ABSTRACT
Despite piezoelectric materials have a long history of application, piezoelectric catalysis has continued to be a hot topic in recent years. Flexible piezoelectric materials have just emerged in recent years due to their versatility and designability. In this paper, we review the recent advances in flexible piezoelectric materials for catalysis, discuss the fundamentals of the catalytic properties of composite materials, and detail the typical structures of these materials. We pay special attention to the types of filler in flexible piezoelectric composites, their role and the interaction between the particles and the flexible substrate. Notable examples of flexible piezoelectric materials for organic pollutants degradation, enhanced piezo-photocatalysis and antibacterial applications are also presented. Finally, we present key issues and future prospects for the development of flexible piezoelectric catalysts.
ABSTRACT
STUDY OBJECTIVE: To summarize and evaluate the available data describing the recovery parameters of xenon anesthesia. DESIGN: Systematic review and meta-analysis. SETTING: Anesthesia for elective surgeries. PATIENTS: Systematic review of randomized controlled trials (RCTs) from databases including Medline (1964-2013), the Cochrane Central Register of Controlled Trials (CENTRAL, 1990-2012), and Google Scholar (1966-2013). INTERVENTIONS: Inhalation of xenon or other anesthetics was administered in elective surgery. MEASUREMENTS: Recovery parameters (time to recovery, alertness/sedation scale scores at "eye opening," bispectral index at "reaction on demand," time to extubation, and time to orientation). MAIN RESULTS: Eleven RCTs (N = 661 patients) met the inclusion criteria. Recovery from xenon anesthesia was significantly faster in terms of the time to eye opening (mean difference [MD], -4.18 minutes; 95% confidence interval [CI], -5.03 to -3.32 minutes; P < .00001), the time to reaction on demand (MD, -5.35 minutes; 95% CI, -6.59 to -4.11 minutes; P < .00001), the time to extubation (MD, -4.49 minutes; 95% CI, -5.40 to -3.58 minutes; P < .00001), and the time to orientation (MD, -4.99 minutes; 95% CI, -6.45 to -3.52 minutes; P < .00001). CONCLUSIONS: This meta-analysis confirmed that recovery from xenon anesthesia is faster than other inhalation anesthesia.
Subject(s)
Anesthesia Recovery Period , Anesthetics, Inhalation/pharmacology , Consciousness/drug effects , Xenon/pharmacology , Airway Extubation , Anesthesia, Inhalation/methods , Elective Surgical Procedures , Humans , Randomized Controlled Trials as Topic , Time FactorsABSTRACT
Hepatic ischemia-reperfusion (I/R) injury contributes to hepatic dysfunction and failure after liver transplantation, major hepatic resection, trauma, and hypovolemic shock. Therefore, reducing I/R injury is an important goal to improve the outcome of these procedures. Recently, high-mobility group box 1 protein (HMGB1) has been identified as a pathogenic mediator in several inflammatory diseases, including hepatic I/R. PNU-282987, a selective α7 nicotinic acetylcholine receptor agonist, prevents nuclear factor κB (NF-κB) activation and thereby inhibits cytokine secretion through a specific cholinergic anti-inflammatory pathway. Our study was designed to evaluate whether PNU-282987 would inhibit HMGB1 expression and prevent I/R-induced liver damage. C57BL/6 mice were randomly divided into 3 groups as follows: sham group, vehicle plus I/R group, and PNU-282987 plus I/R group. Mice were subjected to 70% partial hepatic I/R for 60 min and pretreated with either vehicle or with PNU-282987, and blood and hepatic tissue samples were collected at 3, 6, and 12 h following reperfusion. The results showed that pretreatment with PNU-282987 decreased serum transaminase levels and ameliorated liver injury after hepatic I/R. Moreover, pretreatment with PNU-282987 suppressed NF-κB activation, cytokine production (tumor necrosis factor α, interleukin 1ß), and HMGB1 expression in liver after hepatic I/R. These observations suggest that PNU-282987 protects the liver from I/R injury possibly by inhibiting HMGB1 expression, suppressing cytokine production, and preventing NF-κB activation in mice.
