Objective To explore the expression of EphB4 and VEGF in esophageal cancer tissues and their relationship with microvessel density (MVD ) ,and analysis the curative effect of postoperative esophageal cancer radical under thoracoscope . Methods Theexpression of EphB4 and VEGF was detected by immunohistochemistry in tumor specimens from 76 cases of esopha-geal squamous cell carcinoma and paratumor normal specimens ,used CD34 as marker to count MVD .According to the situation of expression of EphB4 and VEGF ,we analysis their relationship with lymph node metastasis rate ,recurrence and 5-year survival rate . Results The positive expression rate of EphB4 and VEGF in cancerous tissue (57 .89% and 61 .84% ) ,were significantly higher than that in tissue adjacent to carcinoma(0 and 7 .89% )(P<0 .05) .The positive expression rate ofEphB4 and VEGF in high MVD values of patients (67 .44% and 76 .19% ) ,were significantly higher than thatin low MVD values of patients (45 .45% and 44 .11% )(P<0 .05) .The positive expression rate ofEphB4 and VEGF in the patientswith lymph node metastasis group and associ-ated with recurrence ,were significantly higher than that of group without lymph node metastasis and group without recurrence (P<0 .05) .The positive expression rate of EphB4 and VEGF in patients of greater than or equal to 5 years of survival rate(45 .00% and 45 .45% ) ,were significantly lower than in patientsof Less than 5 years of survival rate (80 .36% and 85 .19% )(P<0 .05) .Conclu-sion EphB4 and VEGF are highly expressed in esophageal cancer tissue ,which may be closely associated withmicrovessel density , and lymph node metastasis ,recurrence and 5 years survival rate ;the curative effect of positive expression rate of EphB 4 and VEGF is poor .

Objective To investigate the effect of esmolol pretreatment on Toll like receptor-4 (TLR4)/nuclear factor-kappa-B (NF-кB) pathway in rats with repeated cerebral ischemia/reperfusion (IR) injury. Methods Forty-eight adult male Sprague-Dawley rats were randomly allocated into sham-operated group, IR group and esmolol group (n=16). Rats in the IR group and esmolol group were injected intravenously with esmolol at a dose of 200 g/(kg?min) or normal saline for one h before surgery, and then, bilateral common carotid arteries were clipped to establish the repeated IR injury models. Bilateral common carotid arteries in rats of sham-operated group were only isolated but not clipped, and injected intravenously with normovolemic normal saline for one h. Learning and memory abilities of rats were measured by Morris water maze test before, and one, 3 and 7 d after surgery. Rats were euthanized and hippocampus tissues were excised. The wet to dry (W/D) ratio of the hippocampus was tested. The permeability of blood-brain barrier was determined by Evans blue (EB) method. The levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6 and IL-1β in the hippocampus were tested by enzyme linked immunosorbent assay (ELISA). The NF-кB p65 and TLR4 mRNA expressions in the hippocampus were determined by reverse transcription-polymerase chain reaction (RT-PCR). The NF-кB p65 and TLR4 protein expressions in hippocampus were detected by Western blotting. Results As compared with those in the sham-operated group, the escape latency was significantly prolonged and swimming distance was signficantly longer in rats of IR group one, 3 and 7 d after surgery (P<0.05), the W/D ratio of the hippocampus and the content of EB in brain tissues were significantly increased in the IR group (P<0.05), the levels of TNF-α, IL-6 and IL-1β in hippocampus were significantly increased in the IR group (P<0.05), and the NF-кB p65 or TLR4 mRNA and protein expressions in the hippocampus of IR group were statistically higher (P<0.05). As compared with IR group, the escape latency and swimming distance of rats in the esmolol group were significantly shortened one, 3 and 7 d after surgery (P<0.05), the W/D ratio of the hippocampus and content of EB in brain tissues of esmolol group were significantly decreased (P<0.05), the levels of TNF-α, IL-6 and IL-1β in the hippocampus of esmolol group were signficantly lower(P<0.05), and the NF-кB p65 or TLR4 mRNA and protein expressions in hippocampus of esmolol group were statistically lower in the esmolol group (P<0.05). Conclusion Esmolol preconditioning can alleviate cerebral injury and improve learning and memory abilities of rats with repeated cerebral IR injury, which may be involved in alleviating inflammation and suppressing TLR4/NF-кB pathway.