Objective To evaluate the clinical value of SCTPA and pulmonary V/Q scan in the diagnosis of pulmonary thromboembolism(PTE).Methods Ninety-two patients suspected of having PTE received SCTPA,pulmonary V/Q scan,and other related examinations.Results Thirty-five patients were diagnosed as having PTE in 92 patients investigated,30 cases were revealed by SCTPA,and 20 cases revealed by pulmonary V/Q scan.The area under ROC curve of SCTPA by V/Q scan and combination examination was 0.922,0.824,and 0.933,respectively(P

ObjectiveTo compare the effect of hospital initiative management or patients self management in asthma control and pulmonary function, and improve the control level of asthma. Methods Forty moderate asthma patients enrolled successfully from July to December in 2009 were divided into 2 groups by random digits table:hospital initiative management group (group A) and patient self management group (group B) with 20 cases each, and received the asthma treatment with hospital initiative management or patient self management for 1 year. The acute attack time, emergency visit time, hospitalization time,pulmonary function and Saint George respiratory questionnaire (SGRQ) were compared between two groups.ResultsAfter 1 year management, there were 19 patients in good compliance, satisfaction score was (9.300 ± 0.801 ) scores, 13 total control, 6 partial control and 1 uncontrol in group A, while there were 11 patients in good compliance, satisfaction score was (7.800 ± 1.542) scores, 6 total control, 8 partial control and 6 uncontrol in group B. The compliance, satisfaction and control in group A were much better than those in group B (P＜0.01 or ＜0.05). The forced expiratory volume in 1 second (FEV1)[(2.56 ±0.30) L]and peak expiratory flow (PEF)[(6.26±0.39) t/s]were elevated while SGRQ[(21.55 ±6.35) scores]in group A were better than those in group B[(2.38 + 0.31 ) L, (5.83 ± 0.52 ) L/s,(29.80 ± 12.04) scores](P ＜ 0.05 or ＜ 0.01 ). ConclusionThe compliance, asthma control, pulmonary function and respiratory quality are improved by hospital initiative management, so it is helpful to promote this management model in China via a close cooperation between general hospital and community hospital.

Objectives To evaluate the effect of N-Acetylcysteine on the airway inflammation and remodeling of obese asthma mice with high-fat diets. Methods Forty female C57BL/6J mice were randomly divided into 4 groups, asthma group (A), obese asthma group (B), treatment group (C) and normal control group (D). Group A were sensitized and challenged by ovalbum (OVA) and normal diets. Group B were sensitized and challenged as group A but fed with high-fat diets, while group C were sensitized, challenged and fed as group B, but administrated N-Acetylcysteine 200 mg/kg. d from the third week after challenge. The cells in BALF were counted and classified after staining, IL-6 and 8-iso-PGF2α(8-iso-PGF2α) in lung tissues were detected by ELISA. WAt, WAm, Pbm, as the remodeling indices, measured in lung pathological section. All parameters were compared among 4 groups. Results In comparison with group D, the leukocytes and EOS in BALF, WAt/Pbm, WAm/Pbm in lung section were increased as well as IL-6 and 8-iso-PGF2α in lung tissue elevated in group A and group B, while the maximum changes were observed in group B (P ＜0. 05). After NAC treatment, the IL-6, 8-iso-PGF2α and WAt/ Pbm were decreased significantly (P ＜0. 05). Pearson correlation analysis showed that WAt/Pbm and IL-6 were in positive correlation with 8-iso-PGF2α (r =0. 817, 0. 737, P ＜0. 01). Conclusions N-Acetylcysteine can alleviate the airway inflammation and remodel reaction of asthma by a substantial inhibition of the oxidative stress reaction in lung.

Objective To explore the prevalence and management status of asthma in downtown of Qingdao City.Method A stratified-cluster-disproportional random sampling survey was conducted with uniform procedure and questionnaire.Results The overall incidence of asthma in Qingdao City was 3.12％ (188/6026).The 2 most frequently risk factors of asthma were the allergic history and the asthma heredity (OR =3.562,2.381,P ＜ 0.05 ).In 188 diagnosed asthma patients,only 65 (34.5％)asthma patients accepted the guideline therapy,and 51 (27.1％)of them achieved well-controlled or total control.The 2 common reasons for the poor compliance were fear of adverse drug reaciion and feeling of ineffectiveness of inhaled corticosteroids.Conclusion The population in urban area of Qingdao City is suffered with high prevalence of asthma,poor compliance of guideline treatment and terrible management status.

Objective:To investigate the effect of pterostilbene on the growth, apoptosis and autophagy of a human papillomavirus type 16 (HPV-16) -immortalized cervical epithelial cell line H8.Methods:H8 cells were treated with pterostilbene at different concentrations of 0 (control group) , 25, 50, 75, 100 μmol/L for 24 and 48 hours. Cell counting kit-8 (CCK8) assay was performed to evaluate the cellular proliferative activity, flow cytometry was conducted to detect apoptosis and cell cycle, monodansylcadaverine (MDC) staining and fluorescence microscopy were performed to detect autophagy, and Western blot analysis was conducted to determine the expression of the cell cycle-related protein cyclinD1, apoptosis-related proteins caspase-3 and caspase-9, autophagy-related proteins Beclin1, microtubule-associated protein 1 light chain 3 (LC3) -Ⅱ/Ⅰ, ATG5 and P62, as well as HPV oncoproteins E6 and E7. Statistical analysis was carried out by using one-way analysis of variance, repeated measures analysis of variance and least significant difference- t test. Results:After 48-hour treatment with pterostilbene at different concentrations of 0, 25, 50, 75, 100 μmol/L, the relative cellular proliferation rate significantly differed among the groups (100.00% ± 1.56%, 99.02% ± 4.97%, 93.59% ± 2.01%, 81.28% ± 4.90%, 69.17% ± 7.56%, respectively; F = 77.22, P < 0.05) , and gradually decreased along with the increase in the concentration of pterostilbene; compared with the control group, the pterostilbene groups all showed significantly decreased cellular proliferation rate (all P < 0.05) . After 24-hour treatment with pterostilbene, the proportions of H8 cells at G1, G2 and S phases significantly differed among the above groups ( F = 7 845.00, 51.14, 266.50, respectively, all P < 0.05) ; compared with the control group, the pterostilbene groups showed significantly increased proportions of H8 cells at G1 and G2 phases (all P < 0.05) , but significantly decreased proportions of H8 cells at S phase ( P < 0.05) . After 48-hour treatment with pterostilbene, the apoptosis rate was significantly higher in the 25-, 50-, 75- and 100-μmol/L pterostilbene groups (14.66% ± 0.22%, 13.50% ± 0.49%, 14.56% ± 0.19%, 15.30% ± 0.76%, respectively) than in the control group (11.58% ± 0.50%, all P < 0.05) . After 24-hour treatment with pterostilbene, MDC staining showed only a small number of H8 cells with bright dot-like fluorescence in the control group, but increased number of autophagosome-positive H8 cells with bright dot-like fluorescence in the pterostilbene groups. Western blot analysis revealed that there were significant differences in the protein expression of cyclin D1, caspase-3, caspase-9, Beclin1, LC3-Ⅱ/Ⅰ, ATG5, P62, E6 and E7 among the control and pterostilbene groups after 24- and 48-hour treatment with pterostilbene (all P < 0.05) . The treatment with pterostilbene could down-regulate the expression of cyclin D1, E6 and E7, and up-regulate the expression of caspase-3, caspase-9, Beclin1, LC3-Ⅱ/Ⅰ, ATG5 and P62, with significant differences between the control group and most pterostilbene groups in expression of the above proteins (all P < 0.05) . Conclusion:Pterostilbene can inhibit the proliferation of H8 cells, promote their apoptosis and autophagy, and down-regulate the expression of oncogenes E6 and E7.

Objective:To determine the effects of cytochrome P450 1A1 (CYP1A1) on nitric oxide (NO) production in lipopolysaccharide (LPS)-induced macrophages and the underlying mechanism.Methods:The peritoneal macrophages (PMs) were isolated from healthy C57BL/6 mice and stimulated with 10 mg/L LPS to establish inflammatory response model. The CYP1A1 mRNA and protein expressions in the cells were determined. The mouse macrophages RAW264.7 cell line with CYP1A1 overexpression (CYP1A1/RAW) were cultured in vitro, and they were stimulated by 10 mg/L LPS at logarithmic phase. The negative control-expressed RAW264.7 cells (NC/RAW) were established. The protein and mRNA expressions of activator protein-1 (AP-1) and inducible nitric oxide synthase (iNOS) in the cells as well as the content of NO in the cell supernatant were determined. The RAW264.7 cells were cultured in vitro, and they were stimulated by 10 mg/L LPS and 100 nmol/L 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] only or in combination at logarithmic phase. The blank control group was set up. The expression of iNOS mRNA in the cells and NO content in the cell supernatant were determined to observe whether the effect of CYP1A1 on LPS induced NO production in macrophages was related to 12(S)-HETE produced by metabolism. The RAW264.7 cells with CYP1A1 overexpression and hydroxylase activity mutation (CYP1A1m/RAW) were cultured in vitro, and they were stimulated by 10 mg/L LPS at logarithmic phase. The CYP1A1/RAW cell control group was set up. The iNOS mRNA expression in the cells and NO content in the cell supernatant were determined to observe the effect of hydroxylase activity of CYP1A1 in regulating NO production in macrophages. Results:Compared with the phosphate buffered saline (PBS) control group, the CYP1A1 mRNA expressions were elevated significantly from 2 hours after LPS stimulation and reached a peak at 12 hours [CYP1A1 mRNA (2 -ΔΔCt): 6.41±0.98 vs. 1.00±0.00, P < 0.05], while CYP1A1 protein expressions were increased from 6 hours after LPS stimulation and reached a peak at 24 hours, suggesting that CYP1A1 expression might be involved in LPS-induced macrophage over-activation. Compared with NC/RAW+LPS group, the iNOS mRNA expressions and NO contents both increased in CYP1A1/RAW+LPS group and reached a peak after 12 hours and 24 hours, respectively [12-hour iNOS mRNA (2 -ΔΔCt): 54.42±8.21 vs. 24.22±3.89, 24-hour NO (μmol/L): 66.52±4.09 vs. 41.42±2.09, both P < 0.05], while the iNOS protein expression and AP-1 phosphorylation also enhanced, suggesting that CYP1A1 might increase NO production by promoting AP-1 activation and iNOS expression. LPS and 12(S)-HETE stimulation only or in combination had no effect on iNOS mRNA expression and NO production, and no significant difference was found between the 12 (S)-HETE+LPS group and LPS group [12-hour iNOS mRNA (2 -ΔΔCt): 34.24±4.07 vs. 34.35±4.01, 24-hour NO (μmol/L): 44.02±3.14 vs. 44.56±3.21, both P > 0.05], suggesting that the regulation of CYP1A1 on NO production might not be induced by 12 (S)-HETE. There was no significant difference in the iNOS mRNA expressions or NO content between the CYP1A1m/RAW+LPS group and CYP1A1/RAW+LPS group [12-hour iNOS mRNA (2 -ΔΔCt): 52.11±6.84 vs. 50.21±5.19, 24-hour NO (μmol/L): 60.42±4.14 vs. 52.01±5.12, both P > 0.05], suggesting that CYP1A1 hydroxylase activity deficiency showed no effect on NO production. Conclusions:LPS stimulation significantly increases CYP1A1 expression in macrophages. CYP1A1 overexpression promotes NO production by activated macrophages through AP-1/iNOS pathway, while hydroxylase-deficiency or 12(S)-HETE has no effect on this regulation.

Severe trauma or massive deep burn can cause significant immunosuppression associated with sepsis and multiple organ failure. Dendritic cell (DC), as the professional antigen presenting cells and activating factor of immune response, plays an extraordinary role in initiating and regulating congenital and adaptive immune response. The quantity, functional changes, relevant molecular mechanisms and reverse measures of DC after trauma/burn were reviewed in order to intensively study the changes of DC after trauma/burn and provide a reference for exploring effective intervention measures for trauma/burn.

OBJECTIVE: To investigate the effects of terlipressin (TP) on blood pressure and survival in septic mice following trauma and its mechanism. METHODS: (1) Survival experiment: 120 male C57BL/6 mice aged 6-8 weeks were enrolled, the posttraumatic sepsis mice model was reproduced by traumatic hemorrhage (bilateral femoral fracture + 45% of total blood loss) followed by cecal ligation and puncture (CLP) after 8 hours. Intraperitoneal injection of TP was used for intervention. Sixty model mice were used to observe the effect of 0.05 μg/g TP at different intervention times (the drug was given immediately after traumatic hemorrhage + the administration was repeated after 6 hours, the drug was given immediately after traumatic hemorrhage + the administration was repeated every 6 hours until the end of the experiment, the drug was given at 4 hours after CLP + the administration was repeated every 6 hours until the end of the experiment) on 48-hour cumulative survival rate of mice with posttraumatic sepsis for finding the best intervention time of TP. The other 60 model mice were used to observe the effect of different TP intervention doses (0.01, 0.05, 0.25 μg/g) at the best intervention time on the 48-hour cumulative survival rate of mice with posttraumatic sepsis for finding the best intervention dose of TP. (2) Intervention experiment: the other 45 mice were enrolled, and they were randomly divided into traumatic hemorrhage + sham group (TH+sham group, only laparotomy without CLP), TH+CLP group, and TH+CLP+TP group (the best intervention time and dose of TP shown by survival experiment were used), with 15 mice in each group. Mean arterial pressure (MAP) of mice was monitored continuously. The orbital whole blood was collected at 2 hours after successful reproduction of the model, and the lung tissues were harvested at 12 hours and 24 hours, respectively. The pathological changes in lung tissue were observed with light microscope. The contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum and lung tissue were determined by enzyme linked immunosorbent assay (ELISA). The expressions of IL-1β and TNF-α mRNA in lung tissue were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The expressions of nuclear factor-κB p65 (NF-κB p65) in the nucleus and cytoplasm of lung tissue were determined by Western Blot. RESULTS: (1) Survival experiment results showed that the 48-hour cumulative survival rate of mice was highest with TP intervention by 0.05 μg/g administration immediately after traumatic hemorrhage and repeated every 6 hours, which was the best intervention method of TP. (2) Intervention experiment results showed that the pulmonary alveolar wall fracture accompanied by inflammatory cell infiltration was found at 12 hours after the successful reproduction of traumatic sepsis model, and the pathological damage was gradually increased with time prolongation. MAP was decreased sharply after traumatic hemorrhage, and it was continued to decrease after two-hit of CLP. The contents of IL-1β and TNF-α in serum and lung tissue, the expressions of IL-1β and TNF-α mRNA in lung tissue, and expressions of NF-κB p65 protein in cytoplasm and nucleus of TH+CLP group were significantly higher than those in TH+sham group. Compared with TH+CLP group, the pathological changes in lung tissue were improved significantly, and the MAP was decreased gently after TP intervention, the levels of inflammatory mediators in serum were significantly decreased [IL-1β (pg/L): 164.32±25.25 vs. 233.11±23.02, TNF-α (pg/L): 155.56±31.47 vs. 596.38±91.50, both P < 0.05], and their expressions in lung tissue [IL-1β content (ng/mg): 262.68±16.56 vs. 408.15±17.85, IL-1β mRNA (2^{-Δ ΔCt}): 2.63±0.68 vs. 6.22±0.74; TNF-α content (ng/mg): 311.07±17.35 vs. 405.04±24.83, TNF-α mRNA (2^{-Δ ΔCt}): 2.04±0.62 vs. 5.32±0.55, all P < 0.01], and NF-κB p65 protein expressions were significantly down-regulated (gray value: 0.47±0.01 vs. 1.28±0.05 in cytoplasm, 0.45±0.02 vs. 1.95±0.06 in nucleus, both P < 0.01]. CONCLUSIONS The continuous intervention with TP 0.05 μg/g administration immediately after traumatic hemorrhage and repeated every 6 hours could improve the MAP of mice with traumatic sepsis, and improve the prognosis. The mechanism may be related to alleviating the inflammatory response and inhibiting the activation of the NF-κB signaling pathway in the lung tissue.
Animals ; Blood Pressure ; Interleukin-1beta ; Lypressin/analogs & derivatives* ; Male ; Mice ; Mice, Inbred C57BL ; Sepsis ; Terlipressin ; Tumor Necrosis Factor-alpha

Objective: To investigate the effects of terlipressin (TP) on blood pressure and survival in septic mice following trauma and its mechanism. Methods: ① Survival experiment: 120 male C57BL/6 mice aged 6-8 weeks were enrolled, the posttraumatic sepsis mice model was reproduced by traumatic hemorrhage (bilateral femoral fracture + 45% of total blood loss) followed by cecal ligation and puncture (CLP) after 8 hours. Intraperitoneal injection of TP was used for intervention. Sixty model mice were used to observe the effect of 0.05 μg/g TP at different intervention times (the drug was given immediately after traumatic hemorrhage + the administration was repeated after 6 hours, the drug was given immediately after traumatic hemorrhage + the administration was repeated every 6 hours until the end of the experiment, the drug was given at 4 hours after CLP + the administration was repeated every 6 hours until the end of the experiment) on 48-hour cumulative survival rate of mice with posttraumatic sepsis for finding the best intervention time of TP. The other 60 model mice were used to observe the effect of different TP intervention doses (0.01, 0.05, 0.25 μg/g) at the best intervention time on the 48-hour cumulative survival rate of mice with posttraumatic sepsis for finding the best intervention dose of TP. ② Intervention experiment: the other 45 mice were enrolled, and they were randomly divided into traumatic hemorrhage + sham group (TH+sham group, only laparotomy without CLP), TH+CLP group, and TH+CLP+TP group (the best intervention time and dose of TP shown by survival experiment were used), with 15 mice in each group. Mean arterial pressure (MAP) of mice was monitored continuously. The orbital whole blood was collected at 2 hours after successful reproduction of the model, and the lung tissues were harvested at 12 hours and 24 hours, respectively. The pathological changes in lung tissue were observed with light microscope. The contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum and lung tissue were determined by enzyme linked immunosorbent assay (ELISA). The expressions of IL-1β and TNF-α mRNA in lung tissue were determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The expressions of nuclear factor-κB p65 (NF-κB p65) in the nucleus and cytoplasm of lung tissue were determined by Western Blot. Results: ① Survival experiment results showed that the 48-hour cumulative survival rate of mice was highest with TP intervention by 0.05 μg/g administration immediately after traumatic hemorrhage and repeated every 6 hours, which was the best intervention method of TP. ② Intervention experiment results showed that the pulmonary alveolar wall fracture accompanied by inflammatory cell infiltration was found at 12 hours after the successful reproduction of traumatic sepsis model, and the pathological damage was gradually increased with time prolongation. MAP was decreased sharply after traumatic hemorrhage, and it was continued to decrease after two-hit of CLP. The contents of IL-1β and TNF-α in serum and lung tissue, the expressions of IL-1β and TNF-α mRNA in lung tissue, and expressions of NF-κB p65 protein in cytoplasm and nucleus of TH+CLP group were significantly higher than those in TH+sham group. Compared with TH+CLP group, the pathological changes in lung tissue were improved significantly, and the MAP was decreased gently after TP intervention, the levels of inflammatory mediators in serum were significantly decreased [IL-1β (pg/L): 164.32±25.25 vs. 233.11±23.02, TNF-α (pg/L): 155.56±31.47 vs. 596.38±91.50, both P < 0.05], and their expressions in lung tissue [IL-1β content (ng/mg): 262.68±16.56 vs. 408.15±17.85, IL-1β mRNA (2^-ΔΔCt): 2.63±0.68 vs. 6.22±0.74; TNF-α content (ng/mg): 311.07±17.35 vs. 405.04±24.83, TNF-α mRNA (2^-ΔΔCt): 2.04±0.62 vs. 5.32±0.55, all P < 0.01], and NF-κB p65 protein expressions were significantly down-regulated (gray value: 0.47±0.01 vs. 1.28±0.05 in cytoplasm, 0.45±0.02 vs. 1.95±0.06 in nucleus, both P < 0.01]. Conclusions The continuous intervention with TP 0.05 μg/g administration immediately after traumatic hemorrhage and repeated every 6 hours could improve the MAP of mice with traumatic sepsis, and improve the prognosis. The mechanism may be related to alleviating the inflammatory response and inhibiting the activation of the NF-κB signaling pathway in the lung tissue.

Objective To detect the effect of profound hypothermia on Bax expression and its relationship with cell apoptosis in the rat hippocampus after global ischemia. Methods Animal models of cardiopulmonary bypass (CPB) were established in 30 Wistar rats which were randomized into blank control group (rats were sacrificed 5 min after model making and hippocampus tissues were prepared), normothermia ischemia group (circulatory arrest was performed at [37.0±0.3]°C for 5 min, and then, rats were sacrificed 5 min after model making and hippocampus tissues were prepared) and hypothermia ischemia group (circulatory arrest was performed at [18.0±0.5]°C by ice crumbles for 5 min, and then, rats were sacrificed 5 min after model making and hippocampus tissues were prepared, n=10). Quantitative real-time PCR (qPCR) was used to detect the Bax mRNA expression, immunohistochemical method was used to detect the Bax protein expression, Western blotting was used to detect the cytochrome C (Cyt-C) expression, and TUNEL was used to measure the cell apoptosis. Results The Bax mRNA expression (2.734±0.301), optical density of positive cells (0.326±0.017), Cyt-C protein expression (4.14 ±0.79) and cell apoptosis rate (53.95％±4.23％) increased significantly in the normothermia ischemia group as compared with those in the blank control group (P<0.05). The Bax mRNA expression (1.679 ±0.309), optical density of positive cells (0.209 ±0.019), Cyt-C protein expression (1.45±0.49) and cell apoptosis rate (15.56％±3.02％) in the hypothermia ischemia group decreased significantly as compared with those in the normothermia ischemia group (P<0.05).Conclusion By inhibiting the expression of Bax, profound hypothermia can inhibit release of Cyt-C into the cytoplasm and thus reduce cell apoptosis in the hippocampus after global ischemia in rats, which may be one important way that profound hypothermia has protective effect on brain tissue with ischemic injury.