Objective:To determine the expression of the full-length (NK1R-FL) and truncated (NK1R-Tr) neurokinin-1 receptor (NK1R) and the neurokinin-2 receptor (NK2R) in breast cancer tissues and cell lines, as well as to study the effects of the NK1R and NK2R antagonists on the growth of breast cancer cells. Methods:Immunohistochemistry and Western blot assays were used to detect NK1R, NK1R-FL, and NK2R expression in clinical samples of primary breast cancer tissue, benign lesions, and normal breast tissue, as well as in different breast cancer cell lines. Cell proliferation and soft agar growth tests were performed on cells treated with the NK1R and NK2R antagonists to study the ectopic overexpression of NK1R-FL and NK1R-Tr in breast cancer cell lines. Results:Total NK1R expression was detected in the breast cancer tissues, benign lesions, and normal breast tissues. Compared with the normal breast epithe-lia and benign breast lesions, the expression levels of NK1R-FL and NK2R decreased in the carcinoma. These changes were also relat-ed to the carcinoma type, histological grade, lymph node metastasis, HER2 and Ki-67 expression, and estrogen and progesterone recep-tors in breast cancer. The expression levels of NK1R-FL and NK2R were high in the HBL-100 breast cell lines of para-neoplastic tis-sues, but NK1R-Tr expression was low. The MDA-MB-231, T-47D, and MCF-7 cells only expressed NK1R-Tr. NK1R-Tr or NK1R-FL overexpression caused the decreased inhibition rate or increased levels of the NK1R and NK2R antagonists in the breast cancer cells. Conclusion:NK1R-FL and NK2R are co-expressed in normal cells. NK1R-Tr is highly expressed in breast cancer cells and exerts nega-tive feedback to regulate NK1R-FL and NK2R expression in all cells, especially cancer cells.

Objective:To investigate the preventive and protective effects of Schisandrin B in the mice of Alzheimer's disease (AD),and to clarify its mechanism.Methods:Fifty Balb/c mice were randomly divided into blank group,model group,pasitive control group,low dose of Schisandrin B group(0.1 g·kg-1)and high dose of Schisandrin B group(0.5 g·kg-1);there were 10 mice in each group.Step-through test was conducted after last administration to detect the latencies and number of errors of the mice in various groups,and the brain tissue was taken.Congo red staining was to detect the morphology changes of cells and neuronal amyloidosis in brain tissue of the mice.The levels of ROS in brain tissue of the mice were tested by Flow Cytometry.The contents of MDA,the levels of LDH,and the activities of CAT,GSH-Px and SOD in brain tissue of the mice were tested by biochemical method.Western blotting method was used to detect the expression levels of signaling pathway proteins Nrf2 and Keap1 in brain tissue of the mice.Results:Compared with model group,the latencies of the mice in low and high dose of Schisandrin B groups were increased (P<0.01) and the number of errors in step-through tests was decreased (P<0.05 or P<0.01).The Congo red staining results showed that compared with model group,the neuronal amyloidosis in brain tissue of the mice in Schisandrin B groups was decreased significantly.Compared with model group,the levels of ROS,LDH and the contents of MDA in brain tissue of the mice in low and high doses of Schisandrin B groups were decreased (P<0.05 or P<0.01),and the activities of CAT,SOD and GSH-Px were increased (P<0.01).Compared with low dose of Schisandrin B group,the content of MDA and the activities of SOD and GSH-Px in brain tissue of the mice in high dose of Schisandrin B group were increased (P<0.001).Compared with model group,the expression level of Nrf2 protein in brain tissue of the mice in low dose of Schisandrin B group was increased (P<0.01),while the expression level of Nrf2 protein in brain tissue of the mice in high dose of Schisandrin B group was decreased (P<0.01);the expression levels of Keap1 protein in brain tissue of the mice in low and high doses of Schisandrin B groups was decreased (P<0.01).Conclusion:Schisandrin B could decrease the level of peroxidation in brain tissue of the mice and reduce the oxidative damage and improve the memory function of the AD mice.The mechanism is related to the activation of Nrf2 signaling pathway which improve the activity of antioxidant enzymes.

Objective:To investigate the effect of stroke center on the treatment time and short-term prognosis in patients with ultra-early acute cerebral infarction (ACI) within 6 h treated with intravenous thrombolysis.Methods:The clinical data of 113 patients with ultra-early ACI treated with intravenous thrombolysis from July 2017 to July 2019 in Chaoyang City Central Hospital, Liaoning Province were retrospectively analyzed. Among them, 40 patients who received intravenous thrombolysis before the establishment of the stroke center (from July 2017 to July 2018) were enrolled as control group, and 73 patients who received intravenous thrombolysis after the establishment of the stroke center (from August 2018 to July 2019) were as study group. The treatment time nodes were recorded, including the time of onset, time of ACI initial diagnosis, time of completing blood collection and index reporting, time of completing CT examination and diagnosis, time of informed consent and time of onset of intravenous thrombolysis. The short-term prognosis indexes were recorded, including the mortality rate, effective rate of intravenous thrombolysis, improvement rate of neurological deficit at discharge and length of stay.Results:The time of ACI initial diagnosis, time of informed consent and time of onset of intravenous thrombolysis in study group were significantly shorter than those in control group: (5.16 ± 1.97) min vs. (10.23 ± 7.80) min, (36.26 ± 21.89) min vs. (56.23 ± 40.97) min and (85.12 ± 35.46) min vs. (126.28 ± 50.14) min, and there were statistical differences ( P<0.01); there were no statistical difference in the time of onset, time of completing blood collection and index reporting and time of completing CT examination and diagnosis between 2 groups ( P>0.05). The mortality rate in study group was significantly lower than that in control group: 1.4% (1/73) vs. 12.5% (5/40), the effective rate of intravenous thrombolysis and improvement rate of neurological deficit at discharge were significantly higher than those in control group: 84.9% (62/73) vs. 67.5% (27/40) and 76.7% (56/73) vs. 55.0% (22/40), and there were statistical differences ( P<0.05); there was no statistical difference in length of stay between 2 groups ( P>0.05). Conclusions:The establishment of standard stroke center can shorten the treatment time and improve the prognosis of patients with ultra-early ACI.