Objective To examine the influence of serum on pulmonary surfactant (PS) function.Methods Caesarean section was performed on 26-day pregnant Japanese white rabbits (full term=31 days). The pre-term rabbits weighing 20-34g were anesthetized with intraperitoneal(ip) pentobarbital sodium 0.5mg. Tracheotomy was performed. Test liquids were prepared by suspending PS in rabbit serum or acetate Ringer solution at concentration of 2.0,4.0,6.0,8.0,10,12,24 mg/ml. The surface tension of test liquids was measured by pulsating bubble technique. Test liquid 10ml/kg was instilled in the lungs of PS-deficient pre-term rabbits via tracheotomy cannula.Animals were ramdomly divided into 4 groups according to the test liquid used: group A: 24mg/ml PS suspended in acetate Ringer solution; group B: 24mg/ml PS suspended in serum; group C: 4.0mg/ml PS suspended in acetate Ringer solution; group D: nothing was instilled. Rabbits were placed in plethysmograph. Siemens-Elema ventilator was used for mechanical ventilation. PIP was set at 22.5cmH 2O, PEEP=0,respiratory rate=40 frequency/min, I:E=1:1,FiO 2=100%. Tidal volume was measured at 5,10,15,20 min after the start of mechanical ventilation.Results When concentration of PS suspended in acetate Ringer solution was 2.0 mg/ml, the minimum surface tension (?min) was less than 3.0 mN/m; when suspended in serum, ?min was significantly higher than 30 mN/m (P15 ml/kg, but in group B the mean tidal volume was

Objective The reconstituted pulmonary surfactant (SP) is composed of synthetic lipid(SL) and surfactant- associated protein C (SP-C) . The purpose of this study was to determine the surface tension reducing activity of the reconstituted surfactant containing different concentrations of SP-C.Methods Pulmonary surfactant (SP) was isolated from alveolar lavage fluid of fresh porcine lungs by centrifugation, extraction and precipitateon. SP-C was extracted from PS and SL was prepared by mixing dipalmitoyl-phosphatidyl choline (DPPC), dioleoyl-phosphatidyl choline (DOPC) and palmitoyl-oleoyl-phosphatidyl glycerol (POPG) in the weight ratio of 60: 20: 20. Three synthetically reconstituted surfactants RS-1, RS-2, RS-3, were prepared by adding different concentrations of SP-C to SL. The end concentration of SP-C was 1% , 2% and 3% respectively. Five test liquids (PS, SL. RS-1, RS-2, RS-3) were prepared by suspending the materials mentioned above in nonnal saline. The dynamic surface tension of the five test liquids were measured by a pulsating bubble technique. Thirty-six PS-deficient premature rabbits were studied. The premature rabbits were delivered by cesarean section on the 26 th day of pregnancy. The animals were tracheostomized and mechanically ventilated. 0.1 ml of test liquid PS (group Ⅱ) , SL(group Ⅲ) or RS-3(group Ⅳ) was instilled into the lungs via the tracheostomy cannula. In control group (group Ⅰ) no test liquid was instill. The animals were placed in a body plethysmograph and mechanically ventilated (the maximum inspiratory pressure = 25 cm H2 O, RR = 40 bpm, I: E = 1:1, FiO2 = 100 % made of ventilation IPPV) . Tidal volume was measured at 5, 10, 15 and 20 min after onset of IPPV. Results The minimum surface tension (?min) of PS was 0.9?0.3 mN?m-1 , and of SL was 22.6 ?1.3 mN?m-1 . The ? min of RS-3 was 0.7?0.1 mN ?m-1. The mean tidal volume after 20 min of mechanical ventilation in group Ⅱ(PS) and groupⅢ(RS-3 ) was 25 ?7 ml?kg-1 and 25 ? 4 ml?kg-1 respectively, significantly larger than that in control group (Ⅰ ) and group Ⅲ (SL) . Conclusion The surface tension-reducing activity of SL alone is low. Adding SP-C to SL greatly enhances the surface tension-reducing activity of reconstituted surfactant (RS).

Objective To examine the effects of exogenous pulmonary surfactant (PS)on lung function in rats with meconium aspiration.Methods Twenty Wistar rats of both sexes were anesthetized with intraperitoneal pentobarbital 30 mg?kg-1 , tracheotomized and mechanically ventilated (PIP= 16 cm H2O,RR =40 bpm,I:E= 1 : 1, FiO2 = 1.0) . 3-4 ml? kg -1 of saline suspension of human meconium ( 200 mg ? ml-1 ) was introduced into trachea. Respiratory failure was induced when PaCO2

Objective To investigate the effects of exogenous biliverdin on lung injury induced by brain death (BD) in rats. Methods Twenty-three adult male Wistar rats in which Fogarty balloon catheter was successfully inserted into cranial cavity were randomly divided into 3 groups: group Ⅰ sham operation (group S,n = 7); group Ⅱ brain death (group BD, n = 8) and group Ⅲ biliverdin + BD (group B, n = 8). The animals were anesthetized, intubated and mechanically ventilated. Femoral artery and vein were cannulated for MAP monitoring and drug and fluid administration. Brain death was induced by injecting slowly normal saline into the balloon in group Ⅱ and Ⅲ. BD was confirmed by dilated and fixed pupils, apnea, transient hypertension and EEG changes. In group Ⅲ biliverdin 35 mg/kg was injected intraperitoneally as soon as BD was confirmed. The animals were mechanically ventilated for another 1.5 h during which MAP was maintained at 80-120 mm Hg by iv norepinephrine infusion. Arterial blood samples were obtained before anesthesia, immediately before and at 5, 30,60, 90 min after intraperitoneal biliverdin for blood gas analysis and determination of plasma bilirubin concentration. PaO2/FiO2 was calculated. The animals were sacrificed at 1.5 h after biliverdin administration. The left lung was removed for detection of MDA content, SOD activity, total antioxidant capacity, cell apoptosis and biliverdin reductase expression in lung tissue. Results Brain death significantly decreased PaO2/FiO2, lung SOD activity and total antioxidant capacity and increased lung MDA content and apoptosis as compared with sham operation group. IP biliverdin significantly attenuated BD-induced lung injury in group B as compared with group BD. The plasma bilirubin concentration and biliverdin reductase expression were significantly higher in group B than group BD. Conclusion Exogenous biliverdin can attenuate BD-induced lung injury by inhibiting pulmonary oxidative stress response and apoptosis.

Objective:To study the related factors of severe acute radiation-induced lung injury (SAR) caused by IMRT and concurrent chemotherapy for non-small cell lung cancer. Methods:We retrospectively analyzed the data of 2 323 non-small cell lung cancer pa-tients who underwent IMRT radiotherapy and concurrent chemotherapy at the Department of Radiotherapy of Tianjin Medical Univer-sity Cancer Institute and Hospital from January 2010 to January 2014. We analyzed the clinical factors and parameters that affect dose by univariate and multivariate analysis. Results:A total of 2 323 patients enrolled and 1 241 cases suffering from acute radiation-in-duced lung injury with the rate of 53.4%. Only 185 cases suffered from SARP with a rate of 7.96%. Univariate analysis showed that the gender, histopathological type, total radiation dose, V5 (%), and average dose rate are not related to SARP (P>0.05). By contrast an age of>60 years, 1%predicted FEV, docetaxel+carboplatin/cisplatin chemotherapy, V20 (%), V30 (%), and mean lung dose (MLD) are sig-nificantly related to SARP (P<0.05). Multivariate analysis showed that a patient age of>60 years, docetaxel+carboplatin/cisplatin che-motherapy, V20 (%), and V30 (%) are the independent risk factors of SARP. Conclusion:Among the non-small cell lung cancer patients undergoing IMRT radiotherapy and concurrent chemotherapy, further attention should be given to elderly patients, patients receiving docetaxel and platinum chemotherapy, as well as V20 and V30 with high doses. The necessary preventive treatment should be given to reduce the incidence of SARP, improve the quality of life of patients, and reduce the incidence of respiratory failure and mortality.

Objectlve To investigate the effects of different ventilation modes on the efficacy of exogenous pulmonary surfactant(PS)for the treatment of rats with ventilator-induced lung injury(VILI).Methods Forty-two male Wistar rats weighing 310-356 g were randomly divided into 6 groups(n=7 each):group CVT6,group SVT6,group CVT10,group SVT10,group CVT14 and group SVT14.The tidal volume(VT)was set at 6,10 and 14 ml/kg respectively and the respiratory rate(RR) was 75,45 and 32 bpm respectively.The animals were anesthetized with intraperitoneal 3% Pentobarbital 50 mg/kg,then tracheostomized and intubated.VILI model was induced by high-pressure ventilation (HPV) with peak inspimtory pressure (PIP) 40 cm H2O and without positive end-expiratory pressure (PEEP).The air was injected into the trachea via the airway at the end ofexpiration before HPV (T0,baseline value) and 15-25 min of HPV,the airway pressure monitored and the lung compliance(C) calculated.When C was decreased to half of the baseline value,PEEP was increased to 7.5 cm H20.After the tracheal edema fluid was removed,the PS 100 mg/kg was immediately injected into the trachea in group SVT6,SVT10 and SVT14.The equal volume of air was injected into the trachea in group CVT6,CVT10 and CVr14 instead of PS.Then the rats in different groups were ventilated with the corresponding ventilation modes.MAP was monitored and blood samples were token from femoral artery for blood gas analysis at T0, 5 min after HPV (T1 ), and 15, 30, 60, 90, 120 min (T2-6) after administration of PS. The tracheal edema fluid was collected at T1 and T6.The rats were killed at T6 and the lung tissues taken for microscopic examination. Results With the same ventilation mode, the VILI was significantly alleviated after administration of PS. With different ventilation modes,the lung injury was significantly reduced in group SVT 10 compared with the other groups. Conclusion The efficacy of PS for the treatment of rats with VILI is good using the ventilation strategy with VT of 10 ml/kg and RR of 45 bpm.

Objective:To examine a nomogram model for individualized prediction of the risk for recurrence of early gastric cancer(EGC)in elderly patients undergoing endoscopic submucosal dissection(ESD).Methods:This was a retrospective cohort study, with a total of 3 987 elderly EGC patients who underwent ESD treatment between January 2000 and December 2016 after admission to the gastroenterology department of our hospital.Twenty-eight relapsed patients with complete clinicopathological data and follow-up data were selected as the relapse group, and 276 non-relapsed patients were selected as the control group.General data of all patients were collected and a logistic regression analysis was performed to analyze independent risk factors for the recurrence of EGC in patients after ESD.A corresponding nomogram risk prediction model was established by using the R software.Results:Among the 3 987 elderly EGC patients, 29 relapsed after an average follow-up of 2.7 years, and the recurrence rate was 0.73%(29/3 987). The differences in baseline data such as age(≥75 years old), lesion size(≥3 mm), T stage and lymph node metastasis between the recurrence group and the control group were statistically significant(11 cases or 39.3% vs.171 cases or 62.0%, 19 cases or 67.9% vs.111 cases or 40.0%, 9 cases or 32.1% vs.153 cases or 55.4%, 19 cases or 67.9% vs.102 cases or 39.0%, P<0.05). Logistic regression analysis showed that age over 75 years( OR=2.128, 95% CI: 1.373-3.624), T stage( OR=1.763, 95% CI: 1.079-2.934), lesion size≥3 mm( OR=2.604, 95% CI: 1.363-4.217), and lymph node metastasis( OR=2.871, 95% CI: 1.425-5.639)were independent risk factors for the recurrence after ESD in EGC patients( P<0.05). The nomogram model was established based on the above risk factors, and the validation results showed that the predicted value was basically the same as the actual measured value and had good predictive performance.The internal validation results showed that the consistency index was 0.817(95% CI: 0.722-0.941), suggesting that the model had a high accuracy and discrimination. Conclusions:Before ESD for elderly EGC patients is performed, factors such as age, tumor size, T stage and lymph node metastasis should be fully considered to comprehensively evaluate the recurrence rate of EGC after the procedure.This predictive model can improve the diagnostic efficacy of postoperative recurrence and has high clinical value.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.

This study aims to investigate the effects of astragalus polysaccharide (APS) on diabetic retinopathy through the SHH-Gli1-AQP1 pathway. The anti-type 2 diabetes mellitus (T2DM) targets of APS were identified through comprehensive searches of drug and disease-related databases. A protein-protein interaction network was then constructed, followed by GO and KEGG enrichment analyses.Molecular docking simulations were performed to evaluate the interactions of APS and metformin with Gli1 and AQP1. An in vivo T2DM rat model was established via streptozotocin (STZ) injection and treated with metformin and varying doses of APS for 12 weeks. Histological changes in retinal cells were assessed using H&E and PAS staining. The expression levels of AQP1, Gli1, and SHH in the retina were measured using immunohistochemistry, Western blotting, immunofluorescence, and ELISA. Additionally, mRNA expression of AQP1, Gli1, and SHH was quantified by RT-qPCR. Bioinformatic analyses indicated that Gli1 and AQP1, key components of the SHH-Gli1-AQP1 signaling pathway, may be associated with T2DM. Subsequent experiments demonstrated that the STZ-induced T2DM rats exhibited significant retinal damage, which was notably mitigated by both APS and metformin treatments. Furthermore, the SHH-Gli1-AQP1 signaling pathway was found to be overactivated in STZ-induced T2DM rats. Treatment with APS and metformin significantly reduced the elevated expression levels of SHH, Gli1, and AQP1. APS effectively inhibits retinal damage of STZinduced T2DM rats by restraining the SHH-Gli1-AQP1 signaling pathway.