Comparison of the Effects of Adductor Canal and Femoral Nerve Blocks on Postoperative Opioid Consumption and Inflammatory Factor Levels in Elderly Patients After Total Knee Arthroplasty: A Prospective Observational Study.

Purpose: Total Knee Arthroplasty (TKA) is a highly invasive procedure causing severe postoperative pain, which hampers early mobility. Effective pain management is crucial for optimal recovery. This study aimed to evaluate how adductor canal block (ACB) and femoral nerve block (FNB) affect opioid use and inflammation factor levels in elderly TKA patients. Methods: This prospective observational study included 120 patients who received TKA, and divided them into three groups, based on the different nerve block technique: ACB, FNB, and no intervention before general anesthesia (CON). Postoperative opioid consumption, pain assessment, inflammation factor, knee function recovery and other clinical indicators were recorded. Results: The CON group had significantly higher cumulative sufentanil consumption compared to the ACB and FNB groups at both 12 h and 48h postoperative (P<0.001). Compared with the CON group, the ACB and FNB groups persistently had lower pain scores until 12 h at rest and 24 h during motion after surgery. The ACB group showed significantly lower serum concentrations of C-reactive protein (CRP) and interleukin-6 (IL-6) compared to the CON group at 24 h postoperative (P=0.017, P=0.009), and IL-6 levels remained significantly lower at 72 h postoperative (P=0.005). Both ACB and FNB groups achieved earlier ambulation compared to the CON group (P=0.002). On the first day postoperative, both the ACB and FNB groups showed significantly better knee motion (P<0.001), quadriceps strength (P<0.001), and daily mobilization (P<0.001) compared to the CON group. Additionally, the ACB group exhibited superior quadriceps strength (P<0.001) and daily mobilization (P<0.001) compared to the FNB group. Conclusion: The ACB and FNB groups exhibited comparable clinical efficacy outcomes in terms of pain scores and opioid consumption. However, the ACB group experienced reduced postoperative inflammation and improved knee recovery, especially in quadriceps strength.

Development of implantable electrode based on bioresorbable Mg alloy for tissue welding application.

An implantable electrode based on bioresorbable Mg-Nd-Zn-Zr alloy was developed for next-generation radiofrequency (RF) tissue welding application, aiming to reduce thermal damage and enhance anastomotic strength. The Mg alloy electrode was designed with different structural features of cylindrical surface (CS) and continuous long ring (LR) in the welding area, and the electrothermal simulations were studied by finite element analysis (FEA). Meanwhile, the temperature variation during tissue welding was monitored and the anastomotic strength of welded tissue was assessed by measuring the avulsion force and burst pressure. FEA results showed that the mean temperature in the welding area and the proportion of necrotic tissue were significantly reduced when applying an alternating current of 110 V for 10 s to the LR electrode. In the experiment of tissue welding ex vivo, the maximum and mean temperatures of tissues welded by the LR electrode were also significantly reduced and the anastomotic strength of welded tissue could be obviously improved. Overall, an ideal welding temperature and anastomotic strength which meet the clinical requirement can be obtained after applying the LR electrode, suggesting that Mg-Nd-Zn-Zr alloy with optimal structure design shows great potential to develop implantable electrode for next-generation RF tissue welding application.

Silk-based hybrid microfibrous mats as guided bone regeneration membranes.

The usage of a guided bone regeneration (GBR) membrane that prevents the ingrowth of fibroblast cells and enhances the regeneration rate is an effective strategy for bone regeneration therapy. Herein, LAPONITE® (LAP) nanoplatelets, a bioactive clay with good osteoinductivity, were incorporated within a regenerated silk fibroin (RSF) microfibrous mat via electrospinning. The as-prepared RSF-LAP hybrid microfibrous mats had an interconnected structure with pore size significantly smaller than that of the fibroblast cells, leading to an effective prevention of fibroblast cell ingrowth into the defect sites. As per the water contact angle measurements, the incorporation of LAP significantly improved the hydrophilicity of the RSF microfibrous mats. The in vitro cell experiment results show that the RSF-LAP microfibrous mats exhibited better cell adhesion and proliferation of bone marrow mesenchymal stem cells (BMSCs) than the pristine RSF microfibrous mats. Moreover, the RSF-LAP microfibrous mats promoted osteogenic differentiation by upregulating alkaline phosphatase (ALP) activity and osteo-specific gene expression. Therefore, the results suggest that this easily fabricated LAP-incorporated RSF microfibrous mat has great potential to be a promising biomaterial for GBR applications.

miR­133b­5p contributes to hypoxic preconditioning­mediated cardioprotection by inhibiting the activation of caspase­8 and caspase-3 in cardiomyocytes.

In a previous study using a microRNA (miRNA/miR) microarray assay, we demonstrated that miR-133b-5p was upregulated in response to hypoxic preconditioning (HPC). The present study was designed to investigate the role of the miR­133b­5p in HPC­induced cardioprotection and the underlying mechanisms involving caspase­8 and caspase­3 apoptotic signaling. Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR­133b­5p in myocardium was measured. Neonatal rat cardiomyocytes were isolated and subjected to hypoxia/reoxygenation (H/R) injury, with or without HPC. miR­133b­5p antagomir was transfected into the cardiomyocytes to observe whether it could block HPC­induced cardioprotection. Cellular injury was evaluated by detecting cell viability, lactate dehydrogenase (LDH) activity and apoptotic rate. Reverse transcription­quantitative polymerase chain reaction was used to measure the level of miR­133b­5p. The activation of caspase­8 and caspase­3 were measured by western blot analysis to detect the cleaved fragments as well as a colorimetric assay. Following myocardial I/R injury, the expression of miR­133b­5p was decreased in myocardium, while this decrease was restored by IPC. HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. These protective effects were coupled with the upregulation of miR­133b­5p. However, the knockdown of miR­133b­5p in the cardiomyocytes blocked HPC­mediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. HPC upregulated miR­133b­5p level was markedly suppressed by the antagomir. In addition, the cleavage and activities of caspase­8 and caspase­3 were inhibited by HPC while reversed by knockdown of miR­133b­5p. Upregulation of miR­133b­5p contributes to HPC­mediated cardioprotection in cardiomyocytes, and the mechanism may be associated with inhibition of caspase­8 and caspase­3 apoptotic signaling.

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure.

AIMS: Ischemia reperfusion (I/R) injury is an inevitable event arising during the cardiovascular diseases development and the process of potent surgical treatments. microRNAs (miRNAs) are critical regulators of multiple cell processes including I/R injury. The present study aims to quantify miRNA alterations and regulated genes upon hypoxia-reoxygenation (H/R) injury in a rat heart failure model comparing with normal cardiomyocytes. MAIN METHODS: Chronic heart failure was established by injecting doxorubicin (2mg/kg/week) for 6weeks, then H/R was performed on primary cultured cardiomyocytes isolated from normal and failed heart. Cellular injury was evaluated by detecting LDH release levels, cell variability and apoptotic rate. Dysregulated miRNAs in control, hypoxia preconditioning (HPC) and morphine preconditioning (MPC) groups under two conditions were quantified by microarray analysis. Fas protein expression was analyzed using Western Blotting analysis. KEY FINDINGS: Chronic heart failure was confirmed with lower ejection fraction (EF), and significant cellular injury. HPC could reverse the injury induced by H/R in normal heart rather than failed heart, otherwise, MPC significantly attenuated cellular injury dose dependently in both conditions. There was 12 miRNAs significantly altered after doxorubicin injection, 7 downregulated and 5 upregulated. miR-133b-5p, miR-6216, miR-664-1-5p and let7e-5p were differentially expressed after HPC and MPC treatments. The direct interaction between miR-133b-5p and target gene Fas were established. The Fas protein expression was manipulated by MPC not HPC affording protective effect against H/R injury. SIGNIFICANCE: We investigated that miR-133b-5p might play a particularly important role in the cardioprotective effect of MPC by regulating the target gene Fas.

MicroRNA-133b-5p Is Involved in Cardioprotection of Morphine Preconditioning in Rat Cardiomyocytes by Targeting Fas.

BACKGROUND: MicroRNAs (miRNAs) have been implicated in ischemia-reperfusion injury and ischemic preconditioning. Opioid pre- and postconditioning have powerful protective effects on the heart, but it is still not known whether miRNAs are involved in opioid-induced cardioprotection. The present study was designed to investigate the role of miRNAs in morphine preconditioning (MPC)-induced cardioprotection. METHODS: MiRNA microarray analysis was performed to examine the differentially expressed miRNAs caused by MPC in adult rat cardiomyocytes. A dual-luciferase reporter assay was performed to confirm the direct regulation of miR-133b-5p on the target gene Fas. MiR-133b-5p mimic or inhibitor was separately transfected into myocardial H9c2 cells to examine the role of miR-133b-5p in morphine-induced cardioprotection. RESULTS: MPC protected adult rat cardiomyocytes against hypoxia/reoxygenation (H/R) injury by reducing cell injury and death. MiRNA microarray data showed that a total of 39 miRNAs were differentially expressed after MPC treatment. A Dual-luciferase reporter assay confirmed that miR-133b-5p directly targets the Fas gene. After H/R injury, the decrease in miR-133b-5p and a contemporaneous rise in Fas mRNA and protein levels in adult rat cardiomyocytes were prevented by MPC treatment. In H9c2 cardiomyocytes, overexpression of miR-133b-5p reduced H/R-induced cell injury and apoptosis by inhibiting Fas expression. Knockdown of miR-133b-5p blocked morphine-mediated cardioprotection by reducing miR-133b-5p levels while enhancing the expression of Fas mRNA and protein. CONCLUSIONS: MPC causes a change in miRNA expression in rat cardiomyocytes. Morphine may protect cardiomyocytes against H/R injury through upregulation of miR-133b-5p by targeting Fas.