The objective of this article is to evaluate the effect of dexmedetomidine on emergence agitation (EA) and recovery profiles in children after sevoflurane anesthesia and its pharmacological mechanisms. Standard bibliographic databases, including MEDLINE, EMBASE, PsycINFP, Springer and ISI Web of Knowledge, were artificially searched to identify all randomized controlled trials (RCTs) comparing the impact of dexmedetomidine with placebo, fentanyl and midazolam on EA and recovery profiles after sevoflurane anesthesia in post-anesthesia care unit (PACU). Two authors assessed the quality of each study independently in accordance with strict inclusion criteria and extracted data. RevMan 5.0 software was applied for performing statistic analysis. The outcomes analyzed included: 1) incidence of EA, 2) emergence time, 3) time to extubation, 4) incidence of post-operation nausea and vomiting, 5) number of patients requiring an analgesic, and 6) time to discharge from PACU. A total of 1364 patients (696 in the dexmedetomidine group and 668 in the placebo, fentanyl and midazolam group) from 20 prospective RCTs were included in the meta-analysis. Compared with placebo, dexmedetomidine decreased the incidence of EA (risk ratio [RR] 0.37; 95% CI 0.30 to 0.46), incidence of nausea and vomiting (RR 0.57; 95% CI 0.38 to 0.85) and number of patients requiring an analgesic (RR 0.43; 95% CI 0.31 to 0.59). However, dexmedetomidine had a significantly delayed effect on the emergence time (weighted mean differences [WMD] 1.16; 95% CI 0.72 to 1.60), time to extubation (WMD 0.61; 95% CI 0.27 to 0.95), and time to discharge from recovery room (WMD 2.67; 95% CI 0.95 to 4.39). Compared with fentanyl (RR 1.39; 95% CI 0.78 to 2.48) and midazolam (RR 1.12; 95% CI 0.54 to 2.35), dexmedetomidine has no significantly difference on the incidence of EA. However, the analgesia effect of dexmedetomidine on postoperation pain has no significantly statistical differences compared with fentanyl (RR 1.12; 95% CI 0.66 to 1.91), which implied that its analgesia effect might play an important role in decreasing the incident of EA. No evidence of publication bias was observed.

SummaryThis trial aimed to compare the maternal and neonatal effects of remifentanil given by patient-controlled analgesia (PCA) or continuous infusion for labour analgesia. Patient controlled analgesia was administered using increasing stepwise boluses from 0.1 to 0.4 lg.kg À1 (0.1 lg.kg À1 increment, 2 min lockout, n = 30 Several lines of evidence have shown that intravenous remifentanil is effective for pain relief in parturients who received labour analgesia because of its particular pharmacokinetic characteristics [1][2][3][4][5][6]. Remifentanil has a quick onset time, rapid degradation by plasma and tissue esterase to inactive metabolites (terminal elimination half-life of 9.5 min), a short t 1/2 Keo (time needed for the effect compartment concentration to reach 50% of plasma concentration of 1.3 min) and a constant context sensitive half-life of 3.2 min [7][8][9]. However, labour analgesia with intravenous remifentanil has been reported to be associated with adverse reactions including maternal oversedation and oxygen desaturation as well as fetal heart rate decelerations 236 Anaesthesia

Due to roles in immunoregulation and low immunogenicity, mesenchymal stem cells have been suggested to be potent regulators of the immune response and may represent promising treatments for autoimmune disease. Adipose-derived stem cells (ADSCs), stromal cells derived from adipose tissue, were investigated with allogeneic ADSCs in B6.MRL/lpr mice, a murine model of systemic lupus erythematosus (SLE). We intravenously injected allogeneic ADSCs into SLE mice after disease onset and report that ADSCs reduced anti-ds DNA antibodies in serum and proteinuria in SLE mice. Also, ADSCs decreased IL-17 and IL-6 expression in serum of SLE mice. ADSCs alleviated renal damage and inflammatory cell infiltration and edema of the renal interstitium. Furthermore, ADSCs significantly downregulated renal IL-17 and CD68 expression, suggesting that ADSCs suppressed renal inflammation. ADSCs also decreased IL-17 mRNA expression and increased Foxp3, ROR-γt and miR-23b mRNA expression in renal tissue in SLE mice. ADSCs reduced renal protein expression of TAB 2 and IKK-α in SLE mice. Thus, ADSCs may be a novel potential therapy for treating SLE.

Endometrial injury is a common female disease. This study was designed to illustrate the effects of oxycodone on mifepristone-induced human endometrial stromal cells (hEndoSCs) injury and delineate the underlying molecular mechanism. hEndoSCs were stimulated with mifepristone to generate the endometrial injury in vitro model. hEndoSCs viability, cytotoxicity, and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay, lactate dehydrogenase assay (LDH), and flow cytometry (FCM) analysis, respectively. Meanwhile, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot assay were conducted to evaluate gene and protein expressions. The secretions of inflammatory cytokines (TNF-α, IL-1β, and IL-6) were measured using enzyme-linked immunosorbent assay (ELISA). The data revealed that mifepristone exposure memorably inhibited hEndoSCs viability and promoted cell apoptosis and inflammatory cytokines secretion, and oxycodone had no cytotoxicity on hEndoSCs. Oxycodone increased hEndoSCs growth, blocked cell apoptosis, enhanced Bcl-2 expression, reduced Bax levels, and decreased the secretion of inflammatory cytokines in mifepristone-induced hEndoSCs, exhibiting the protective effects in endometrial injury. In addition, the TLR4/NF-κB pathway-related protein levels (TLR4 and p-p65) in mifepristone-treated hEndoSCs were enhanced, while these enhancements were inhibited by oxycodone treatment. In conclusion, oxycodone exhibited the protective role in mifepristone-triggered endometrial injury via inhibiting the TLR4/NF-κB signal pathway.

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Purpose: This study aimed to investigate the comprehensive differential expression profile of miRNAs by screening for miRNA expression in ischemic stroke and normal samples. Methods: Differentially expressed miRNA analysis was conducted by using limma R Bioconductor package. Target genes of differential expression miRNAs (DEMs) were identified from TargetScanHuman and miRTarBase databases. Functional enrichment analysis of the target genes was performed using clusterProfiler R Bioconductor package. The miRNA-based ischemic stroke diagnostic signature was constructed via logistic regression analysis. Results: Compared with the normal cohort, a total of 14 DEMs, including 5 upregulated miRNAs and 9 downregulated miRNAs, were identified in ischemic stroke patients. These DEMs have 1600 regulatory targets. Using a logistic regression model, the top 5 miRNAs were screened for constructing a miRNA-based ischemic stroke diagnostic signature. Using the miRNA–mRNA interaction pairs, two target genes (SP1 and AGO1) were speculated to be the primary genes of ischemic stroke. Discussion and Conclusion: Here, several potential miRNAs biomarkers were identified and a miRNA-based diagnostic signature for ischemic stroke was established, which can be a valuable reference for future clinical researches.

Background: The present study analyzed whole-lesion histogram parameters from intravoxel incoherent motion diffusion-weighted imaging (IVIM-DWI) to explore the clinical value of IVIM histogram features in the differentiation of liver lesions.Methods: In this retrospective study, 33 cases of hepatic hemangioma (HH), 22 cases of hepatic cysts (HC), and 34 cases of hepatocellular carcinoma (HCC) were underwent IVIM-DWI (b =0-600 s/mm 2 ), which were confirmed pathologically and clinically. The data were processed by IVIM model to obtain the following quantitative indicators: perfusion fraction (f), slow diffusion coefficient (D), and pseudo-diffusion coefficient (or fast diffusion coefficient, D*). The region of interest in the largest solid part of the lesion was delineated for histogram analysis of the correlation between tissue image and lesion type. The relevant histogram parameters were obtained and statistically analyzed. The characteristic histogram parameters for HH, HC, and HCC were compared to find significantly different parameters. The diagnostic efficacies of these parameters for HH, liver cysts, and HCC were assessed using the receiver operating characteristic (ROC) curves.Results: There were significant differences in the maximum diameter, maximum value, minimum value, mean, median, standard deviation, uniformity, skewness, kurtosis, volume, 10th percentile (P10) of D, and 90th percentile (P90) of D between the three groups (P<0.05). The maximum diameter, minimum value, entropy, and volume of D* differed significantly between the three groups (P<0.05). The maximum diameter, minimum value, mean, median, skewness, kurtosis, volume, P10, and P90 of f differed significantly between the three groups (P<0.05). The largest area under the ROC curve (AUC) for both D* and f was that of volume (AUC =0.883 for both). When 1438.802 was used as the volume cut-off, the sensitivity and specificity of volume in differentiating between HH and HC were 87.88 and 77.27, respectively, and the sensitivity and specificity of volume in differentiating between HC and HCC were 77.27 and 85.29. Conclusions:A multiparametric histogram from IVIM-DWI magnetic resonance imaging (MRI) is an effective means of identifying HH, HC, and HCC that provides valuable reference information for clinical diagnosis.

Previously, we have shown that the phosphoinositide-3-kinase (PI3K) mediated acute (24 h) post-conditioning neuroprotection induced by propofol. We also found that propofol post-conditioning produced long term neuroprotection and inhibited the internalization of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluR2 subunit up to 28 days post middle cerebral artery occlusion (MCAO). However, the relationship between PI3K with AMPA receptor GluR2 subunit trafficking in propofol post-conditioning has never been explored. Here we showed that propofol post-conditioning promoted the binding of PI3K to the C-terminal of AMPA receptor GluR2 subunit and formed a complex within 1 day after transient MCAO. Interestingly, the enhanced activity of PI3K was observed in the hippocampus of post-conditioning rats at day 1 post ischemia, whereas the decrease of AMPA receptor GluR2 subunit internalization was found up to 28 days in the same group. Administration of PI3K selective antagonist wortmannin inhibited the improvement of spatial learning memory and the increase of neurogenesis in the dentate gyrus up to 28 days post ischemia. It also reversed the inhibition of AMPA receptor GluR2 internalization induced by propofol post-conditioning. Together, our data indicated the critical role of PI3K in regulating the long term neuroprotection induced by propofol post-conditioning. Moreover, this role was established by first day activation of PI3K and formation of PI3K-AMPA receptor GluR2 complex, thus stabilized the structure of postsnaptic AMPA receptor and inhibited the internalization of GluR2 subunit during the early stage of propofol post-conditioning.