Research trends and hotspots in the field of electrical impedance tomography for mechanical ventilation: a bibliometric analysis.

Background: Electrical impedance tomography (EIT) is a relatively recent functional imaging technique that is both noninvasive and radiation free. EIT measures the associated voltage when a weak current is applied to the surface of the human body to determine the distribution of electrical resistance within tissues. We performed a bibliometrics-based review to explore the geographic hotspots of current research and future trends developing in the field of EIT for mechanical ventilation. Methods: The Web of Science database was searched from its inception to June 25, 2023. CiteSpace software was used to visualize and analyze the relevant literature and identify the most impactful literature, trends, and hotspots. Results: 363 articles describing EIT use in mechanical ventilation were identified. A fluctuating growth in the number of publications was observed from 1998 to 2023. Germany had the highest number of articles (n=154), followed by Italy (n=53) and China (n=52). A cluster analysis of keyword co-occurrence revealed that "titration", "ventilator-related lung injury", and "oxygenation" were the most actively researched terms associated with the use of EIT in mechanically ventilated patients. Conclusions: Significant progress has been made in EIT research for mechanical ventilation. EIT research is limited to a small number of countries with a present research focus on the prevention and treatment of ventilator-related lung injury, oxygenation status, and prone ventilation. These topics are expected to remain research hotspots in the future.

Regulation of depressive-like behaviours by palmitoylation: Role of AKAP150 in the basolateral amygdala.

BACKGROUND AND PURPOSE: Protein palmitoylation is involved in learning and memory, and in emotional disorders. Yet, the underlying mechanisms in these processes remain unclear. Herein, we describe that A-kinase anchoring protein 150 (AKAP150) is essential and sufficient for depressive-like behaviours in mice via a palmitoylation-dependent mechanism. EXPERIMENTAL APPROACH: Depressive-like behaviours in mice were induced by chronic restraint stress (CRS) and chronic unpredictable mild stress (CUMS). Palmitoylated proteins in the basolateral amygdala (BLA) were assessed by an acyl-biotin exchange assay. Genetic and pharmacological approaches were used to investigate the role of the DHHC2-mediated AKAP150 palmitoylation signalling pathway in depressive-like behaviours. Electrophysiological recording, western blotting and co-immunoprecipitation were performed to define the mechanistic pathway. KEY RESULTS: Chronic stress successfully induced depressive-like behaviours in mice and enhanced AKAP150 palmitoylation in the BLA, and a palmitoylation inhibitor was enough to reverse these changes. Blocking the AKAP150-PKA interaction with the peptide Ht-31 abolished the CRS-induced AKAP150 palmitoylation signalling pathway. DHHC2 expression and palmitoylation levels were both increased after chronic stress. DHHC2 knockdown prevented CRS-induced depressive-like behaviours, as well as attenuating AKAP150 signalling and synaptic transmission in the BLA in CRS-treated mice. CONCLUSION AND IMPLICATIONS: These results delineate that DHHC2 modulates chronic stress-induced depressive-like behaviours and synaptic transmission in the BLA via the AKAP150 palmitoylation signalling pathway, and this pathway may be considered as a promising novel therapeutic target for major depressive disorder.

Efficacy and safety of remimazolam compared with propofol in hypertensive patients undergoing breast cancer surgery: a single-center, randomized, controlled study.

BACKGROUND: Remimazolam, as a novel anesthetic, has recently been shown to improve hemodynamic stability during anesthesia induction and maintenance; however, it has not been reported in the hypertensive population. This study aimed to compare the effects of remimazolam and propofol on hemodynamic stability in hypertensive patients undergoing breast cancer surgery. METHODS: We enrolled 120 hypertensive patients undergoing breast cancer surgery in this prospective study and randomly allocated them to remimazolam (n = 60) or propofol (n = 60) groups. Anesthesia regimens were consistent between groups, except for the administration of remimazolam and propofol. Our primary outcome was the incidence of post-induction hypotension, which was either an absolute mean arterial pressure (MAP) < 60 mmHg or a > 30% relative drop in MAP compared to baseline within 20 min of induction or from induction to the start of surgery. Secondary outcomes included minimum MAP and MAP at different time points during anesthesia, the application of vasoactive drugs, adverse events, and the patient's self-reported Quality of Recovery-40 scale for the day after surgery. RESULTS: The incidence of post-induction hypotension was lower and the minimum MAP during induction was higher in the remimazolam group than those in the propofol group. There were no significant differences between the two groups in the remaining outcomes. CONCLUSION: Remimazolam is safe and effective in hypertensive patients undergoing breast cancer surgery. Induction with remimazolam in hypertensive patients may result in more stable hemodynamics than propofol. TRIAL REGISTRATION: This study was registered at the Chinese Clinical Trials Registry ( http://www.chictr.org.cn ) on 03/12/2020, with registration number ChiCTR2000040579.

Gut microbiota of old mice worsens neurological outcome after brain ischemia via increased valeric acid and IL-17 in the blood.

BACKGROUND: Aging is a significant risk factor for ischemic stroke and worsens its outcome. However, the mechanisms for this worsened neurological outcome with aging are not clearly defined. RESULTS: Old C57BL/6J male mice (18 to 20 months old) had a poorer neurological outcome and more severe inflammation after transient focal brain ischemia than 8-week-old C57BL/6J male mice (young mice). Young mice with transplantation of old mouse gut microbiota had a worse neurological outcome, poorer survival curve, and more severe inflammation than young mice receiving young mouse gut microbiota transplantation. Old mice and young mice transplanted with old mouse gut microbiota had an increased level of blood valeric acid. Valeric acid worsened neurological outcome and heightened inflammatory response including blood interleukin-17 levels after brain ischemia. The increase of interleukin-17 caused by valeric acid was inhibited by a free fatty acid receptor 2 antagonist. Neutralizing interleukin-17 in the blood by its antibody improved neurological outcome and attenuated inflammatory response in mice with brain ischemia and receiving valeric acid. Old mice transplanted with young mouse feces had less body weight loss and better survival curve after brain ischemia than old mice transplanted with old mouse feces or old mice without fecal transplantation. CONCLUSIONS: These results suggest that the gut microbiota-valeric acid-interleukin-17 pathway contributes to the aging-related changes in the outcome after focal brain ischemia and response to stimulus. Valeric acid may activate free fatty acid receptor 2 to increase interleukin-17.

Perspective Review of Myeloid Immune Cell Responses and Poststroke Immunosuppression.

Ischemic stroke profoundly influences the peripheral immune system, which responds quickly to brain ischemia and participates in the evolution of poststroke neuroinflammation, while a period of systemic immunosuppression ensues. Poststroke immunosuppression brings harmful consequences, including increased infection rates and escalated death. As the most abundant cell population in the fast-responding innate immune system, myeloid cells including neutrophils and monocytes play an indispensable role in systemic immunosuppression after stroke. The change in myeloid response after stroke can be regulated by circulating DAMPs (damage-associated molecular patterns) and neuromodulatory mechanisms, which contain sympathetic nervous system, hypothalamic-pituitary-adrenal, and parasympathetic nervous system. In this review, we summarize the emerging roles and newly identified mechanisms underlying myeloid cell response in poststroke immunosuppression. Deeper understanding of the above points may pave the way for future development of novel therapeutic strategies to treat poststroke immunosuppression.

A MODIFIED SURGICAL SEPSIS MODEL SATISFYING SEPSIS-3 AND HAVING HIGH CONSISTENCY OF MORTALITY.

ABSTRACT: Background : Cecal ligation and perforation (CLP) is currently considered the criterion standard model of sepsis; however, there are some deficiencies, such as low clinical relevance, inconsistency in severity grading, and an unknown proportion of CLP animals meeting the requirements of sepsis-3. Methods : Adult rats were randomly divided into the following three groups: modified CLP (M-CLP) group, CLP group, and sham group. The vital organ function of rats was evaluated 24 hours postoperatively by blood pressure, behavioral testing, histopathology, and blood test. Cytokine levels were determined by enzyme-linked immunosorbent assay, and T-cell suppression was assessed by flow cytometry. The stability of the model was evaluated by comparing the survival rates of repeated experiments in all groups from day 1 to day 14. Results : More rats in the M-CLP group met Sepsis-3 criteria than those in the CLP group 24 hours postoperatively (53.1% vs. 21.9%, P = 0.01). Rats in the M-CLP group developed more serious hepatic, pulmonary, and renal dysfunction. Similar to human sepsis, rats in the M-CLP group demonstrated more serious immunosuppression and systemic inflammation compared with the CLP group. In addition, disease development and severity, which was indicated by the stable survival rates of model animals, were more stable in the M-CLP group. Conclusions : More rats could meet Sepsis-3 criteria with this novel surgical procedure, which may reduce the number of animals needed in preclinical sepsis experiments. This stable M-CLP model may contribute to the development of new therapies.

Trends in perivascular macrophages research from 1997 to 2021: A bibliometric analysis.

INTRODUCTION: Perivascular macrophages (PVMs) play pivotal roles in maintaining the physiological function of the brain. Dysfunction of PVMs is emerging as an important mechanism in various disease conditions in the brain. METHODS: In this work, we analyzed recent research advances in PVMs, especially in the brain, from the Web of Science (WoS) core database using bibliometric analysis based on the search terms "perivascular macrophages" and "perivascular macrophage" on October 27, 2021. Visualization and collaboration analysis were performed by Citespace (5.8 R3 mac). RESULTS: We found 2384 articles published between 1997 and 2021 in the field of PVMs, which were selected for analysis. PVMs were involved in several physio-pathological fields, in which Neurosciences and Neurology, Neuroscience, Immunology, Pathology, and Cardiovascular System and Cardiology were most reported. The research focuses on PVMs mainly in the central nervous system (CNS), inflammation, macrophage or T-cell, and disease, and highlights the related basic research regarding its activation, oxidative stress, angiotensin II, and insulin resistance. Tumor-associated macrophage, obesity, myeloid cell, and inflammation were relatively recent highlight keywords that attracted increasing attention in recent years. Harvard Univ, Vrije Univ Amsterdam, occupied important positions in the research field of PVMs. Meanwhile, PVM research in China (Peking Univ, Sun Yat Sen Univ, Shanghai Jiao Tong Univ, and Shandong Univ) is on the rise. Cluster co-citation analysis revealed that the mechanisms of CNS PVMs and related brain diseases are major specialties associated with PVMs, while PVMs in perivascular adipose tissue and vascular diseases or obesity are another big category of PVMs hotspots. CONCLUSION: In conclusion, the research on PVMs continues to deepen, and the hotspots are constantly changing. Future studies of PVMs could have multiple disciplines intersecting.

Emergency tracheal intubation peri-operative risk factors and prognostic impact after esophagectomy.

BACKGROUND: Emergent endotracheal intubation (ETI) is a serious complication after Oesophagectomy. It is still unclear that perioperative risk factors and prognosis of these patients with ETI. METHODS: Between January 2015 and December 2018, 21 patients who received ETI after esophagectomy were enrolled (ETI group) at the department of thoracic surgery, Fujian Union hospital, China. Each study subject matched one patient who underwent the same surgery in the current era were included (control group). Patient characteristics and perioperative factors were collected. RESULTS: Patients with ETI were older than those without ETI (p = 0.022). The patients with history of smoking in ETI group were significantly more than those in control group (p = 0.013). The stay-time of postanesthesia care unit (PACU) in ETI group was significantly longer than that in control group (p = 0.001). The incidence of anastomotic leak or electrolyte disorder in ETI group was also higher than that in control group (p = 0.014; p = 0.002). Logistic regression analysis indicated history of smoke (HR 6.43, 95%CI 1.39-29.76, p = 0.017) and longer stay time of PACU (HR 1.04, 95%CI 1.01-1.83, p = 0.020) both were independently associated with higher risks of ETI. The 3-year overall survival (OS) rates were 47.6% in patients with ETI and 85.7% in patients without ETI (HR 4.72, 95%CI 1.31-17.00, p = 0.018). COX regression analysis indicated ETI was an independent risk factor affecting the OS. CONCLUSION: The study indicated that history of smoking and longer stay-time in PACU both were independently associated with higher risks of ETI; and ETI was an independent risk factor affecting the OS of patients after esophagectomy. TRIAL REGISTRATION: This trial was retrospectively registered with the registration number of ChiCTR2000038549.

Preoperative environment enrichment preserved neuroligin 1 expression possibly via epigenetic regulation to reduce postoperative cognitive dysfunction in mice.

AIMS: Postoperative cognitive dysfunction (POCD) is a common and significant syndrome. Our previous studies have shown that surgery reduces dendritic arborization and spine density and that environment enrichment (EE) reduces POCD. Neuroligin 1 is a postsynaptic protein involved in the formation of postsynaptic protein complex. This study was designed to determine the role of neuroligin 1 in the protection of EE against POCD and the mechanisms for EE to affect neuroligin 1 expression. METHODS: Eight-week-old C57BL/6J male mice with or without EE for 3, 7, or 14 days had right carotid artery exposure under isoflurane anesthesia. An anti-neuroligin 1 antibody at 1.5 µg/mouse was injected intracerebroventricularly at one and two weeks before the surgery. Mice were subjected to the Barnes maze and fear conditioning tests from one week after the surgery. Cerebral cortex and hippocampus were harvested after surgery. RESULTS: Mice with surgery had poorer performance in the Barnes maze and fear conditioning tests than control mice. EE for 2 weeks, but not EE for 3 or 7 days, improved the performance of surgery mice in these tests. Surgery reduced neuroligin 1 in the hippocampus. Preoperative EE for 2 weeks attenuated this reduction. The anti-neuroligin 1 antibody worsened the performance of mice with surgery plus EE in the Barnes maze and fear conditioning tests. Surgery increased histone deacetylase activity and decreased the acetylated histone in the hippocampus. EE attenuated these surgery effects. CONCLUSION: Our results suggest that preoperative EE for 2 weeks reduces POCD. This effect may be mediated by preserving neuroligin 1 expression via attenuating surgery-induced epigenetic dysregulation in the brain.

Modified long-axis in-plane ultrasound-guided radial artery cannulation in adult patients: A randomized controlled trial.

INTRODUCTION: For adults with small radial arteries, ultrasound-guided radial artery cannulation remains challenging and the relevant data is currently lacking. The study aimed to test the hypothesis that modified long-axis in-plane ultrasound guidance (M-LAIP) would improve success rates of radial artery cannulation in this population. PATIENTS AND METHODS: This was a prospective, randomised, and controlled clinical study that enrolled 201 adult patients with diameters of the radial artery less than 2.2 mm. Patients were randomised to M-LAIP, short-axis out-of-plane (SAOP), or conventional palpation (C-P) group according to different approaches of radial artery cannulation (M-LAIP, SAOP, and C-P). Outcome measurements included the success rate, cannulation time, and cannulation-related adverse events. RESULTS: The cannulation success rate was significantly higher in the M-LAIP group than in the SAOP or C-P groups (first success rate: 80.3% vs. 53.8% or 33.8%; P < 0.001; total success rate: 93.9% vs. 78.5% or 50.8%; P < 0.001). Total cannulation time in the M-LAIP group was shorter than that in the SAOP group (P = 0.002) or the C-P group (P < 0.001). The rates of posterior wall puncture and haematoma in the M-LAIP group were lower than that in the SAOP group or C-P group (P < 0.008). CONCLUSION: The use of the M-LAIP approach significantly improved the success rate of radial artery cannulation, shortened procedure time, and lowered the rates of posterior wall puncture and haematoma in adults with radial artery diameters less than 2.2 mm, compared with that achieved by the SAOP or C-P approach.

Mdivi-1 improves postoperative neurocognitive disorders in aged rats undergoing splenectomy by inhibiting dynamin-related protein-1.

Background: The regulatory role of mitochondria in the inflammatory response of the nervous system postoperatively remains unclear. This study explored the relationship between mitochondria and postoperative neurocognitive dysfunction (PNCD) by regulating mitochondrial function in aged rats undergoing splenectomy. Methods: A total of 120 aged rats were randomly divided into five groups (n=24) as follows: Control group (not subjected to any form of treatment), Sham group (subjected only to sham-splenectomized operation after anesthesia), Splenectomy group (only underwent splenectomy after anesthesia), Synonyms Mitochondrial division inhibitor 1 (Mdivi-1) group [treated with Mdivi-1, a dynamin-relatedprotein 1 (Drp1) inhibitor], and Dimethyl Sulfoxide (DMSO) group (treated with DMSO, a solvent). Inflammatory markers, namely interleukin-1ß (IL-1ß) and tumor necrosis factor α (TNF-α), were measured in the plasma and brains of the rats. Cognitive function was assessed using the Morris water maze test. Results: During the perioperative period, the physiological parameters did not differ among the five groups (P>0.05). The results of the Morris water maze experiments showed that the memory of the rats was significantly impaired after splenectomy, which was alleviated by Mdivi-1 administration (P=0.04). Postoperatively, the proinflammatory cytokine levels in the serum and hippocampus tissue were upregulated, while Mdivi-1 administration reduced this increase. The electron microscopy and hematoxylin-eosin (HE) staining results indicated that the structure of neurons and mitochondria was minimally impaired in the Mdivi-1 group. Conclusions: Aged rats that underwent splenectomy exhibited significant postoperative cognitive impairments. The selective inhibitor of Drp1, Mdivi-1, exerted protective effects against PNCD by ameliorating mitochondrial dysfunction and reducing the inflammatory response.

Appropriate exercise level attenuates gut dysbiosis and valeric acid increase to improve neuroplasticity and cognitive function after surgery in mice.

Postoperative cognitive dysfunction (POCD) affects the outcome of millions of patients each year. Aging is a risk factor for POCD. Here, we showed that surgery induced learning and memory dysfunction in adult mice. Transplantation of feces from surgery mice but not from control mice led to learning and memory impairment in non-surgery mice. Low intensity exercise improved learning and memory in surgery mice. Exercise attenuated surgery-induced neuroinflammation and decrease of gut microbiota diversity. These exercise effects were present in non-exercise mice receiving feces from exercise mice. Exercise reduced valeric acid, a gut microbiota product, in the blood. Valeric acid worsened neuroinflammation, learning and memory in exercise mice with surgery. The downstream effects of exercise included attenuating growth factor decrease, maintaining astrocytes in the A2 phenotypical form possibly via decreasing C3 signaling and improving neuroplasticity. Similar to these results from adult mice, exercise attenuated learning and memory impairment in old mice with surgery. Old mice receiving feces from old exercise mice had better learning and memory than those receiving control old mouse feces. Surgery increased blood valeric acid. Valeric acid blocked exercise effects on learning and memory in old surgery mice. Exercise stabilized gut microbiota, reduced neuroinflammation, attenuated growth factor decrease and preserved neuroplasticity in old mice with surgery. These results provide direct evidence that gut microbiota alteration contributes to POCD development. Valeric acid is a mediator for this effect and a potential target for brain health. Low intensity exercise stabilizes gut microbiota in the presence of insult, such as surgery.

Surgery Trauma Severity but not Anesthesia Length Contributes to Postoperative Cognitive Dysfunction in Mice.

BACKGROUND: Perioperative, modifiable factors contributing to perioperative neurocognitive disorders (PND) have not been clearly defined. OBJECTIVE: To determine the contribution of anesthesia lengths and the degrees of surgical trauma to PND and neuroinflammation, a critical process for PND. METHODS: Three-month-old C57BL/6J mice were subjected to 2 h or 6 h isoflurane anesthesia plus a 5 min or 15 min left common carotid artery exposure (surgery) in a factorial design (two factors: anesthesia with two levels and surgery with three levels). Their learning and memory were tested by Barnes maze and novel object recognition paradigms. Blood, spleen, and hippocampus were harvested for measuring interleukin (IL)-6 and IL-1ß. Eighteen-month-old C57BL/6J mice (old mice) were subjected to 6 h isoflurane anesthesia or 2 h isoflurane anesthesia plus 15 min surgery and then had learning and memory tested. RESULTS: Three-month-old mice with 15 min surgery (long surgery) under 2 h or 6 h anesthesia performed poorly in the learning and memory tests compared with controls. Anesthesia alone or anesthesia plus 5 min surgery did not affect mouse performance in these tests. Similarly, only mice with long surgery but not mice with other experimental conditions had increased IL-6 and IL-1ß in the blood, spleen, and hippocampus and decreased spleen weights. Splenocytes were found in the hippocampus after surgery. Similarly, old mice with long surgery but not the mice with isoflurane anesthesia alone had poor performance in the Barnes maze and novel object recognition tests. CONCLUSION: Surgical trauma, but not anesthesia, contributes to the development of PND and neuroinflammation. Splenocytes may modulate these processes.

Emergency tracheal intubation during off-hours is not associated with increased mortality in hospitalized patients: a retrospective cohort study.

BACKGROUND: The prognosis of hospitalized patients after emergent endotracheal intubation (ETI) remains poor. Our aim was to evaluate the 30-d hospitalization mortality of subjects undergoing ETI during daytime or off-hours and to analyze the possible risk factors affecting mortality. METHODS: A single-center retrospective study was performed at a university teaching facility from January 2015 to December 2018. All adult inpatients who received ETI in the general ward were included. Information on patient demographics, vital signs, ICU (Intensive care unit) admission, intubation time (daytime or off-hours), the department in which ETI was performed (surgical ward or medical ward), intubation reasons, and 30-d hospitalization mortality after ETI were obtained from a database. RESULTS: Over a four-year period, 558 subjects were analyzed. There were more male than female in both groups (115 [70.1%] vs 275 [69.8%]; P = 0.939). A total of 394 (70.6%) patients received ETI during off-hours. The patients who received ETI during the daytime were older than those who received ETI during off-hours (64.95 ± 17.54 vs 61.55 ± 17.49; P = 0.037). The BMI of patients who received ETI during the daytime was also higher than that of patients who received ETI during off-hours (23.08 ± 3.38 vs 21.97 ± 3.25; P < 0.001). The 30-d mortality after ETI was 66.8% (373), which included 68.0% (268) during off-hours and 64.0% (105) during the daytime (P = 0.361). Multivariate Cox regression analysis found that the significant factors for the risk of death within 30 days included ICU admission (HR 0.312, 0.176-0.554) and the department in which ETI was performed (HR 0.401, 0.247-0.653). CONCLUSIONS: The 30-d hospitalization mortality after ETI was 66.8%, and off-hours presentation was not significantly associated with mortality. ICU admission and ETI performed in the surgical ward were significant factors for decreasing the risk of death within 30 days. TRIAL REGISTRATION: This trial was retrospectively registered with the registration number of ChiCTR2000038549 .

Modified long-axis in-plane ultrasound technique versus conventional palpation technique for radial arterial cannulation: A prospective randomized controlled trial.

BACKGROUND: A low first-pass success rate of radial artery cannulation was obtained when using the conventional palpation technique (C-PT) or conventional ultrasound-guided techniques, we; therefore, evaluate the effect of a modified long-axis in-plane ultrasound technique (M-LAINUT) in guiding radial artery cannulation in adults. METHODS: We conducted a prospective, randomized and controlled clinical trial of 288 patients undergoing radial artery cannulation. Patients were randomized 1:1 to M-LAINUT or C-PT group at Fujian Medical University Union Hospital between 2017 and 2018. Radial artery cannulation was performed by 3 anesthesiologists with different experience. The outcome was the first and total radial artery cannulation success rates, the number of attempts and the cannulation time, and incidence of complications. RESULTS: Two hundred eighty-five patients were statistically analyzed. The success rate of first attempt was 91.6% in the M-LAINUT group (n = 143) and 57.7% in the C-PT group (n = 142; P < .001) (odds ratio, 7.9; 95% confidence interval, 4.0-15.7). The total success rate (≤5 minutes and ≤3 attempts) in the M-LAINUT group was 97.9%, compared to 84.5% in the palpation group (P < .001) (odds ratio, 8.5; 95% confidence interval, 2.5-29.2). The total cannulation time was shorter and the number of attempts was fewer in the M-LAINUT group than that in the C-PT group (P < .05). The incidence of hematoma in the C-PT group was 19.7%, which was significantly higher than the 2.8% in the M-LAINUT group (P < .001). CONCLUSIONS: Modified long-axis in-plane ultrasound-guided radial artery cannulation can increase the first and total radial artery cannulation success rates, reduce the number of attempts, and shorten the total cannulation time in adults.

MicroRNA-574-5p promotes cell growth of vascular smooth muscle cells in the progression of coronary artery disease.

Coronary artery disease (CAD) is caused by atherosclerotic plaque development in the walls of coronary arteries. Aberrant proliferation of vascular smooth muscle cells (VSMCs) promotes atherosclerotic plaque formation, whereas VSMC apoptosis may promote CAD-related inflammation. microRNAs are potential diagnostic biomarkers in cardiovascular disease, especially CAD. Previous reports found that, among patients with CAD, microRNA-574-5p (miR-574-5p) expression was significantly increased and associated with disease severity. However, the specific mechanism by which miR-574-5p affects CAD is unknown. We used quantitative real-time PCR to detect the mRNA expression levels of miR-574-5p in the sera and VSMCs of patients with CAD. We also detected cell proliferation by MTT assay and apoptosis by the Cell Death Detection ELISA-Plus apoptosis assay. We found that miR-574-5p expression was elevated in the sera and VSMCs of patients with CAD. Additionally, miR-574-5p overexpression promoted cell proliferation and inhibited apoptosis in VSMCs. A dual-luciferase reporter assay showed that miR-574-5p directly targets ZDHHC14. In conclusion, our findings indicate that miR-574-5p promotes cell proliferation and inhibits apoptosis by inhibiting ZDHHC14 gene expression, suggesting that miR-574-5p is a CAD-related factor that may serve as a potential molecular target for CAD treatment.

Monitoring the end-tidal concentration of sevoflurane for preventing awareness during anesthesia (MEETS-PANDA): A prospective clinical trial.

OBJECTIVE: It was hypothesized that monitoring end-tidal sevoflurane (ETS) during endoscopic surgery could reduce the incidence of intraoperative awareness in patients undergoing general anesthesia. Herein, the incidence of intraoperative awareness and other correlative factors was recorded and compared. METHODS: Two thousand five hundred ASA I-III patients aged 18-80 years who underwent general anesthesia were randomly divided into 2 groups (n = 1250): routine care group (R) and ETS concentration group (E). ETS concentration was monitored in group E and maintained at a sevoflurane minimum alveolar concentration (MAC) of 0.7-1.3; group R was monitored using routine care, and the sevoflurane was maintained. Patients were assessed for intraoperative awareness with a questionnaire on their explicit memory 24-48 h after surgery. RESULTS: A total of 2532 patients were selected, and 86 patients were excluded. As for the groups, 1219 patients were assigned to group E, and 1227 patients were assigned to group R. As for intraoperative awareness, group E had 2 patients, and group R had 14. Compared with group R, the incidence of intraoperative awareness in group E was significantly lower (p = 0.003); the time-averaged ETS concentration and sevoflurane dosage were lower in group E (p < 0.05); and no significant changes were found in tracheal extubation time, intravenous general anesthetic dosage, or postoperative complication incidence in either group (p > 0.05). The incidence of intraoperative awareness was higher in women than men in group R (p < 0.05). CONCLUSION: Using ETS-guided anesthesia and maintaining the sevoflurane concentration (0.7-1.3 MAC) can decrease the incidence of patient awareness during endoscopic surgery.

Sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage rats via the PI3K/Akt-mPTP pathway.

BACKGROUND: Volatile anesthetic postconditioning has been documented to provide neuroprotection in adult animals. Our aim was to investigate whether sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage (HIBD) rats, and whether the PI3K/Akt pathway and mitochondrial permeability transition pore (mPTP) opening participate in the effect. METHODS: Seven-day-old Sprague-Dawley rats were subjected to brain HI and randomly allocated to 10 groups (n=24 each group) and treated as follows: (1) Sham, without hypoxia-ischemia; (2) HI/Control, received cerebral hypoxia-ischemia; (3) HI+Atractyloside (Atr), (4) HI+Cyclosporin A (CsA), (5) HI+sevoflurane (Sev), (6) HI+Sev+ LY294002 (LY), (7) HI+Sev+ L-NAME (L-N), (8) HI+Sev+ SB216763 (SB), (9) HI+Sev+Atr, and (10) HI+Sev+CsA. Twelve rats in each group underwent behavioral testing and their brains were harvested for hippocampus neuron count and morphology study. Brains of the other 12 animals were harvested 24h after intervention to examine the expression of Akt, p-Akt, eNOS, p-eNOS, GSK-3ß, p-GSK-3ß by Western bolting and mPTP opening. RESULTS: Sevoflurane postconditioning significantly improved the long-term cognitive performance of the rats, increased the number of surviving neurons in CA1 and CA3 hippocampal regions, and protected the histomorphology of the left hippocampus. These effects were abolished by inhibitors of PI3K/eNOS/GSK-3ß. Although blocking mPTP opening simulated sevoflurane postconditioning-induced neuroprotection, it failed to enhance it. CONCLUSIONS: Sevoflurane postconditioning exerts a neuroprotective effect against HIBD in neonatal rats via PI3K/Akt/eNOS and PI3K/Akt/GSK-3ß pathways, and blockage of mPTP opening may be involved in attenuation of histomorphological injury.

Involvement of AQP 1 in the cardio-protective effect of remifentanil post-conditioning in ischemia/reperfusion rats.

BACKGROUND: our research aim to study the role of AQP1 in the cardioprotective effect of remifentanil post-conditioning for myocardial ischemia/reperfusion injury. METHODS: Ninety Sprague-Dawley (SD) rats were divided into 6 groups: sham operation group (Sham group), myocardial ischemia and reperfusion group (I/R group), postconditioning of remifentanil group (R-post), postconditioning of remifentanil plus AQP1 inhibitor acetazolamide group (R-post +Ace), postconditioning of remifentanil plus opioid-receptor antagonist compounds (R-post +AC), postconditioning of remifentanil plus AQP1 enhancer arginine vasopressin (R-post +AV). All groups except the sham operation group were given 30 min ischemia in left anterior descending (LAD) coronary arteries. All groups were then given 120 min reperfusion to the LAD. Before reperfusion, the R-post, R-post +Ace, R-post +AC, R-post +AV groups were given 10 min remifentanil post-conditioning. Hemodynamic data were measured every 30 min after initiation of ischemia. The rats' hearts were exercised for detecting infarct size and water content in the left ventricle, and AQP1 expression were also detected. RESULTS: The R-post group showed a significant reduction of the infarct size compared to the I/R group. The effect of R-post for reducing infarct size was slightly enhanced by adding acetazolamide to R-post, so significant differences could still be found when compared R-post+Ace group to the I/R group. The effect of infarct size reduction brought by R-post was blocked by the opioid-receptor antagonist compounds. This effect was also blocked by the AQP1 enhancer. Similar outcomes were found considering the water content of the left ventricle and the AQP1 expression. CONCLUSION: Cardioprotective effect of remifentanil post-conditioning may initiate through inhibiting the function of AQP1.