One hundred and ninety one patients with esophageal carcinoma underwent surgical resection from January 2004 to January 2009. The gastroesophageal anastomosis was performed with auto suture instrument at superior aperture of the thorax in 107 cases (group A) and the instrument anastomosis was performed above or below the aorta arch in 84 cases ( group B ). The electron gastroscopy was performed and biopsy of mucosa at 3cm above the anastomosis was taken during the postoperative follow-up in all patients. Results showed that the incidence rate of reflux esophagitis in group A ( 5% ) was much lower than that in group B (51% ).

Objective To investigate the effects of propofol and sevoflurane on adriamycin chemotherapy-induced myocardial damage in rats.Methods Twenty-four healthy male Wistar rats, aged 3 months, weighing 212-270 g, were randomly divided into 4 groups (n =6 each) using a random number table: control group (group C) , adriamycin group (group ADM) , adriamycin-propofol group (group ADM-Pro) , and adriamycin-sevoflurane group (group ADM-Sevo).The equal volume of normal saline was injected intraperitoneally in group C.In group ADM, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times (11 days in total).In group ADM-Pro, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, propofol anesthesia was performed as follows : the total amount of propofol injected intraperitoneally was 200 mg/kg, the initial dose was 100 mg/kg, and 1 h later the remaining amount was added, and the duration of anesthesia was about 2 h.In group ADM-Sevo, adriamycin 2.5 mg/kg was injected intraperitoneally once every other day for 6 times, and at 3 days after the last administration of adriamycin, sevoflurane anesthesia was performed as follows: 1.5％-3.0％ sevoflurane was inhaled for 2 h.After the end of anesthesia, blood samples were collected for determination of serum cardiac troponin (cTnI) concentrations.Myocardial specimens were collected for detection of caspase-3 expression by immuno-histochemistry.Results Compared with group C, the serum cTnI concentration was significantly increased, and the caspase-3 expression was up-regulated in ADM, ADM-Pro and ADM-Sevo groups (P＜ 0.05).Compared with group ADM, the serum cTnI concentration was significantly decreased, and the caspase-3 expression was down-regulated in ADM-Pro and ADM-Sevo groups (P＜0.05).There was no significant difference in the parameters mentioned above between group ADM-Pro and group ADM-Sevo (P＞0.05).Conclusion Propofol and sevoflurane both can mitigate adriamycin chemotherapy-induced myocardial damage in rats, without significant difference in the efficacy.

ObjectiveTo investigate the role of δ-opioid receptor in remifentanil-induced N-methyl-D-aspartate (NMDA) receptor miniature excitatory postsynaptic currents (mEPSCs) in rat spinal dorsal horn neurons.MethodsMale 14-18 d old Wistar rats weighing 50-60 g were used in this study.The animals were anesthetized with intraperitoneal choral hydrate 400 mg/kg and sacrificed.Their lumbar segments of spinal cord (L1-S1 ) were immediately removed and sliced.Twenty-four slices were randomly divided into 4 groups ( n =6 each): control group (group C) ; glycine group (group G) ; remifentanil group (group R) and remifentanil + naltrindole(a δ receptor antagon) (group RN).Slices were cultured in artificial cerebrospinal fluid (ACSF) (group C) or incubated in ACSF containing glycine 0.24 μmol/L (group G) or remifentanil 4 nmol/L (group R) or remifentanil 4 nmol/L+ naltrindole 1 nmol/L (group RN) for 60 min.Whole cell patch clamp technique was used to measure NMDA receptor mEPSCs.ResultsThe amplitude and frequency of mEPSCs were significantly higher in group R than in groups C and RN ( P ＜ 0.01).There were no significant differences in amplitude and frequency of mEPSCs among gorups C,G and RN ( P ＞ 0.05).ConclusionActivation of δ-receptor can enhance NMDA receptor function in spinal dorsal horn neurons in rats which may be the mechanism of remifentanil-induced hyperalgesia.

Ghrelin and motilin (MTL) are mainly secreted by digestive tract,and they both can promote gastrointestinal motility. Disorder of gastrointestinal motility (DGIM)is a gastrointestinal motility or sensory disease mainly caused by neuroregulatory disorder,its main symptoms are nausea,vomiting,abdominal pain and abdominal distension. More and more studies have indicated that ghrelin,MTL and their receptor agonists are closely related to DGIM. This article reviewed the advances in studies on relationship between ghrelin/ GHS-R agonist,MTL/ MTL-R agonist and DGIM.

Aged ; Coronary Artery Disease ; diagnosis ; Coronary Vessel Anomalies ; diagnosis ; Coronary Vessels ; pathology ; Humans ; Male

[Abstract] Objective: To study the effect and possible mechanism of TGF-β2 on the invasion of glioma stem cells (GSCs). Methods: Tumor tissues of 8 patients with glioblastoma multiforme, who underwent resection at Department of Neurosurgery of the FirstAffiliated Hospital of China Medical University duringApril 2016 toApril 2017, were collected. The primary culture of glioma cells were conducted with trypsin digestion. Partial primary glioma cells were seeded into serum-free DMEM/F12 culture medium containing EGF, bFGF and B27 to obtain suspension of tumor spheres. Immunoflurenscent staining and differentiation assay were used to detect whether the tumor spheres were GSCs. TGF-β2 secretion ability of GSCs was determined by ELISAassay.After transfection of TGF-β2 siRNA, the invasion ability of glioma stem cells was determined by Transwell assay. Western blotting was used to examine the effect of TGF-β2 on expression of matrix metalloproteinases (MMP) in glioma stem cells. Results: The suspended tumor spheres were proved to be GSCs by immunofluorescent staining and differentiation assay; the tumor spheres expressed the marker of GSCs（CD133）and had the ability to multi-differentiate (glia and neuronal cells). Compared with the primary glioma cells, Glioma stem cells exerted significantly improved TGF-β2 secretion ability ([74.13±3.63] vs [46.13±2.61] pg/ml, P<0.05); and TGF-β2 silencing significantly reduced the invasion ability of glioma stem cells ([105.71±8.69] vs [63.67±5.93], P<0.05) and inhibited MMP-2 and MMP-9 expressions. Conclusion: TGF-β2 can promote the invasiveness of glioma stem cells through MMP-2 and MMP-9 pathway.