continued for 700 s. The total duration of the experiment was 1 500 s. Neurons were extracted and data were analyzed using MATLAB software.Results:When mice were subjected to inhalation anesthesia with desflurane, the calcium fluorescence intensity and percentage of active neurons in the cortex 2/3 layers initially increased significantly, then continuously declined, stabilizing after about 100 s of inhalation. After cessation of inhalation, it gradually recovered to the pre-anesthetic level around 50 s post-inhalation. During the induction period of anesthesia, the percentage of active neurons was significantly higher in the retrosplenial cortex than in the other brain regions ( P<0.05). Conclusions:The disappearance and recovery of consciousness induced by desflurane anesthesia at the neuronal level is not a " symmetrical" process. Neuronal activity in the brain exhibits asymmetry when entering and recovering from an anesthetized state. The retrosplenial cortex, which is related to sleep-wake cycles, may play a crucial role in maintaining consciousness during induction of anesthesia with desflurane.

Dopaminergic neurons in the ventral tegmental area (VTA) play an important role in cognition, emergence from anesthesia, reward, and aversion, and their projection to the cortex is a crucial part of the "bottom-up" ascending activating system. The prelimbic cortex (PrL) is one of the important projection regions of the VTA. However, the roles of dopaminergic neurons in the VTA and the VTA^DA-PrL pathway under sevoflurane anesthesia in rats remain unclear. In this study, we found that intraperitoneal injection and local microinjection of a dopamine D1 receptor agonist (Chloro-APB) into the PrL had an emergence-promoting effect on sevoflurane anesthesia in rats, while injection of a dopamine D1 receptor antagonist (SCH23390) deepened anesthesia. The results of chemogenetics combined with microinjection and optogenetics showed that activating the VTA^DA-PrL pathway prolonged the induction time and shortened the emergence time of anesthesia. These results demonstrate that the dopaminergic system in the VTA has an emergence-promoting effect and that the bottom-up VTA^DA-PrL pathway facilitates emergence from sevoflurane anesthesia.
Anesthesia ; Animals ; Dopaminergic Neurons/metabolism* ; Rats ; Receptors, Dopamine D1/metabolism* ; Sevoflurane/pharmacology* ; Ventral Tegmental Area/metabolism*

Objective:To observe and analyze the changes in activity of layer 2/3 cortical neurons in isoflurane-anesthetized mice by Real-time Ultra-large-Scale High-resolution (RUSH) imaging platform.Methods:Clean-grade healthy male Rasgrf2-Cre/Ai148d mice, aged 8-12 weeks, weighing 18-25 g, were studied.The mice recovered ten days after the skull replacement surgery and proceeded to the next experiment.Imaging data of calcium fluorescence signals from layer 2/3 cortical neurons were acquired by RUSH imaging platform after fixing the head of mice.The time of imaging data acquisition in the awake state, during anesthesia with 1.2% isoflurane, and after the end of anesthesia was 100, 600 and 600 s, respectively.Imaging data were analyzed using Image J and MATLAB softwares.Results:The overall trend of activity of layer 2/3 cortical neurons decreased first and then stabilized with the inhalation of 1.2% isoflurane.The cortical neural activity were gradually increased when isoflurane inhalation was stopped.The recovery rate of neural activity was different in different brain regions after isoflurane inhalation was stopped.The recovery of neural activity in the primary motor cortex was delayed obviously.During the maintenance of anesthesia, the activities of most layer 2/3 cortical neurons in the retrosplenial cortex were weakened, however, some of the neurons became more active.Conclusions:The neural activity in the 2/3 layer of cortex in isoflurane anesthetized mice is inconsistent in observation region, brain region and single cell, suggesting that different neural pathways are involved in the process of anesthesia induction and recovery from anesthesia.

There is a certain relationship between chemotherapy and stroke in cancer patients. Its mechanism may be associated with the increase of the prevalence of traditional vascular factors, the promotion of coagulation dysfunction, the induction of anemia, the impairment of cardiac function, and vascular inflammation. The pathophysiological mechanism of chemotherapy-associated stroke is still in the exploratory stage. This article reviews the pathophysiological mechanism, monitoring indicators, and diagnosis and treatment progress of stroke in cancer patients during chemotherapy.

ObjectiveTo explore the difference of learning and memory function between permanent cerebral ischemia and ischemia-reperfusion rat models by filament-occluded method after three weeks of natural recovery, and to observe the changes of brain structure. MethodsA total of 21 SPF male Sprague-Dawley rats were randomly divided into sham group (n = 7), permanent ischemia group (n = 7) and ischemia-reperfusion group (n = 7). The latter two group underwent left middle cerebral artery occlusion, and the ischemia-reperfusion group was reperfused after 90 minutes of ischemia. All the rats were tested with Morris Water Maze 16 to 22 days after modeling, to record escape latency in the navigation experiment, as well as first latency, platform quadrant swimming time ratio and distance ratio, boundary swimming time ratio and distance ratio, average speed, and the swimming path in the space exploration experiment. On the 22nd day after modeling, four rats with similar Longa scores in each group were scanned by magnetic resonance by diffusion tensor imaging, to measure the fractional anisotropy (FA) of cerebral ischemic cortex, striatum, hippocampus and their corresponding contralateral regions, to calculate ratio of FA (rFA); as well as the volume of infarct (VI) and ratio of VI (rVI). ResultsFor navigation experiment, the escape latency decreased in all the groups with the time (F = 36.202, P < 0.001), but it was not significant for the permanent ischemia group (F = 4.004, P > 0.05). The escape latency was longer in the permanent ischemia group than in the other two groups at each time points (P < 0.05). For space exploration experiment, the boundary time ratio and distance ratio were more in the permanent ischemia group and the ischemia-reperfusion group than in the sham group (P < 0.017), and the first latency was longer in the permanent ischemia group than in the sham group (P < 0.017). The swimming path of ischemia-reperfusion group and sham operation group was better than that of the permanent ischemia group. FA and rFA in left cortex and striatum were less in the permanent ischemia group and the ischemia-reperfusion group than in the sham group (P < 0.05), while FA and rFA of left cortex and FA of left striatum were less in the permanent ischemia group than in the ischemia-reperfusion group (P < 0.05). The VI and rVI were larger in the permanent ischemia group than in the ischemia-reperfusion group (t > 4.185, P < 0.01). FA and rFA of left cortex and striatum correlated with escape latency, boundary time ratio and distance ratio (|r| > 0.498, P < 0.05). The VI and rVI correlated with escape latency and boundary time ratio (|r| > 0.538, P < 0.05). ConclusionCognitive impairment is more severe in the rat model of permanent cerebral ischemia, which may relate to the larger damage of structure of nerve fibers in ischemic cortex and striatum, and larger infarct size.

Based on 18 hospitals including the Chinese People's Liberation Army General Hospital and Peking University People's Hospital, and based on the "Specifications for Perioperative Data", explore the construction and application of perioperative multi-center data centers in the era of medical big data. The use of data ferry technology avoids hidden safety hazards in hospitals, realizes the integration and sharing of perioperative medical data of various medical institutions, and forms a complete data chain combining patient medical data and follow-up data.
Hospitals, Military ; Humans ; Military Personnel ; United States