Objective:To explore whether perioperative intravenous flurbiprofen axetil can reduce the incidence and intensity of chronic pain for breast cancer atfer surgical treatment. Methods:This randomized, double-blind, controlled trial enrolled 60 patients undergoing mastectomy and axillary lymph node dissection under general anesthesia. All patients accepted Hospital Anxiety and Depression Scale (HAD) tests the day before the surgery to evaluate depression and anxiety. hTe patients were randomly assigned to receive either 50 mg lfurbiprofen axetil intravenously 15 minutes before the surgical incision and 6 hours later (group F) or intravenous 5 mL intralipid as a control (group C). All patients received patient-controlled intravenous analgesia (PCIA) with fentanyl postoperatively. Peripheral venous blood samples were drawn before the surgery, at 4 and 24 h atfer the surgery to detect the plasma level of PGE2 and tumor necrosis factor-α(TNF-α). Postoperative fentanyl consumption, Numerical Rating Scale (NRS) scores and adverse effects were recorded at 2, 6, 12, 24 and 48 h after the surgery. hTe duration and intensity of pain were followed up by telephone at the 2nd-12th month atfer the surgery. Results:The incidence of pain at 2, 4, 6, and 12 months after the breast surgery was 33%, 20%, 15%, and 10%, respectively, and the average pain score was 0.77, 0.57, 0.28, and 0.18, respectively. Compared with group C, the scores of pain in group F were significantly lower at 2, 4, 6 and 12 months postoperatively (F=7.758, P=0.007). The incidence of pain in group F was significantly lower at 2, 4 and 6 months postoperatively (P<0.05). There was no significant difference in the incidence of pain between the groups at 12 months postoperatively (P>0.05). Preoperatively and at 4 and 24 h atfer the surgery, there was no signiifcant difference in the level of TNF-αbetween the two groups (F=0.530, P=0.470);but plasma concentration of PGE2 in group F was significantly lower than that in group C (F=5.646, P=0.021). No patients developed abnormal bleeding, peptic ulcer, impaired liver or renal function and respiratory depression. Conclusion:Perioperative intravenous infusion of 100 mg flurbiprofen axetil can decrease the intensity and incidence of chronic pain for breast cancer atfer surgical treatment.

Objective To investigate the level of resilience in male patients of open ocular trauma, and to analyze its related factors. Methods A cross-section study was conducted in 116 male open ocular trauma patients in Zhongshan Ophthalmic Center from November 2016 to March 2017. The patients were investigated with general situation questionnaire, Connor- Davidson Resilience Scale, Medical Coping Modes Questionnaire, and Perceived Social Support Scale. Results The Connor- Davidson Resilience Scale score of male suffers was (65.69 ± 14.31) points with the low level. The patients at their own expense, poor, with higher suffering had lower resilience score(P <0.05). Social support, avoidance was positively related with resilience(r =0.308-0.558, P <0.01), acceptance was negatively related with resilience(r=-0.385, P<0.05). Multiple liner regression analysis showed that social support, acceptance, payment were influencing factors of resilience(P<0.05). Conclusions The level of resilience is lower in male patients with open ocular trauma, and which is impacted by economic factors, social support and coping method.

OBJECTIVETo study the effect of emodin on the proliferation, cell cycle distribution, apoptosis and expression of hematopoietic growth factors in bone marrow mesenchymal stem cells (BMSCs).

METHODSThe proliferation of rat BMSCs exposed to emodin was analyzed using MTT assay, and flow cytometry was used to detect the apoptosis and cell cycle changes of the exposed cells. Real-time quantitative PCR was used to determine the mRNA expression of the hematopoietic growth factors.

RESULTSExposure to 0.1 and 1 µg/ml emodin for 48 and 72 h significantly enhanced the proliferation of BMSCs (P<0.01). The cells exposed to 0.1 µg/ml emodin showed significantly increased percentage of cells in G2/M phase (P<0.05), and 1 µg/ml emodin exposure caused increased cells in S phase (P<0.01) and decreased cells in G1/G0 phase (P<0.05). Emodin exposure for 48 h resulted in significantly decreased cell apoptosis (P<0.05). BMSCs treated with 0.1 µg/ml emodin showed a significant increase in the expression of thrombopoietin mRNA (P<0.05).

CONCLUSIONEmodin can promote the proliferation of BMSCs in vitro possibly by regulating the cell cycle distribution, cell apoptosis and thrombopoietin expression.

Animals ; Apoptosis ; Cell Cycle ; Cell Proliferation ; drug effects ; Emodin ; pharmacology ; Hematopoietic Cell Growth Factors ; metabolism ; Mesenchymal Stromal Cells ; cytology ; drug effects ; RNA, Messenger ; Rats

Animals ; Embryonic Stem Cells ; virology ; Gene Expression Regulation, Enzymologic ; Histone Deacetylase 6 ; Histone Deacetylases ; biosynthesis ; genetics ; Infection ; genetics ; pathology ; virology ; Mice ; Mice, Knockout