[Purpose]To analyze the trend of gastric cancer incidence and age characteristics in Jiangsu cancer registration areas from 2009 to 2019.[Methods]Cancer registration data from 2009 to 2019 meeting quality control requirements were collected from 16 cancer registries in Jiangsu Province.The crude incidence rate and age-standardized incidence rate by Chinese standard population in 2000(ASIRC)were calculated by gender,urban/rural areas and age groups.The inci-dence trends were analyzed by Joinpoint.A birth cohort model was constructed to calculate the in-cidence rate of gastric cancer for men and women born between 1929 and 2019.The age composi-tion of gastric cancer incidence in Jiangsu Province between 2009 and 2019 was calculated and compared.[Results]The crude incidence rate and ASIRC of gastric cancer in Jiangsu cancer regi-stration areas from 2009 to 2019 showed a significant decreasing trend in both male and female or urban and rural areas,in which the decrease in male(AAPC=-1.28％,P＜0.001)was higher than that of female(AAPC=-1.17％,P=0.030),and the decrease in urban(AAPC=-1.66％,P＜0.001)was higher than that of rural(AAPC=-0.72％,P＜0.001).The incidence rates of gastric cancer in age groups of 40～79 years old showed a significant decreasing trend from 2009 to 2019 with the AAPC ranging from-6.75％to-3.54％(all P＜0.05).In age groups of 40～79 years old,the inci-dence rates of gastric cancer among people with different years of birth showed a decreasing trend with the increase of the birth year.For ASIRC,the composition of patients aged 60 years old above increased by 0.63％(95％CI:0.46％～0.81％)per year from 2009 to 2019.[Conclusion]The inci-dence rate of gastric cancer in cancer registration areas of Jiangsu Province from 2009 to 2019 showed a decreasing trend,the average age of incidence showed a trend of backward moving,and for age-standardized incidence the proportion of patients over 60 years old was increased.

Objective:To investigate the role of NF-E2-related factor 2 (Nrf2) in lung injury caused by seawater drowning in mice.Methods:A total of 48 6-8 weeks old male wild-type C57 mice were randomly divided into two groups for experiment: (1) control group, day 1 group after drowning(Day1), day 3 group after drowning(Day3) and day 7 group after drowning(Day7) to determine the time point of seawater drowning; (2) control group, seawater drowning model group(SW), dimethyl fumarate treatment group(DMF) and seawater drowning+ DMF reatment group(SW+ DMF) to determine the role of Nrf2 in lung injury in mice caused by drowning, 6 mice per group. And 12 male C57 background Nrf2 knockout mice (Nrf2 KO) at 6-8 weeks old were divided into Nrf2 KO control group and Nrf2 KO+ seawater drowning group; 6 mice in each group. Three days after the drowning model was established, we observed the gross morphology and the pathological changes of the lung tissue, calculated the wet-to-dry weight ratio of the lungs, and tested the reduced glutathione and malondialdehyde levels.Results:Seawater drowning caused alveolar space rupture, pulmonary hemorrhage and pulmonary edema in mice. Compared with the wild-type mice, knockout of Nrf2 aggravated lung injury and oxidative stress in mice caused by seawater drowning. Nrf2 agonist DMF treatment significantly improved lung injury in mice, increased the reduced glutathione content, and decreased malondialdehyde level.Conclusion:The activation of Nrf2 can relieve lung injury and oxidative stress levels in mice caused by seawater drowning, which can play an important role in reducing lung damage caused by seawater drowning.

Objective:To investigate the role of NF-E2-related factor 2 (Nrf2) in lung injury caused by seawater drowning in mice.Methods:A total of 48 6-8 weeks old male wild-type C57 mice were randomly divided into two groups for experiment: (1) control group, day 1 group after drowning(Day1), day 3 group after drowning(Day3) and day 7 group after drowning(Day7) to determine the time point of seawater drowning; (2) control group, seawater drowning model group(SW), dimethyl fumarate treatment group(DMF) and seawater drowning+ DMF reatment group(SW+ DMF) to determine the role of Nrf2 in lung injury in mice caused by drowning, 6 mice per group. And 12 male C57 background Nrf2 knockout mice (Nrf2 KO) at 6-8 weeks old were divided into Nrf2 KO control group and Nrf2 KO+ seawater drowning group; 6 mice in each group. Three days after the drowning model was established, we observed the gross morphology and the pathological changes of the lung tissue, calculated the wet-to-dry weight ratio of the lungs, and tested the reduced glutathione and malondialdehyde levels.Results:Seawater drowning caused alveolar space rupture, pulmonary hemorrhage and pulmonary edema in mice. Compared with the wild-type mice, knockout of Nrf2 aggravated lung injury and oxidative stress in mice caused by seawater drowning. Nrf2 agonist DMF treatment significantly improved lung injury in mice, increased the reduced glutathione content, and decreased malondialdehyde level.Conclusion:The activation of Nrf2 can relieve lung injury and oxidative stress levels in mice caused by seawater drowning, which can play an important role in reducing lung damage caused by seawater drowning.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.

ObjectiveTo evaluate CT and MRI findings of the intrathoracic ganglioneuroma and to improve its diagnosis and differential diagnosis ability.MethodsClinical,CT( n = 14),MRI (n = 6) and pathology manifestations of 20 patients with the intrathoracic ganglioneuroma were retrospectively analyzed.All 20 cases had chest CT and MRI plain scanning and multiphase enhance scanning before operation.ResultsSeventeen of 20 lesions were located in posterior mediastinum,2 in pleura side and 1 in right thorax cavity.The CT value of the plain scans ranged from 20 to 40 HU ( mean 30.5 HU),Tubercle calcification were detected in four masses,one case with fat density was showed on CT scanning.After injecting contrast media,CT value ranged from 0 to 12 HU (mean 6.2 HU) in artery phase,ranging from 10 to 20 HU ( mean 14.3 HU) in delay phase.Five of 6 cases of MRI signals were homogeneously low intensity on T1 WI,1 case with fat signal was imhomogeneously low intensity on T1WI.Six cases were imhomogeneously high intensity on T2WI.A whorled appearance was visualized in one tumor on T2WI.The post-contrast enhancement MR images was slight enhancement imhomogeneously in artery phase and gradual increasing enhancement in delay phase.ConclusionOn CT and MR imaging,no enhancement or slight enhancement in artery phase and gradual increasing enhancement in delay phase are characteristic manifestations of ganglioneuroma in the thorax.

Traditional EP analysis is developed under the condition that the background noises in EP are Gaussian distributed. Alpha stable distribution, a generalization of Gaussian, is better for modeling impulsive noises than Gaussian distribution in biomedical signal processing. Conventional blind separation and estimation method of evoked potentials is based on second order statistics (SOS). In this paper, we propose a new algorithm based on minimum dispersion criterion and Givens matrix. The simulation experiments show that the proposed new algorithm is more robust than the conventional algorithm.
Algorithms ; Artifacts ; Brain ; physiology ; Electroencephalography ; methods ; Evoked Potentials ; physiology ; Humans ; Normal Distribution ; Signal Processing, Computer-Assisted