Objective To investigate the effect of sevoflurane preconditioning on lung injury induced by limb ischemia-reperfusion in rats and the relationship with endoplasmic reticulum stress.Methods Forty-five healthy male Sprague-Dawley rats,aged 6-8 weeks,weighing 250-300 g,were randomly allocated into 3 groups (n =15 each) using a random number table:sham operation group (group S),limb ischemia-reperfusion group (group LIR),and sevoflurane preconditioning group (group SP).Limb ischemia-reperfusion was induced by clamping bilateral femoral arteries for 3 h followed by 3 h reperfusion in LIR and SP groups.In group SP,2.5％ sevoflurane was inhaled for 30 min,and 15 min later the model was established.Before ischemia and at 3 h of reperfusion (at the corresponding time point in group S),arterial blood samples were collected for blood gas analysis,and arterial oxygen partial pressure (PaO2) and arterial carbon dioxide partial pressure (PaCO2) were recorded.The rats were sacrificed at 3 h of reperfusion,and lung specimens were obtained for determination of wet to dry lung weight ratio (W/D ratio) and total lung water content (TLW) and for microscopic examination of the pathological changes,and index of quantitative evaluation for alveolar damage (IQA) was calculated.The expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) protein and mRNA in lung tissues was detected by Western blot and real-time polymerase chain reaction,respectively.Results Compared to group S,the PaO2was significantly decreased at 3 h of reperfusion,the W/D ratio,TLW and IQA were significantly increased,the expression of GRP78 and CHOP protein and mRNA was significantly up-regulated (P＜0.05),and no significant change was found in PaCO2 in group LIR (P＞0.05).Compared to group LIR,the PaO2 was significantly increased at 3 h of reperfusion,the W/D ratio,TLW and IQA were significantly decreased,the expression of GRP78 and CHOP protein and mRNA was significantly down-regulated (P＜ 0.05),and no significant change was found in PaCO2 in group SP (P＞0.05).Conclusion Sevoflurane preconditioning can ameliorate lung injury induced by limb ischemia-reperfusion in the rats,and the mechanism is related to inhibition of endoplasmic reticulum stress.

Objective To analyze the regulation of estrogen receptor α (ERα) on truncated neurokinin-1 receptor (NK1R-Tr), and the influence of this regulation on cell proliferation in estrogen receptor-positive breast cancer cell lines. Methods The chromatin immune coprecipitation (CHIP) was used to observe the transcriptional regulation function of ERαon NK1R-Tr in breast cancer cells. Luciferase reporter gene assay was used to verify whether ERα played a positive regulatory role in the expression of NK1R-Tr. Western blot assay and real-time-PCR were used to detect the expression of ERα and NK1R-Tr in breast cancer cells, MCF-7 and T47D, as well as the expression of NK1R-Tr protein and mRNA level. NK1R-Tr levels were also detected after using estradiol (E2, ERα agonist) and small interfering RNA (knock out ERα). CCK-8 and clone formation experimen were used to detect the proliferation ability of breast cancer cells after knocking out NK1R-Tr with small interfering RNAs. Results CHIP test and Luciferase reporter gene assay proved that ERα can positively regulate the expression of NK1R-Tr via the ERα sequences in the upstream of the NK1R-Tr gene promoter. The expression of NK1R-Tr at both protein level and mRNA level dropped in the estrogen receptor-positive breast cancer cell line MCF-7 upon knocking out ERα. After knocking out NK1R-Tr, the proliferation ability of estrogen receptor-positive breast cancer cells was lower than that of the control group. Conclusion The ERα positively regulates the expression of NK1R-Tr, resulting in the increased cell proliferation in estrogen positive breast cancer cells.

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 correlation between depression, anxiety and sleep disturbance. Methods 93 patients with the main complaint of insomnia were selected and performed a retrospective study. Results Four factors including anxiety factors, manifest anxiety, subjective depression and dominant depression of the insomnia patients were significantly higher than normal people, while the Ego Strength scores are significantly lower than the normal people. Conclusion When confronting patients with sleep disturbance, doctors must pay attention to identifying any psychological disorders including depression and anxiety in the patients, and psychological support should also be strengthened to such patients.