Objective To predict the burden caused by fatal road traffic injuries from 2015 to 2030. Methods We searched the websites of United Nations Population Division,United States Department of Agriculture,World Health Organization,China Energy Research Foundation and other agencies to obtain the predictive values of gross domestic product(GDP)per capita,urbanization, motorization and education from 2015 to 2030 in China. Predicted values were then applied to log-linear models to estimate the numbers and years of life lost due to road traffic injuries from 2015 to 2030. Results The mortality rate caused by road traffic injury decreased slightly,from 13.7/100 000 in 2015 to 11.8/100 000 in 2030. 191,189,183,169 thousand persons were estimated to die from road traffic crashes in 2015,2020,2025 and 2030,respectively,showing a declining trend. Years of Life Lost(YLLs)caused by road traffic deaths were predicted to be 6 918,6 634,6 189,5 513 thousand years in 2015,2020,2025 and 2030,respectively,also showing a gradual downward trend. But the YLLs displayed an increase among people at 55 years of age or older,between 2015 and 2030. Results from the sensitivity analysis showed a stable forecasting result. Conclusion Mortality, number of deaths and YLLs from road traffic crashes were predicted to decrease slightly,between 2015 and 2030 but the number of deaths and YLLs due to road traffic injuries will continue to increase from 2015 to 2030.

OBJECTIVE: To determine the prevalence and incidence of illness of two-week duration, and the factors influencing these, among residents 15 years and older in four counties of Hunan Province. METHODS: Data were sampled from four counties of Hunan Province for the Fourth National Health Service Survey. Incidence and two-week prevalence of disease were used to assess the health service needs of residents. A non-conditional, stepwise logistic regression was employed to explore the influencing factors. RESULTS: The two-week prevalence and incidence were 11.5% and 3.9%, respectively, in four counties of Hunan. The three leading diseases of two-week prevalence were: respiratory diseases, digestive diseases, and musculoskeletal diseases. Non-conditional stepwise logistic regression showed that urban residents had 0.64 times the risk of two-week illness compared with the rural residents (P< 0.05); residents in the 45-59 year age group and the 60+ year age group had 1.69 and 2.62 times the risk of two-week illness compared with residents in the 15-44 year age group, respectively (P<0.05). The widowed had 1.91 times the risk of prevalence of two-week illness contrasted to singles (P<0.05); the students had 0.29 times the risk of two-week illness contrasted to the workers (P<0.05); urban residents had 0.63 times the risk of two-week illness compared with the rural (P<0.05); the widowed had 2.37 times the risk of incidence of two-week illness compared with singles (P<0.05). CONCLUSION The majority of health service needs of residents of four counties is generated by three diseases: respiratory diseases, digestive diseases, and musculoskeletal diseases. Relatively, rural residents, the elderly, employed persons and the widowed have higher health service needs than others and deserve specific attention.
Adolescent ; Adult ; Aged ; China ; epidemiology ; Community Health Services ; statistics & numerical data ; Digestive System Diseases ; epidemiology ; Female ; Humans ; Incidence ; Male ; Middle Aged ; Musculoskeletal Diseases ; epidemiology ; Respiratory Tract Diseases ; epidemiology ; Sampling Studies ; Surveys and Questionnaires ; Young Adult

Objective:To investigate whether annexin A1 (ANXA1) improves sepsis-induced lung injury by activating G protein-coupled formyl peptide receptor type 2 (FPR2)-dependent endothelial nitric oxide synthase (eNOS) pathway.Methods:Twenty-four male SD rats were randomly divided into normal group (Control group), lipopolysaccharide (LPS) induced lung injury model group (LPS group), LPS+ANXA1 mimetic peptide group (LPS+Ac2-26 group) and LPS+ANXA1 mimetic peptide+FPR2 inhibitor group (LPS+Ac2-26+WRW4 group), with 6 rats in each group. On the third day before modeling, rats of the LPS+Ac2-26 group were injected with 1 mg/kg Ac2-26 by the tail vein and rats of LPS+Ac2-26+WRW4 group were injected with 1 mg/kg Ac2-26 and 2.2 mg/kg WRW4 by the tail vein. The rats of control group and LPS group were injected same volume of physiological saline. After 48 hours of modeling, the rats were anesthetized and the carotid blood was taken to detect the oxygenation index (OI). Lung tissue was taken from the euthanized rats. The wet/dry (W/D) ratio was determined. The pathological changes of lung tissue were observed under light microscope and pathological score was performed. The levels of tumor necrosis factor-α (TNF-α), interleukins (IL-1β, IL-6, IL-10), malondialdehyde (MDA) and myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA). The protein expressions of eNOS, inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NF-κB) were detected by Western blotting.Results:Under light microscope, compared with LPS group, the infiltration degree of inflammatory cells in the lung tissue of LPS+Ac2-26 group was reduced, and the thickness of the alveolar septum was improved. The degree of inflammatory cell infiltration in the lung tissue of LPS+Ac2-26+WRW4 group was more severe than that of LPS+Ac2-26 group, and the thickness of the alveolar septum increased. These findings suggested that ANXA1 significantly inhibited inflammatory cell infiltration and improved alveolar septal thickness, WRW4 reversed the lung improvement effects of ANXA1. Compared with control group, OI in LPS group was significantly decreased, and W/D ratio, pathological score and TNF-α, IL-1β, IL-6, MDA and MPO levels in lung tissue were significantly increased. Compared with LPS group, OI and IL-10 levels in lung tissue were significantly increased in LPS+Ac2-26 group, while W/D ratio, pathological score, TNF-α, IL-1β, IL-6, MDA and MPO levels in lung tissue were significantly decreased. These results indicated that ANXA1 can improve the oxygenation capacity, improve lung tissue leakage, reduce edema, and inhibit lung tissue inflammation in rats with lung injury. Compared with LPS+Ac2-26 group, the LPS+Ac2-26+WRW4 group showed significant decreases in OI and lung tissue IL-10 level [OI (mmHg, 1 mmHg≈0.133 kPa): 132.16±24.00 vs. 248.67±18.70, IL-10 (ng/L): 27.30±3.04 vs. 36.10±3.92, both P < 0.05], the lung tissue W/D ratio, pathological score and levels of TNF-α, IL-1β, IL-6, MDA and MPO were significantly increased [W/D ratio: 5.29±0.02 vs. 4.83±0.02, pathological score: 5.00±0.28 vs. 2.67±0.52, TNF-α (ng/L): 39.80±4.36 vs. 32.10±2.15, IL-1β (ng/L): 200.00±15.68 vs. 152.60±9.74, IL-6 (ng/L): 181.50±18.02 vs. 148.50±7.34, MDA (mmol/mg): 82.01±8.22 vs. 70.43±5.69, MPO (pg/mg): 6.50±0.32 vs. 4.60±0.56, all P < 0.05]. These results suggested that WRW4 could block the above improvement of ANXA1. Western blotting results showed that compared with control group, the expression of eNOS, iNOS and NF-κB in LPS group was significantly up-regulated. Compared with LPS group, the protein expression of eNOS in LPS+Ac2-26 group was significantly up-regulated (eNOS/β-actin: 0.25±0.01 vs. 0.14±0.01, P < 0.05), and the protein expression of iNOS and NF-κB was significantly down-regulated (iNOS/β-actin: 0.09±0.02 vs. 0.12±0.02, NF-κB/β-actin: 0.35±0.06 vs. 0.59±0.13, both P < 0.05). These findings suggested that ANXA1 might activate the eNOS pathway and down-regulate the expression of NF-κB. Compared with LPS+Ac2-26 group, the protein expression of eNOS in LPS+Ac2-26+WRW4 group was significantly down-regulated (eNOS/β-actin: 0.17±0.02 vs. 0.25±0.01, P < 0.05), while the protein expression of iNOS and NF-κB was significantly up-regulated (iNOS/β-actin: 0.12±0.02 vs. 0.09±0.02, NF-κB/β-actin: 0.52±0.10 vs. 0.35±0.06, both P < 0.05). These results suggested that WRW4 blocked the activation of the eNOS pathway by ANXA1. Conclusion:ANXA1 can improve lung injury associated with sepsis by activating FPR2-dependent eNOS pathway.

OBJECTIVETo predict the burden caused by fatal road traffic injuries from 2015 to 2030.

METHODSWe searched the websites of United Nations Population Division,United States Department of Agriculture, World Health Organization, China Energy Research Foundation and other agencies to obtain the predictive values of gross domestic product (GDP) per capita, urbanization, motorization and education from 2015 to 2030 in China. Predicted values were then applied to log-linear models to estimate the numbers and years of life lost due to road traffic injuries from 2015 to 2030.

RESULTSThe mortality rate caused by road traffic injury decreased slightly, from 13.7/100 000 in 2015 to 11.8/100 000 in 2030. 191, 189, 183, 169 thousand persons were estimated to die from road traffic crashes in 2015, 2020, 2025 and 2030, respectively, showing a declining trend. Years of Life Lost (YLLs) caused by road traffic deaths were predicted to be 6 918, 6 634, 6 189, 5 513 thousand years in 2015, 2020, 2025 and 2030, respectively, also showing a gradual downward trend. But the YLLs displayed an increase among people at 55 years of age or older, between 2015 and 2030. Results from the sensitivity analysis showed a stable forecasting result.

CONCLUSIONMortality, number of deaths and YLLs from road traffic crashes were predicted to decrease slightly, between 2015 and 2030 but the number of deaths and YLLs due to road traffic injuries will continue to increase from 2015 to 2030.

Accidents, Traffic ; mortality ; Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; China ; epidemiology ; Cost of Illness ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Young Adult