To investigate the changes in arterial oxygenation and intrapulmonary shunt during one-lung ventilation (OLV) with intravenous infusion of dexmedetomidine combined with isoflurane inhalation. ASA I-II 60 patients aged 18-70 year, undergoing OLV during elective thoracic surgery were randomly allocated to two groups: (1) isoflurane + saline (group NISO, n = 30) and (2) isoflurane + dexmedetomidine (group DISO, n = 30). After induction, anesthesia was maintained with intravenous infusion of remifentanil 0.1-0.2 μg kg(-1) min(-1) and inhalation isoflurane (1.0-2.0%). In addition, anesthesia was maintained with intravenous infusion of dexmedetomidine 0.7 μg kg(-1) h(-1) in DISO group and saline 0.25 ml kg(-1) h(-1) in NISO group. Bispectral Index values were maintained within 40-60 by changing the concentration of isoflurane in all groups. Arterial blood gas samples and central venous blood gas samples were taken as follows: during two-lung ventilation before OLV and during the first 40 min of OLV. 45 Patients completed the study, with 23 patients in DISO group and 22 patients in NISO group. The two groups were comparable in terms of demographic variables, hemodynamic, PaO2, Qs/QT, end expiration isoflurane and BIS levels during the operation. Compared with patients in the group NISO, there were significant increases with PaO2, significant decrease with Qs/QT, significant decrease with end expiration isoflurane, and significant decrease with HR in the group DISO during the first 40 min of OLV (P < 0.05). Dexmedetomidine infusions decrease the requirement for isoflurane, decrease intrapulmonary shunt, and moderate the change in PaO2 and may be useful in managing OLV.
Aberrant activation of Wnt signaling is implicated in gliomagenesis. Propofol, the most commonly used intravenous anesthetic agent in clinics, exhibits potent antitumor activity in a variety of cancer cells through different mechanisms. However, the role of propofol on Wnt signaling and glioma cell growth remains to be fully elucidated. In the present study, propofol was identified as a potent inhibitor of Wnt signaling. In 293T cells transfected with Wnt1 or Wnt3 expression plasmids or treated with Wnt3A-conditioned medium, propofol significantly inhibited the transcriptional activity of the SuperTopFlash reporter and the expression of Wnt target genes. The inhibitory effect of propofol on Wnt signaling was also observed in glioma cells. Further experiments demonstrated that propofol suppressed glioma cell growth by decreasing cell proliferation and enhancing cell apoptosis. Finally, the potential antitumor efficiency of propofol was confirmed using xenograft experiments . Taken together, the results indicated a novel mechanism for the anticancer activity of propofol and provide supporting evidence for its use as a prospective anticancer drug to treat glioma in patients with deregulated Wnt signaling.
Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3 0 UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (Po0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (Po0.01). Moreover, miR-455 decreased the expression of HDAC2 (Po0.01). miR-455 remarkably decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after transfection while inducing cell apoptosis (Po0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.
Background: Adductor canal block has become a popular mode of pain management after total knee arthroplasty. This study compared a single-injection adductor canal block (SACB) with continuous adductor canal block (CACB). The hypothesis was that the 2 groups would have equivalent analgesia at 48 hours post-neural blockade. Methods: This is a double-blinded, randomized, controlled, equivalency trial that is conducted at a single university hospital in China. A total of 60 patients who meet inclusion criteria are randomized in a ratio of 1:1 to either CACB (0.5% ropivacaine 20 mL followed by continuous infusion of 0.2% ropivacaine at 5 mL/h for 48 hours) or SACB (0.5% ropivacaine 20 mL) group. The primary outcome is pain scores at 48 hours utilizing the visual analog scale, whereas the secondary outcomes include opioid consumption, Timed Up & Go test, ambulation distances at discharge, length of stay, and maximal flexion at discharge. All pain scores are assessed by an independent observer who is blinded to the allocation of groups. Results: This study has limited inclusion and exclusion criteria and a well-controlled intervention. This clinical trial is expected to provide evidence of better therapy for the pain management after total knee arthroplasty. Trial registration: This study protocol was registered in Research Registry (researchregistry5431).
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