Effects of perioperative hydrogen inhalation on brain edema and prognosis in patients with glioma: a single-center, randomized controlled study.

Introduction: Brain edema is a life-threatening complication that occurs after glioma surgery. There are no noninvasive and specific treatment methods for brain edema. Hydrogen is an anti-inflammatory and antioxidant gas that has demonstrated therapeutic and preventative effects on several diseases, particularly in the nervous system. This study aimed to determine the therapeutic effects of hydrogen administration on brain edema following glioma surgery and elucidate its mechanism. Methods: A single-center, randomized controlled clinical trial of hydrogen inhalation was conducted (China Clinical Trial Registry [ChiCTR-2300074362]). Participants in hydrogen (H) group that inhaled hydrogen experienced quicker alleviation of postoperative brain edema compared with participants in control (C) group that inhaled oxygen. Results: The volume of brain edema before discharge was significantly lower in the H group (p < 0.05). Additionally, the regression rate of brain edema was higher in the H group than in the C group, which was statistically significant (p < 0.05). Furthermore, 3 days after surgery, the H group had longer total sleep duration, improved sleep efficiency, shorter sleep latency, and lower numerical rating scale (NRS) scores (p < 0.05). Discussion: In conclusion, hydrogen/oxygen inhalation effectively reduced postoperative brain edema in glioma patients. Further research is necessary to understand the underlying mechanisms of hydrogen's therapeutic effects. Hydrogen is expected to become a new target for future adjuvant therapy for brain edema.

The effect of intraoperative intermittent pneumatic compression on deep venous thrombosis prophylaxis in patients undergoing elective craniotomy.

Objective: Postoperative deep venous thrombosis (DVT) is commonly observed in patients undergoing craniotomy and is associated with a high incidence of pulmonary embolism and poor clinical outcomes. Herein, we investigated the prophylactic effect of DVT of intraoperative intermittent pneumatic compression (IPC) in patients undergoing craniotomy. Methods: A total of 516 patients who underwent elective craniotomy between December 2021 and December 2022 were enrolled in this study. Patients were randomly assigned to the intervention group (received intraoperative IPC) or control group (without IPC). Lower extremity ultrasound was performed on both legs before and after surgery (1 h, 24 h, and 7 days post-intervention). DVT was defined as the visualization of a thrombus within the vein lumen of the leg. Coagulation and platelet function were measured at the start and end of the craniotomy. Results: A total of 504 patients (251 in the intervention group and 253 in the control group) completed the study. Among these patients, 20.4% (103/504) developed postoperative DVT within the first week after surgery, with 16.7% occurring within 24 h. The incidence of postoperative DVT in the intervention group (9.6%, 24/251) was significantly lower than that in the control group (22.9%, 58/253, p < 0.001). Intraoperative IPC reduced the risk of DVT by 64.6% (0.354, 95% CI, 0.223-0.564, p < 0.001). There was no significant difference in coagulation and platelet function between the two groups (all p > 0.05). Conclusion: DVT may develop within 24 h after the craniotomy. Intraoperative application of IPC reduces the incidence of postoperative DVT.

Hydrogen mitigates brain injury by prompting NEDD4-CX43- mediated mitophagy in traumatic brain injury.

BACKGROUND: Hydrogen (H2) has emerged as a potential therapeutic intervention for traumatic brain injury (TBI). However, the precise mechanism underlying H2's neuroprotective effects in TBI remain incompletely understood. METHODS: TBI mouse model was induced using the controlled cortical impact (CCI) method, and a cell model was established by exposing astrocytes to lipopolysaccharide (LPS). Cell viability was detected by CCK-8 kits. Cell apoptosis was measured by flow cytometry. ELISA was used to detect cytokine quantification. Protein and gene expression was detected by western blot and RT-PCR analysis. Co-immunoprecipitation (CO-IP) were employed for protein-protein interactions. Morris water maze test and rotarod test were applied for TBI mice. RESULTS: H2 treatment effectively inhibited the LPS-induced cell injury and cell apoptosis in astrocytes. NEDD4 expression was increased following H2 treatment coupled with enhanced mitophagy in LPS-treated astrocytes. Overexpression of NEDD4 and down-regulation of connexin 43 (CX43) mirrored the protective effects of H2 treatment in LPS-exposed astrocytes. NEDD4 interacts CX43 to regulates the ubiquitinated degradation of CX43. While overexpression of CX43 reversed the protective effects of H2 treatment in LPS-exposed astrocytes. In addition, H2 treatment significantly alleviated brain injury in TBI mouse model. CONCLUSION: H2 promoted NEDD4-CX43 mediated mitophagy to protect brain injury induced by TBI, highlighting a novel pathway underlying the therapeutic effects of H2 in TBI.

Impact of Preoperative Sleep Disturbances on Postoperative Delirium in Patients with Intracranial Tumors: A Prospective, Observational, Cohort Study.

Background: Postoperative delirium (POD) is prevalent in craniotomy patients and is associated with high mortality. Sleep disturbances are receiving increasing attention from clinicians as associated risk factors for postoperative complications. This study aimed to determine the impact of preoperative sleep disturbances on POD in craniotomy patients. Methods: We recruited 130 patients undergoing elective craniotomy for intracranial tumors between May 1st and December 30th, 2022. Preoperative subjective sleep disturbances were assessed using the Pittsburgh Sleep Quality Index on the day of admission. We also measured objective perioperative sleep patterns using a dedicated sleep monitoring device 3 days before and 3 days after the surgery. POD was assessed twice daily using the Confusion Assessment Model for the Intensive Care Unit within the first week after craniotomy. Results: Preoperative sleep disturbances were diagnosed in 49% of the study patients, and POD was diagnosed in 22% of all the study patients. Sleep disturbances were an independent risk factor for POD (OR: 2.709, 95% CI: 1.020-7.192, P = 0.045). Other risk factors for POD were age (OR: 3.038, 95% CI: 1.195-7.719, P = 0.020) and the duration of urinary catheterization (OR: 1.246, 95% CI: 1.025-1.513, P = 0.027). Perioperative sleep patterns (including sleep latency, deep sleep duration, frequency of awakenings, apnea-hypopnea index, and sleep efficiency) were significantly associated with POD. Conclusion: This study demonstrated that preoperative sleep disturbances predispose patients undergoing craniotomy to POD, also inferred a correlation between perioperative sleep patterns and POD. The targeted screening and intervention specifically for sleep disturbances during the perioperative period are immensely required.

Associations between perioperative sleep patterns and clinical outcomes in patients with intracranial tumors: a correlation study.

Objective: Although the quality of perioperative sleep is gaining increasing attention in clinical recovery, its impact role remains unknown and may deserve further exploration. This study aimed to investigate the associations between perioperative sleep patterns and clinical outcomes among patients with intracranial tumors. Methods: A correlation study was conducted in patients with intracranial tumors. Perioperative sleep patterns were assessed using a dedicated sleep monitor for 6 consecutive days. Clinical outcomes were gained through medical records and follow-up. Spearman's correlation coefficient and multiple linear regression analysis were applied to evaluate the associations between perioperative sleep patterns and clinical outcomes. Results: Of 110 patients, 48 (43.6%) were men, with a median age of 57 years. A total of 618 days of data on perioperative sleep patterns were collected and analyzed. Multiple linear regression models revealed that the preoperative blood glucose was positively related to the preoperative frequency of awakenings (ß = 0.125; 95% CI = 0.029-0.221; P = 0.011). The level of post-operative nausea and vomiting was negatively related to perioperative deep sleep time (ß = -0.015; 95% CI = -0.027--0.003; P = 0.015). The level of anxiety and depression was negatively related to perioperative deep sleep time, respectively (ß = -0.048; 95% CI = -0.089-0.008; P = 0.020, ß = -0.041; 95% CI = -0.076-0.006; P = 0.021). The comprehensive complication index was positively related to the perioperative frequency of awakenings (ß = 3.075; 95% CI = 1.080-5.070; P = 0.003). The post-operative length of stay was negatively related to perioperative deep sleep time (ß = -0.067; 95% CI = -0.113-0.021; P = 0.005). The Pittsburgh Sleep Quality Index was positively related to perioperative sleep onset latency (ß = 0.097; 95% CI = 0.044-0.150; P < 0.001) and negatively related to perioperative deep sleep time (ß = -0.079; 95% CI = -0.122-0.035; P < 0.001). Conclusion: Perioperative sleep patterns are associated with different clinical outcomes. Poor perioperative sleep quality, especially reduced deep sleep time, has a negative impact on clinical outcomes. Clinicians should, therefore, pay more attention to sleep quality and improve it during the perioperative period. Clinical trial registration: http://www.chictr.org.cn, identifier: ChiCTR2200059425.

Propofol suppresses hormones levels more obviously than sevoflurane in pediatric patients with craniopharyngioma: A prospective randomized controlled clinical trial.

OBJECTIVE: General anesthesia can disturb the hormone levels in surgical patients. Hormone deficiency is one of the major symptoms of craniopharyngioma (CP) in pediatric patients. The aim of this prospective randomized controlled clinical study is to evaluate whether propofol and sevoflurane influence the perioperative hormone levels in these patients and to determine which anesthesia technique causes less impact on hormone levels. MATERIALS: Sixty-four ASA I and II pediatric patients with CP undergoing elective neurosurgery were randomly divided into the sevoflurane group (S group, n = 32) and the propofol group (P group, n = 32). Anesthesia was maintained with sevoflurane and propofol until the end of the operation. Demographic information, operation information and hemodynamic variables were recorded. The levels of hormones were evaluated preoperatively as the baseline (T0), 1h after the beginning of the operation (T1), immediately at the end of the operation (T2) and 72 h postoperatively (T3). RESULTS: There were no significant differences in the two groups in terms of patients' demographics and intraoperative information, such as operation duration, blood loss and transfusion volumes, and fluid infusion volume (P>0.05). In both groups, compared to those at T0, the levels of TSH, FT3, TT3 and ACTH at T1, T2 and T3 were significantly lower. The levels of FSH, PRL and GH at T3 were also significantly lower (P<0.05). The FT3 and TT3 levels of both groups at T2 and T3 were significantly lower than those at T1, but the ACTH level was significantly increased (P<0.05). Compared to the levels at T2, the TSH, FT3, FT4 and ACTH levels of the two groups at T3 were significantly reduced (P<0.05). The baseline hormone levels of both groups were similar (P>0.05). At T1, the FT3, TT3, FT4, TT4 and ACTH levels in the P group were significantly lower than those in the S group (P<0.05). At T2, the TT3 and ACTH levels of the P group were significantly lower than those of the S group (P<0.05) At T3, the TT4 level in the P group was significantly lower than that of the S group (P<0.05). CONCLUSION: Propofol and sevoflurane could reduce the levels of hormones intraoperatively and postoperatively in pediatric patients with craniopharyngioma. However, propofol reduced hormone levels more intensively, mainly intraoperatively. Postoperatively, propofol and sevoflurane had similar inhibition effects on the shift in hormone levels. Therefore, in pediatric patients with craniopharyngioma undergoing neurosurgery, sevoflurane might be the preferred anesthetic because it causes less interruption of hormone levels. However, because of their similar postoperative effects, which long-term effects of sevoflurane or propofol could produce optimal clinical situations? Thus more extensive clinical studies are needed. TRIAL REGISTRATION: Clinical trial registration. This trail was registered at Chinese Clinical Trial Registry (http://www.chictr.org.cn, Jun Xiong) on 28/12/2021, registration number was ChiCTR2100054885.

The Effects of Perioperative Probiotics on Postoperative Gastrointestinal Function in Patients with Brain Tumors: A Randomized, Placebo-Controlled Study.

The incidence of postoperative gastrointestinal dysfunction among neurosurgical patients is as high as 80%. Probiotics help to maintain gastrointestinal barrier defense, provide competitive adherence to mucus and epithelial cells, and regulate gastrointestinal motility. Therefore, the purpose of this study was to investigate whether probiotics enhance gastrointestinal health after craniotomy in patients with brain tumors. This study was a 15-day, prospective, randomized, double-blind, placebo-controlled trial for patients being treated with elective craniotomy for brain tumors. Participants were randomly divided into the probiotics group (4 g probiotics, twice daily) and placebo group. The primary outcome was the time of first stool after surgery. The secondary outcomes included assessments of the gastrointestinal function, changes in gastrointestinal permeability and clinical outcomes. We enrolled a total of 200 participants (probiotics: 100; placebo: 100) and followed the principles of intention-to-treat analysis. The time of first stool and flatus were significantly shorter in the probiotics group compared to the placebo group (P < 0.001, respectively). No significant trends were observed for any other of the secondary outcome variables. Our findings suggest that probiotics can improve the gastrointestinal mobility of patients received craniotomy, and this improvement cannot be explained by changes in gastrointestinal permeability.

Dexmedetomidine premedication increases preoperative sedation and inhibits stress induced by tracheal intubation in adult: a prospective randomized double-blind clinical study.

OBJECTIVE: The aim of this prospective randomized double-blind study is to evaluate whether oral dexmedetomidine (DEX) premedication could increase sedation in order to reduce preoperative anxiety and inhibit stress response during general anesthesia tracheal intubation. MATERIALS: A total of 100 ASA I and II adult patients undergoing elective neurosurgery were randomly divided into the control group (C group, n = 50) and the oral DEX premedication (DEX group, n = 50). Patients were administrated 4 µg/kg dexmedetomidine orally pre-anesthesia 120 min. Hemodynamic variables were monitored and recorded from premedication to 10 min after tracheal intubation. The primary outcome, the sedation level of all participants, was evaluated by Richmond Agitation Sedation Scale (RASS), and Numerical Rating Scale was to measure their intensity of thirst and satisfaction of patients' family members. During general anesthesia induction, the total dosage of induction anesthetics and complications relative to anesthesia induction were recorded. After tracheal intubation, blood sample was drain from radial atrial line to measure levels of adrenocorticotropic hormone (ACTH) and cortisol. RESULTS: RASS scores at 60 min after premedication and on arrival in the operating room were significantly reduced in the DEX group (P < 0.001). Oral DEX premedication not only increased the intensity of thirst but also the satisfaction of their family members (P < 0.001). The cortisol level after tracheal intubation was deduced by oral DEX premedication (P < 0.05). Oral DEX premedication reduced heart rate (HR) and mean arterial pressure (MAP) on arrival in the operating room, and HR when tracheal intubation (P < 0.05). During the whole process of anesthesia induction, although the lowest MAP in two groups were not significantly different, the lowest HR was significantly lower in the DEX group (P < 0.05). Oral DEX premedication might reduce HR from premedication to 10 min after tracheal intubation. However MAP was reduced just from premedication to on arrival in the operating room. Total induction dosages of propofol, midazolam, sulfentanil and rocuronium were similar in two groups (P > 0.05), as well as the complications relative to anesthesia induction and cases of rescue dopamine therapy were similar (P > 0.05). CONCLUSION: Oral DEX 4 µg/kg premedication was an efficient intervention to increase preoperative sedation and reduce stress reaction induced by general anesthesia tracheal intubation, but also it was with the stable hemodynamic during the process of general anesthesia tracheal intubation, and improved the satisfaction of patients' family members. In this study, the sparing-anesthetic effect of 4 µg/kg DEX oral premedication was not significant, and this would be needed to study in future. TRIAL REGISTRATION: This trail was registered at Chinese Clinical Trial Registry ( https://www.chictr.org.cn , Jie Gao) on 15/04/2021, registration number was ChiCTR2100045458.

Characteristics, surgical outcomes, and influential factors of epilepsy in Sturge-Weber syndrome.

Few studies have reported the clinical presentation, surgical treatment, outcomes and influential factors for patients with epilepsy and Sturge-Weber syndrome. This large-scale retrospective study continuously enrolled 132 patients with Sturge-Weber syndrome and epilepsy from January 2008 to December 2018 at our hospital to analyse their characteristics. Among these patients, 90 underwent epilepsy surgery, and their postoperative 2-year follow-up seizure, cognitive and motor functional outcomes were assessed and analysed. Univariable and multivariable logistic analyses were conducted to explore the influential factors. Among the patients with Sturge-Weber syndrome for whom characteristics were analysed (n = 132), 76.52% of patients had their first epileptic seizures within their first year of life. The risk factors for cognitive decline were seizure history ≥ 2 years [adjusted odds ratio (aOR) = 3.829, 95% confidence interval (CI): 1.810-9.021, P = 0.008)], bilateral leptomeningeal angiomas (aOR = 3.173, 95% CI: 1.970-48.194, P = 0.013), age at onset <1 year (aOR = 2.903, 95% CI: 1.230-6.514, P = 0.013), brain calcification (aOR = 2.375, 95% CI: 1.396-5.201, P = 0.021) and left leptomeningeal angiomas (aOR = 2.228, 95% CI: 1.351-32.571, P = 0.030). Of the patients who underwent epilepsy surgery (n = 90), 44 were subject to focal resection, and 46 underwent hemisphere surgery (19 anatomical hemispherectomies and 27 modified hemispherotomies). A postoperative seizure-free status, favourable cognitive outcomes, and favourable motor outcomes were achieved in 83.33%, 44.44% and 43.33% of surgical patients, respectively. The modified hemispherotomy group had similar surgical outcomes, less intraoperative blood loss and shorter postoperative hospital stays than the anatomical hemispherectomy group. Regarding seizure outcomes, full resection (aOR = 11.115, 95% CI: 1.260-98.067, P = 0.020) and age at surgery < 2 years (aOR = 6.040, 95% CI: 1.444-73.367, P = 0.031) were positive influential factors for focal resection. Age at surgery < 2 years (aOR = 15.053, 95% CI: 1.050-215.899, P = 0.036) and infrequent seizures (aOR = 8.426, 95% CI: 1.086-87.442, P = 0.042; monthly versus weekly) were positive influential factors for hemisphere surgery. In conclusion, epilepsy surgery resulted in a good postoperative seizure-free rate and favourable cognitive and motor functional outcomes and showed acceptable safety for patients with epilepsy and Sturge-Weber syndrome. Modified hemispherotomy is a less invasive and safer type of hemisphere surgery than traditional anatomic hemispherectomy with similar surgical outcomes. Early surgery may be helpful to achieve better seizure outcomes and cognitive protection, while the risk of surgery for young children should also be considered.

Detection of Electrophysiological Activity of Amygdala during Anesthesia Using Stereo-EEG: A Preliminary Research in Anesthetized Epileptic Patients.

Recent studies of anesthesia mechanisms have focused on neuronal network and functional connectivity. The stereo-electroencephalography (SEEG) recordings provide appropriate temporal and spatial resolution to study whole-brain dynamics; however, the feasibility to detect subcortical signals during anesthesia still needs to be studied with clinical evidence. Here, we focus on the amygdala to investigate if SEEG can be used to detect cortical and subcortical electrophysiological activity in anesthetized epileptic patients. Therefore, we present direct evidence in humans that SEEG indeed can be used to record cortical and subcortical electrophysiological activity during anesthesia. The study was carried out in propofol-anesthetized five epileptic patients. The electrophysiology activity of the amygdala and other cortical areas from anesthesia to the recovery of consciousness was investigated using stereo-EEG (SEEG). Results indicated that with the decrease of propofol concentration, power spectral density (PSD) in the delta band of the amygdala significantly decreased. When it was close to recovery, the correlation between the amygdala and ipsilateral temporal lobe significantly decreased followed by a considerable increase when awake. The findings of the current study suggest SEEG as an effective tool for providing direct evidence of the anesthesia mechanism.

Transient visual acuity loss after spine surgery in the prone position: a case report and literature review.

Visual loss after spine surgery in the prone position is a disastrous postoperative complication because it is almost irreversible. Additionally, the optimal treatments and recommended professional guidelines for visual loss after spine surgery are deficient. A 43-year-old man developed visual loss after spine surgery in the prone position. Immediate ophthalmic consultation confirmed central retinal artery occlusion. Therefore, combined therapies were administered, including neurotrophy, anticoagulation, vasodilation, and adequate fluid infusion, followed by hyperbaric oxygen treatment. After active treatment, his visual acuity gradually recovered from 5 hours postoperatively and continued to improve thereafter. We reviewed the literature on postoperative visual loss with a focus on spine surgery in the prone position. Because the etiology of this complication is complex and has few effective treatments, the best method for its avoidance is to pay close attention to preventing it during surgery.

Peripheral Blood Occludin Level as a Biomarker for Perioperative Cerebral Edema in Patients with Brain Tumors.

OBJECTIVE: Cerebral edema is a common complication of brain tumors in the perioperative period. However, there is currently no reliable and convenient method to evaluate the extent of brain edema. The objective is to explore the effectiveness of serum occludin on predicting the extent of perioperative brain edema and outcome in patients with brain tumors. METHODS: This prospective study enrolled 55 patients with brain tumors and 24 healthy controls in Sanbo Brain Hospital from June 2019 through November 2019. Serum occludin levels were measured preoperatively and on postoperative day 1. Peritumoral edema was assessed preoperatively using MRI. Pericavity brain edema on postoperative day 1 was evaluated using CT. RESULTS: Compared with healthy controls, the serum occludin level was higher in patients with brain tumors both preoperatively and postoperatively (P < 0.001). The serum occludin level correlated positively with the degree of brain edema preoperatively (r = 0.78, P < 0.001) and postoperatively (r = 0.59, P < 0.001). At an optimal cutoff of 3.015 ng/mL, the preoperative serum occludin level discriminated between mild and severe preoperative brain edema with a sensitivity of 90.48% and specificity of 84.62%. At an optimal cutoff value of 3.033 ng/mL, the postoperative serum occludin level distinguished between mild and severe postoperative brain edema with a sensitivity of 97.30% and specificity of 55.56%. CONCLUSIONS: The serum occludin level is associated with cerebral edema and could potentially be used as a biomarker for perioperative cerebral edema. This trial is registered with ChiCTR1900023742.

Electric vagal nerve stimulation inhibits inflammation and improves early postoperation cognitive dysfunction in aged rats.

BACKGROUND: This study aimed to evaluate effects of electric vagal nerve stimulation on early postoperation cognitive dysfunction in aged rats. METHODS: A total of 33 male Sprague Dawley rats were selected and assigned randomly to three groups, control group (C, n = 10), splenectomy group (S, n = 10) and splenectomy+vagal nerve stimulation group (SV, n = 13). Behavior and memory of rats were evaluated by Open Field Test and Morris Water Maze. Levels of TNF-α, IL-6 and IL-10 in serum were measured by ELISA. The level of TNF-α protein in hippocampus was assessed by Western blotting. rt-PCR was used to detect mRNA expression of NF-κB in hippocampus. RESULTS: During anesthesia/operation, vital life signs of rats were stable. In SV group, vagal nerve stimulation decreased heart rate lower than 10% of basic level and kept it at a stable range by regulating stimulation intensity. After stimulation stop, heart rate returned to the basic level again. This indicated that the model of vagal nerve stimulation was successful. Serum levels of TNF-α and IL-6 increased by the operation/anesthesia, but they decreased with vagal nerve stimulation (all P < 0.05). TNF-α protein and mRNA expression of NF-κB in hippocampus were also eliminated by vagal nerve stimulation compared to S group (P < 0.05). Results of Morris Water Maze showed escape latency of postoperation in S group was significantly longer than C group (P < 0.05), and times of crossing platform in S group was lower than that of C group (P < 0.05). Although escape latency of postopration in SV group was shorter than that of S group, there was no significant difference between two groups. Meanwhile there were no significant differences of behavior test in Open Field test between three groups, although vagal nerve stimulation improved partly active explore behavior compared to S group. CONCLUSION: The inflammation caused by operation and general anesthesia was an important reason of early postoperation cognitive dysfunction, and electric vagal nerve stimulation could inhibit the inflammation. Meanwhile, vagal nerve stimulation could ameliorate early postoperation cognitive dysfunction partly, but its protective effects were not enough and should be studied and improved in future.

MiR-125b-5p Inhibitor Might Protect Against Sevoflurane-induced Cognitive Impairments by Targeting LIMK1.

PURPOSE: Research has shown that exposure to anesthesia might increase the risks of cognitive impairments and learning difficulties. MiR-125b-5p contributed to anesthesia-induced hippocampal apoptosis. However, the role of miR-125b-5p in sevoflurane-induced cognitive impairments remains unclear. METHODS: Firstly, sevoflurane was used to establish a rat model and cognitive impairment was detected by the Morris water maze (MWM) test. The hippocampus was observed by HE staining. The lentivirus-miR-125b-5p antagomiR was transfected into rats to decrease miR-125b-5p. The interaction between miR-125b-5p and LIM domain kinase 1 (LIMK1) was confirmed by the luciferase reporter assay. The mRNA and expression levels of related genes and mRNA were examined by the Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and western blot. RESULTS: Sevoflurane induced the cognitive dysfunction presenting with longer latency time and few platform crossings in rats. Moreover, miR-125b-5p was observed to be up-regulated in both sevoflurane-anesthesia rats and sevoflurane-treated SH-SY5Y cells. More importantly, a decrease in miR-125b-5p could prevent sevoflurane-induced hippocampal apoptosis and inflammation in rats. Moreover, LIMK1 was the target gene of miR-125b-5p. Interestingly, si-LIMK1 could restore the sevoflurane-induced cell apoptosis in SH-SY5Y cells, which was alleviated by miR-125b-5p inhibitor. Finally, the miR-125b-5p inhibitor shortened the time to find the platform and increased the number of platform crossings compared to sevoflurane-anesthesia rats in the Morris water maze test. At the same time, the expression of LIMK1 was dramatically increased. CONCLUSION: Altogether, these findings suggested that miR-125b-5p inhibitor could protect against the sevoflurane-induced cognitive impairments by targeting LIMK1.

Negative pressure pulmonary edema: a case report.

BACKGROUND: The negative pressure pulmonary edema is rare clinical situation which caused mainly by upper airway obstruction. However except upper airway obstruction, there may be other pathophysiological disorders making patients more vulnerable to pulmonary edema. Based on these disorders, upper airway obstruction is the trigger to induce negative pressure pulmonary edema. CASE PRESENTATION: This case was a 5-year-old girl with tumor on saddle area, her hormones level were abnormal preoperatively, such as cortisol, adrenocorticotrophic hormone, free T4 and total T4. During the stage of induction, negative pressure pulmonary edema took place due to mild upper airway obstruction. And the instant chest Computer tomography proved diagnosis clue. After intensive care, most lung field of this girl recovered to normal within 48 h. CONCLUSION: The patient with abnormal hormone levels is vulnerable to pulmonary edema, mild upper airway obstruction triggered negative pressure pulmonary. Thus pre-operation hormones supplement is as important as keeping upper airway unobstructed.

Burst strength of tubing and casing based on twin shear unified strength theory.

The internal pressure strength of tubing and casing often cannot satisfy the design requirements in high pressure, high temperature and high H2S gas wells. Also, the practical safety coefficient of some wells is lower than the design standard according to the current API 5C3 standard, which brings some perplexity to the design. The ISO 10400: 2007 provides the model which can calculate the burst strength of tubing and casing better than API 5C3 standard, but the calculation accuracy is not desirable because about 50 percent predictive values are remarkably higher than real burst values. So, for the sake of improving strength design of tubing and casing, this paper deduces the plastic limit pressure of tubing and casing under internal pressure by applying the twin shear unified strength theory. According to the research of the influence rule of yield-to-tensile strength ratio and mechanical properties on the burst strength of tubing and casing, the more precise calculation model of tubing-casing's burst strength has been established with material hardening and intermediate principal stress. Numerical and experimental comparisons show that the new burst strength model is much closer to the real burst values than that of other models. The research results provide an important reference to optimize the tubing and casing design of deep and ultra-deep wells.

Glucose may attenuate isoflurane-induced caspase-3 activation in H4 human neuroglioma cells.

BACKGROUND: The commonly used inhaled anesthetic isoflurane has been shown to induce caspase-3 activation. However, the underlying mechanism(s) and targeted intervention(s) remain largely to be determined. Isoflurane may induce caspase-3 activation via causing accumulation of reactive oxygen species (ROS), mitochondrial dysfunction, and reduction in adenosine triphosphate (ATP) levels. Therefore, we performed a hypothesis-generation study to determine whether glucose could attenuate isoflurane-induced caspase-3 activation, ROS accumulation, mitochondrial dysfunction, and ATP reduction in cultured cells. METHODS: H4 human neuroglioma cells (H4 cells) were treated with 2% isoflurane or the control condition plus saline or 50 mM glucose for 6 or 3 hours. Caspase-3 activation, cell viability, levels of ROS and ATP, and mitochondrial membrane potential were determined at the end of the experiments by Western blot analysis and fluorescence assay. RESULTS: We found that the glucose treatment might attenuate isoflurane-induced caspase-3 activation and reduction of cell viability in H4 cells. Moreover, the glucose treatment mitigated the isoflurane-induced increase in ROS levels and reduction in ATP levels in H4 cells. Unexpectedly, we observed that the glucose treatment might not inhibit the isoflurane-induced decrease in mitochondrial membrane potential in H4 cells. CONCLUSIONS: Pending further studies, these results suggested that glucose might attenuate isoflurane-induced caspase-3 activation through a mitochondria-independent reduction in ROS levels and enhancement in ATP levels. These findings have established a system and suggest that it is worth performing more research to further investigate whether glucose can attenuate anesthesia neurotoxicity.

Time-Dependent Effects of Anesthetic Isoflurane on Reactive Oxygen Species Levels in HEK-293 Cells.

The inhalation anesthetic isoflurane has been reported to induce caspase activation and apoptosis, which may lead to learning and memory impairment. However, the underlying mechanisms of these effects are largely unknown. Isoflurane has been shown to induce elevation of cytosol calcium levels, accumulation of reactive oxygen species (ROS), opening of the mitochondrial permeability transition pore, reduction in mitochondria membrane potential, and release of cytochrome c. The time course of these effects, however, remains to be determined. Therefore, we performed a pilot study to determine the effects of treatment with isoflurane for various times on ROS levels in HEK-293 cells. The cells were treated with 2% isoflurane plus 21% O2 and 5% CO2 for 15, 30, 60, or 90 min. We then used fluorescence imaging and microplate fluorometer to detect ROS levels. We show that 2% isoflurane for 60 or 90 min, but not 15 or 30 min, induced ROS accumulation in the cells. These data illustrated that isoflurane could cause time-dependent effects on ROS levels. These findings have established a system to further determine the time course effects of isoflurane on cellular and mitochondria function. Ultimately, the studies would elucidate, at least partially, the underlying mechanisms of isoflurane-induced cellular toxicity.