Morphine promotes glioblastoma cell proliferation through activating ERK1/2 signaling pathway / 基础医学与临床

Objective To observe the effect of morphine on the proliferation of glioblastoma T98G and U118MG cells and to explore the possible mechanism. Methods Glioblastoma T98G and U118MG cells were cultured in plates for 24 h and randomly divided into five groups: control (con), morphine 0.1 μmol/L(M1),1.0 μmol/L (M2),10.0 μmol/L (M3) and 100.0 μmol/L (M4). MTS and BrdU methods were used to detect the prolifera-tion of glioblastoma T98G and U118MG cells-treated with morphine for 24 h and 48 h. Western blot analysis was applied for determing the level of p-ERK1/2 and cyclin D1 protein expression.Results Compared with the control group,morphine in M3 and M4 groups significantly promoted the proliferation of T98G and U118MG cells (P<0.05) in a concentration-and time-dependent manner. In addition,the level of ERK1/2 phosphorylation and cyclin D1 protein expression significantly increased in both M3 and M4 groups as compared with those of control group (P<0.05). Conclusions Morphine may promote the proliferation of glioblastoma T98G and U118MG cells through activating the ERK1/2 signaling pathway.

Changes in Rat Brain MicroRNA Expression Profiles Following Sevoflurane and Propofol Anesthesia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Sevoflurane and propofol are widely used anesthetics for surgery. Studies on the mechanisms of general anesthesia have focused on changes in protein expression properties and membrane lipid. MicroRNAs (miRNAs) regulate neural function by altering protein expression. We hypothesize that sevoflurane and propofol affect miRNA expression profiles in the brain, expect to understand the mechanism of anesthetic agents.</p><p><b>METHODS</b>Rats were randomly assigned to a 2% sevoflurane group, 600 μg·kg - 1·min - 1 propofol group, and a control group without anesthesia (n = 4, respectively). Treatment group was under anesthesia for 6 h, and all rats breathed spontaneously with continuous monitoring of respiration and blood gases. Changes in rat cortex miRNA expression profiles were analyzed by miRNA microarrays and validated by quantitative real-time polymerase chain reaction (qRT-PCR). Differential expression of miRNA using qRT-PCR among the control, sevoflurane, and propofol groups were compared using one-way analysis of variance (ANOVA).</p><p><b>RESULTS</b>Of 677 preloaded rat miRNAs, the microarray detected the expression of 277 miRNAs in rat cortex (40.9%), of which 9 were regulated by propofol and (or) sevoflurane. Expression levels of three miRNAs (rno-miR-339-3p, rno-miR-448, rno-miR-466b-1FNx01) were significantly increased following sevoflurane and six (rno-miR-339-3p, rno-miR-347, rno-miR-378FNx01, rno-miR-412FNx01, rno-miR-702-3p, and rno-miR-7a-2FNx01) following propofol. Three miRNAs (rno-miR-466b-1FNx01, rno-miR-3584-5p and rno-miR-702-3p) were differentially expressed by the two anesthetic treatment groups.</p><p><b>CONCLUSIONS</b>Sevoflurane and propofol anesthesia induced distinct changes in brain miRNA expression patterns, suggesting differential regulation of protein expression. Determining the targets of these differentially expressed miRNAs may help reveal both the common and agent-specific actions of anesthetics on neurological and physiological function.</p>

Propofol ameliorates calpain-induced collapsin response mediator protein-2 proteolysis in traumatic brain injury in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Collapsin response mediator protein-2 (CRMP2), a multifunctional cytosolic protein highly expressed in the brain, is degraded by calpain following traumatic brain injury (TBI), possibly inhibiting posttraumatic neurite regeneration. Lipid peroxidation (LP) is involved in triggering postinjury CRMP2 proteolysis. We examined the hypothesis that propofol could attenuate LP, calpain-induced CRMP2 degradation, and brain injury after TBI.</p><p><b>METHODS</b>A unilateral moderate controlled cortical impact injury was induced in adult male Sprague-Dawley rats. The animals were randomly divided into seven groups: Sham control group, TBI group, TBI + propofol groups (including propofol 1 h, 2 h, and 4 h groups), TBI + U83836E group and TBI + fat emulsion group. The LP inhibitor U83836E was used as a control to identify that antioxidation partially accounts for the potential neuroprotective effects of propofol. The solvent of propofol, fat emulsion, was used as the vehicle control. Ipsilateral cortex tissues were harvested at 24 h post-TBI. Immunofluorescent staining, Western blot analysis, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling were used to evaluate LP, calpain activity, CRMP2 proteolysis and programmed cell death. The data were statistically analyzed using one-way analysis of variance and a paired t-test.</p><p><b>RESULTS</b>Propofol and U83836E significantly ameliorated the CRMP2 proteolysis. In addition, both propofol and U83836E significantly decreased the ratio of 145-kDa αII-spectrin breakdown products to intact 270-kDa spectrin, the 4-hydroxynonenal expression and programmed cell death in the pericontusional cortex at 24 h after TBI. There was no difference between the TBI group and the fat emulsion group.</p><p><b>CONCLUSIONS</b>These results demonstrate that propofol postconditioning alleviates calpain-mediated CRMP2 proteolysis and provides neuroprotective effects following moderate TBI potentially by counteracting LP and reducing calpain activation.</p>

Effect of epidural analgesia with 0.075% ropivacaine versus 0.1% ropivacaine on the maternal temperature during labor: a randomized controlled study / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>A wealth of evidence has indicated that labor epidural analgesia is associated with an increased risk of hyperthermia and overt clinical fever. Recently, evidence is emerging that the epidural analgesia-induced fever is associated with the types of the epidural analgesia and the variations in the epidural analgesia will affect the incidence of fever. The aim of the present study was to investigate the effects of epidural analgesia with 0.075% or 0.1% ropivacaine on the maternal temperature during labor.</p><p><b>METHODS</b>Two hundred healthy term nulliparas were randomly assigned to receive epidural analgesia with either 0.1% ropivacaine or 0.075% ropivacaine. Epidural analgesia was initiated with 10 ml increment of the randomized solution and 0.5 µg/ml sufentanyl after a negative test dose of 5 ml of 1.5% lidocaine, and maintained with 7 ml bolus doses of the above mentioned mixed analgesics every 30 minutes by the patient-controlled epidural analgesia. The measurements included the maternal oral temperature, visual analog scale pain scores, labor events and neonatal outcomes.</p><p><b>RESULTS</b>Epidural analgesia with 0.075% ropivacaine could significantly lower the mean maternal temperature at 4 hours after the initiation of analgesia and the oxytocin administration during labor compared with the one with 0.1% ropivacaine. Moreover, 0.075% ropivacaine treatment could provide satisfactory pain relief during labor and had no significant adverse effects on the labor events and neonatal outcomes.</p><p><b>CONCLUSION</b>Epidural analgesia with 0.075% ropivacaine may be a good choice for the epidural analgesia during labor.</p>

Effect of electroacupuncture on Sevoflurane anesthesia in patients undergoing resection of supratentorial tumor / 中国针灸

<p><b>OBJECTIVE</b>To observe the supplementary analgesic effect of electroacupuncture and its influence on the maintenance of anesthesia and the speed of recovery of patients undergoing craniotomy.</p><p><b>METHODS</b>Eighty cases of supratentorial tumor resection were randomly divided into group A and group S, 40 cases in each group. All the patients were anesthetized with 2% Sevoflurane. The patients in group A received electroacupuncture at Hegu (LI 4) and Waiguan (TE 5), Jinmen (BL 63) and Taichong (LR 3), Zusanli (ST 36) and Qiuxu (GB 40) from anesthesia beginning to the end of operation, and in group S without electroacupuncture. The end-tidal Sevoflurane concentration, minimum alveolar concentration (MAC), bispectral index (BIS) and the information during anesthesia recovery stage were recorded, respectively.</p><p><b>RESULTS</b>The end-tidal concentration and MAC of Sevoflurane in group A at all times were significant lower than those in group S (P<0.05, P<0.01) with a Sevoflurane saving of 9.62% on average. The BIS in group A during a few phases were higher than that in group S (all P<0.05). During anesthesia recovery stage, the time of each phase in group A was significantly shorter than that in group S (all P<0.01). No dysphoria and one case with nausea and vomiting were shown in group A, but in group S, 2 patients had dysphoria and 3 patients had nausea and vomiting.</p><p><b>CONCLUSION</b>Electroacupuncture combined with Sevoflurane anesthesia can decrease the dosage of Sevoflurane, shorten the recovery time of anesthesia and improve the quality of anesthesia recovery of the patients undergoing resection of supratentorial tumor.</p>

Effect of Low Dose Dexamethasone on Blood Glucose Concentration in Patients Undergoing Craniotomy / 中国康复理论与实践

@#ObjectiveTo evaluate the effect of low dose of dexamethasone on the blood glucose concentration in patients undergoing craniotomy. Methods20 consecutive patients undergoing craniotomy without a preexisting metabolic disorder were prospectively randomized into 1 of 2 groups: Dexamethasone (group D, n=10) and Normal Saline (group S, n=10), who were given dexamethasone 10 mg intravenous bolus or a saline placebo preoperatively. Arterial glucose concentrations were measured immediately before and after treatment and hourly for 5 hours intraoperatively. ResultsThe arterial glucose concentration in group D increased significantly(F=3.133,P<0.05), while those in group S keep stable. Compared with group S, arterial glucose concentration in group D increased significantly 180 min after dosing(P<0.01). ConclusionIf dexamethasone is used during craniotomy, perioperative blood glucose level should be carefully monitored and controled.

Transient Neurologic Syndrome after Spinal Anaesthesia / 中国康复理论与实践

@#A number of reports have appeared implicating neurotoxicity of local anesthetics as a possible cause of neurologic complications after spinal anesthesia. Transient neurologic syndrome is one of neurologic complications. This article reviews the etiology, occurred mechanism, clinical symptoms, risk factors, prevention and treatment of transient neurologic syndrome.

The effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery.</p><p><b>METHODS</b>Thirty consecutive patients under-going intracranial aneurysmal surgery were prospectively randomized into two groups: Isoflurane (group A, n = 15) and nimodipine (group B, n = 15). The patients in group A were maintained with 1 minimum alveolar concentration (MAC) isoflurane anesthesia during the whole procedure. The patients in group B were given nimodipine infusion continuously (20 microg.kg(-1).h(-1)) after induction of anesthesia and anesthetized with 1 MAC isoflurane. S100B levels in cerebrospinal fluid were determined before aneurysm clipping and 0, 2, 4 h after aneurysm clipping by enzyme linked immunosorbent assay. Assessment of mean blood flow velocity of parent arterial and arterial branches were performed before and after aneurysm clipping.</p><p><b>RESULTS</b>(1) S100B in cerebrospinal fluid was increased significantly at 4 h after aneurysm was clipped in group A (F = 4.11, P < 0.05). However, S100B in cerebrospinal fluid was stable in group B in the whole procedure. (2) Mean arterial flow velocity of parent vessels in group B was lower significantly than that in group A (t = 2.08, P < 0.05). However, mean arterial flow velocity of distal vessels in both groups has no significant difference.</p><p><b>CONCLUSION</b>Intraoperative nimodipine infusion may prevent cerebral vasospasm during intracranial aneurysm surgery.</p>