Effectiveness and safety of ultrasound-guided thoracic paravertebral block versus local anesthesia for percutaneous kyphoplasty in patients with osteoporotic compression fracture.

BACKGROUND: Kyphoplasty for osteoporotic vertebral compression fractures (OVCF) is a short but painful intervention. Different anesthetic techniques have been proposed to control pain during kyphoplasty; however, all have limitations. OBJECTIVE: To compare the effectiveness and safety of ultrasound-guided thoracic paravertebral block with local anesthesia for percutaneous kyphoplasty (PKP). METHODS: In this prospective study, non-randomized patients with OVCF undergoing PKP received either ultrasound-guided thoracic paravertebral block (group P) or local anesthesia (group L). Perioperative pain, satisfaction with anesthesia, and complications were compared between the groups. RESULTS: Mean intraoperative (T1-T4) perioperative visual analog scale (VAS) scores were significantly lower in group P than in group L (2 [1-3] vs. 3 [2-4], 2 [2-3] vs. 4 [2-4], 2 [2-3] vs. 5 [3-5], and 3 [2-3] vs. 5 [3-5], respectively; P< 0.05). Investigators' satisfaction scores, patients' anesthesia satisfaction scores, and anesthesia re-administration intention rate were significantly higher in group P than in group L (4 [3-5] vs. 3 [2-4], 2 [2-3] vs. 2 [1-3], 90.63% vs. 69.70%; P< 0.05). There was no significant intergroup difference in complications. CONCLUSIONS: Ultrasound-guided thoracic paravertebral block has similar safety to and better effectiveness than local anesthesia in PKP.

Prevalence and risk factors for postoperative delirium in total joint arthroplasty patients: A prospective study.

BACKGROUND: The aim of this prospective study was to investigate the incidence and clinical features of delirium after total joint arthroplasty, and to establish the potential risk factors for postoperative delirium. METHODS: A total of 212 consecutive patients undergoing hip or knee arthroplasty, who met the inclusion and exclusive criteria were enrolled. The general characteristics, preoperative and postoperative hematological variables were documented respectively. According to the presence of delirium, all patients were divided into the delirium group and non-delirium group. Univariate and multivariate logistic regression were performed to identify the possible predictors for postoperative delirium. RESULTS: At a minimum of 6months of follow-up, 35 patients were observed with postoperative delirium at an estimated total incidence of 16.5%. The incidence of delirium was statistically higher in hip arthroplasty (22.8%) than that in knee arthroplasty (7.1%). The multivariate regression analysis identified older age (OR=1.590, P=0.023), a history of stroke (OR=190.23, P=0.036), preoperative PaO2 (OR=1.277, P=0.018) and equivalent fentanyl dose (OR=1.010, P=0.012) as the predictive factors for postoperative delirium after total joint arthroplasty. CONCLUSIONS: The incidence of postoperative delirium after total joint arthroplasty is higher than expected. Based on our findings, we suggest that the surgeons should focus on those patients who have these risk factors and ensure the appropriate management to avoid postoperative delirium.

Activation of mitochondria apoptotic pathway is involved in the sevoflurane-induced hippocampal neuronal HT22 cells toxicity through miR-145/Binp3 axis.

Sevoflurane is a commonly used inhalation anesthesia, which has been previously demonstrated to impair long-term emotional memory consolidation and induce learning dysfunction through inducing hippocampal dysfunction. However, the underlying molecular mechanisms remain largely unknown. MicroRNAs (miRNAs) play critical roles in multiple cells apoptosis, including hippocampal neural. The present study, therefore, was aimed to investigate the miR-145 function on the hippocampal neural apoptosis induced by sevoflurane exposure. A hippocampal neural cell line HT22 was used, and treated with 4.1% sevoflurane. Cell viability and apoptosis were determined by MTT assay and flow cytometry, respectively. microRNA microarray was used to select differentially expression miRNAs in cells with sevoflurane exposure and controls. Results showed that sevoflurane could significantly induce the hippocampal neural cell apoptosis via mitochondria apoptotic pathway. Then, miR-145 was selected as a significantly down expression microRNA in sevoflurane treated HT22 cell lines, by microarray analysis and real-time PCR verification. Furthermore, we found that miR-145 overexpression could protect HT22 cells against apoptosis caused by sevoflurane. Bioinformatics analysis and dual-luciferase reporter assays indicated that Bnip3, which has a key role in the mitochondrial dysfunction, is a novel target of miR-145. Finally, we found that over expression of Bnip3 by pcDNA-Bnip3 transfection significantly induced apoptosis in HT22 cells, which was inhibited by miR-145 mimic. Therefore, it concluded that miR-145 could protect against sevoflurane-induced hippocampal apoptosis through the mitochondrial pathway at least by directly inhibiting its target gene-Bnip3 expression in hippocampal neural cell lines.

Sevoflurane induces endoplasmic reticulum stress mediated apoptosis inmouse hippocampal neuronal HT22 cells via modulating miR-15b-5p/Rab1A signaling pathway.

Sevoflurane (Sev) is a widely used anaesthetic agent in clinical patients. Growing evidences indicated that Sev resulted in cognitive impairment via inducing endoplasmic reticulum (ER) stress mediated neurons apoptosis in vivo. However, the underlying molecular mechanisms have not yet fully understood. In this study, we found that Sev exposure suppresses cell viability, and induces apoptosis by activating caspase-3 apoptotic signaling pathway. Our results further verified that Sevtriggers ER stress via upregulating its markers glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), caspase-12 and cleaved-PARP proteins. Recently, microRNAs (miRNAs) have been proven to regulate ER stress in a variety of cells, especially neuronal cells. Therefore, we performed the microarray analysis to identified miRNA levels in HT22 cells after treatment with Sev. Our results showed that Sev induces miRNAs aberrant expression and miR-15b-5p was one of the miRNAs being most upregulated in HT22 cells. Furthermore, the Sev-induced apoptosis and ER stress were rescued by knockdown of miR-15b-5p. Additionally, we demonstrated that miR-15b-5p suppresses Rab1A, a regulator in inducing ER stress, by directly targeting its 3'-UTR in HT22 cells. These results suggested that Sev exposure induces ER stress mediated apoptosis in HT22 cells via regulating miR-15b-5p/Rab1A signaling pathway. These data may provide an important therapeutic strategy for fighting against Sev through ER stress mediated neuronal apoptosis in clinical patients.

Facile solid-phase synthesis of the diammoniate of diborane and its thermal decomposition behavior.

The recent mechanistic finding of the hydrogen release pathways from ammonia borane (AB) has sparked new interest in the chemistry and properties of the diammoniate of diborane (DADB), an ionic isomer of AB. We herein report a facile one-step solid-phase synthesis route of DADB using inexpensive starting materials. Our study found that mechanically milling a 1 : 1 NaBH(4)/NH(4)F powder mixture causes the formation of crystalline DADB via a NH(4)BH(4) intermediate. The produced DADB can be readily separated from the sodium fluoride (NaF) by-product by a purification procedure using liquid ammonia at -78 °C. The thermal decomposition behavior of DADB was studied using synchronous thermal analyses, particularly in comparison with AB. It was found that the decomposition steps and products of DADB are similar to those of AB. But meanwhile, DADB exhibits a series of advantages over AB that merit its potential hydrogen storage application, such as lower dehydrogenation temperature, free of foaming and lack of an induction period in the thermal decomposition process. Our study further found that the volatile non-hydrogen products from DADB can be effectively suppressed by milling with MgH(2).