[Psychological health of nurses in operating room participating in organ donation and intervention effect].

Objective: To understand the effect of organ donation surgery on the mental health of nurses in operating room, and to explore the intervention effects. Methods: From Jan.2015 to Dec. 2018, 60 operating room nurses in our hospital participating in organ donation surgery were selected for investigation of mental health, and were intervened by group psychological training, positive psychological intervention, improving shift arrangement system and financial support. The SCL-90 scale and DAP-R scale were used to evaluate before and after intervention. Results: The mean scores of somatization, interpersonal sensitivity, depression, anxiety, terror, paranoia and psychoticism in SCL-90 scale of 60 operating room nurses were (2.07±0.63) , (2.07±0.69) , (1.88±0.62) , (1.71±0.57) , (1.78±0.67) , (1.71±0.68) , (1.73±0.60) before intervention respectively, which were significantly higher than the Chinese norm (P<0.01) and those[ (1.64±0.60) , (1.46±0.57) , (1.53±0.62) , (1.48±0.60) , (1.28±0.50) , (1.45±0.56) , (1.43±0.52) ] after intervention were lower than before (P<0.01) . Before and after the intervention, the scores of DAP-R scale tended to be death fear dimension and acceptance dimension, the proportion of the death fear dimension was 16.7% (10/60) and 6.7% (4/60) , respectively, and the approaching acceptance dimension was 83.3% (50/60) and 93.3% (56/60) . The proportion of the nurses with scores of SCL-90 scale ≥160 after the intervention was significantly lower than that before the intervention (χ(2)=5.82, P<0.05) . Conclusion: The mental health of nurses in the operating room participating in organ donation surgery is lower; After intervention, the investigated nurses present improved mental health and positively emotional attitude towards death.

ROR2 modulates neuropathic pain via phosphorylation of NMDA receptor subunit GluN2B in rats.

BACKGROUND: Neuropathic pain, a type of chronic pain as a result of direct central or peripheral nerve damage, is associated with significant quality of life and functional impairment. Its underlying mechanisms remain unclear. We investigated whether ROR2, a member of the receptor tyrosine kinase-like orphan receptor (ROR) family, participates in modulation of neuropathic pain. METHODS: Thermal hyperalgesia and mechanical allodynia were measured using radiant heat and von Frey filament testing. Immunofluorescence staining was used to detect expression of ROR2 in neuronal nuclei. Fos expression was determined by immunocytochemistry. Phosphorylation status was detected by western blot and immunoprecipitation. Small interfering RNA was used to knock down ROR2 expression. RESULTS: ROR2 was upregulated and activated in spinal neurones after chronic constriction injury (CCI) in mice [1.3 (0.1) to 2.1 (0.1)-fold of sham, P<0.01] from Day 1-21. CCI induced significant demethylation of the CpG island in the ROR2 gene promoter [0.37 (0.06) vs 0.12 (0.03)% CpG methylation, P<0.001]. Knockdown of ROR2 in the spinal cord prevented and reversed CCI-induced pain behaviours and spinal neuronal sensitisation [Fos expression: 130 (12) vs 81 (8) cells, P<0.05; 120 (11) vs 70 (7) cells, P<0.05]. In contrast, activation of spinal ROR2 by intrathecal injection of Wnt5a induced pain behaviours and spinal neuronal sensitisation [Fos expression: 11 (1) vs 100 (12) cells, P<0.001] in wild-type mice. Furthermore, ROR2-mediated pain modulation required phosphorylation of N-methyl-D-aspartate receptor 2B subunit (GluN2B) at Ser 1303 and Tyr1472 by pathways involving protein kinase C (PKC) and Src family kinases. Intrathecal injection of GluN2B, PKC, or Src family kinase-specific inhibitors significantly attenuated Wnt5a-induced pain behaviours. CONCLUSIONS: ROR2 in the spinal cord regulates neuropathic pain via phosphorylation of GluN2B, suggesting a potential target for prevention and relief of neuropathic pain.

[Clinical efficacy of enhanced recovery after surgery in atrial caval shunting for type â ¡ Budd-Chiari syndrome].

Objective: To investigate the clinical efficacy of enhanced recovery after surgery(ERAS) in atrial caval shunting (ACS) for type Ⅱ Budd-Chiari syndrome(BCS). Methods: The clinical data of patients underwent ACS for type Ⅱ BCS in the Henan Province People's Hospital from January 2014 to June 2016 were prospectively analyzed.Randomized and single-blind, controlled study was performed among the patients, and all of them underwent ACS and were divided into control group (patients underwent traditional perioperative management) and ERAS group (patients underwent ERAS perioperative management) based on a random number table.Operational and postoperative data, levels of inflammatory cytokines, stress state evaluation and postoperative complications were observed.The comparison between the two groups was evaluated with an independent sample t test.The trend analyses for variables were done using repeated measures ANOVA.The count data were analyzed using the chi-square test or Fisher exact. Results: Eighty-two patients were screened for eligibility, and allocated into the control group (40 patients) and the ERAS group (42 patients). All patients underwent ACS successfully with no death.Comparison of intraoperative status: operation time, volume of intraoperative blood and number of patients receiving blood transfusion were (211.0±12.9) minutes vs. (207.7±10.7) minutes, (167.5±28.3) ml vs. (165.0±28.4) ml and 3 cases vs. 1 case between the control group and the ERAS group, respectively, showing no difference between the two groups (t=0.90, 0.29, χ2=0.32, all P>0.05). Comparison of postoperative status: time of gastric tube removal, time of catheter removal, time of chest tube, time to flatus, time of food intake, duration of postoperative infusion, duration of postoperative hospital stay and numeric rating scale were (3.7±0.5)days vs. (0.0±0.0)days, (2.3±0.7)days vs. (1.4±0.5)days, (3.7±0.7)days vs. (2.3±0.5)days, (75.2±3.8)hours vs. (46.6±4.2)hours, (75.7±4.7)hours vs. (21.4±2.1)hours, (10.0±1.0)days vs. (5.8±0.9)days, (11.4±1.0)days vs. (7.8±0.6)days, 2.9±0.4 vs. 1.9±0.6 between the control group and the ERAS group, respectively, with statistically differences (t=35.03, 4.36, 8.10, 22.89, 47.78, 14.75, 14.22, 6.13, all P<0.05). Stress state evaluation: the levels of IR were (2.7±0.1) vs.(2.7±0.1), (8.8±0.7) vs. (5.2±0.3), (11.0±0.5) vs. (7.3±0.5), (4.9±0.2) vs. (3.9±0.1), and the levels of C-reaction protein were (14.6±1.3)mg/L vs.(14.6±1.1) mg/L, (101.2±13.6) mg/L vs. (89.5±6.9) mg/L, (62.7±8.6) mg/L vs. (56.4±8.4) mg/L, (46.4±6.7) mg/L vs. (40.0±5.6) mg/L from pre-operation to postoperative day 1, 3 and 5 between the control group and the ERAS group, respectively, with statistically significant differences in changing trends(F=136.61, 4.97, both P<0.05). Comparisons of levels of inflammatory cytokines: the levels of IL-6 were (43.1±2.7) ng/L vs. (43.6±3.6) ng/L, (135.1±6.4) ng/L vs. (117.4±5.7) ng/L, (145.4±6.7) ng/L vs. (128.5±5.5) ng/L, (93.3±3.7) ng/L vs. (88.0±3.9) ng/L, and the levels of TNF-α were (10.4±0.3)mmol/L vs. (10.4±0.3) mmol/L, (14.4±0.4) mmol/L vs. (12.6±0.4) mmol/L, (15.6±0.4) mmol/L vs. (13.8±0.4) mmol/L, (12.3±0.7) mmol/L vs. (11.4±0.6) mmol/L from pre-operation to postoperative day 1, 3 and 5 between the control group and the ERAS group, respectively, with statistically significant differences in changing trends (F=15.15, 21.45, both P<0.05). Comparison of postoperative complications: incidence of complications was 30.0%(12/40) in the control group and 11.9%(5/42) in the ERAS group, and the numbers of patients with nausea and vomiting, respiratory complications and cardiovascular complications were 4, 3, 5 cases in the control group and 3, 1, 1 case in the ERAS group, respectively, showing statistically differences in the incidence of complications(χ2=4.08, P<0.05). All the 82 patients were followed up for 2 to 22 months (median time, 12 months), no patients received reoperation or re-admitted to the hospital duo to complications. Conclusion: ERAS management in the perioperative period of ACS for BCS is beneficial to postoperative recovery of patients, and can relieve postoperative stress state and inflammatory response, reduce the duration of hospital stay, and incidence of postoperative complications.

Spinal ephrinB/EphB signalling contributed to remifentanil-induced hyperalgesia via NMDA receptor.

BACKGROUND: One of the major unresolved issues in treating pain is the paradoxical hyperalgesia produced by opiates, and accumulating evidence implicate that EphBs receptors and ephrinBs ligands are involved in mediation of spinal nociceptive information and central sensitization, but the manner in which ephrinB/EphB signalling acts on spinal nociceptive information networks to produce hyperalgesia remains enigmatic. The objective of this research was to investigate the role of ephrinB/EphB signalling in remifentanil-induced hyperalgesia (RIH) and its downstream effector. METHODS: We characterized the remifentanil-induced pain behaviours by evaluating thermal hyperalgesia and mechanical allodynia in a rat hind paw incisional model. Protein expression of EphB1 receptor and ephrinB1 ligand in spinal dorsal horn cord was determined by Western blotting, and Fos was determined by immunohistochemistry assay, respectively. To figure out the manner in which ephrinB/EphB signalling acts with N-methyl-d-aspartic acid (NMDA) receptor, we used MK-801, an antagonist of NMDA receptor, trying to suppressed the hyperalgesia induced by ephrinB1-Fc, an agonist of ephrinB/EphB. RESULTS: Continuing infusion of remifentanil produced a thermal hyperalgesia and mechanical allodynia, which was accompanied with increased protein expression of spinal-level EphB1 receptor, ephrinB1 ligand and Fos; what appeared above was suppressed by pretreatment with EphB1-Fc, an antagonist of ephrinB/EphB or MK-801, and increased pain behaviours induced by intrathecal injection of ephrinB1-Fc, an agonist of ephrinB/EphB, were suppressed by MK-801. CONCLUSIONS: Our findings indicated that ephrinB/EphB signalling is involved in RIH. EphrinB/EphB signalling might be the upstream of NMDA receptor.