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OBJECTIVE: To investigate the current disease burden of chronic obstructive pulmonary disease (COPD) in China and globally using the Global Burden of Disease (GBD) data in 2019, as well as to analyse the changes in its risk factors, providing a scientific basis for the formulation of a comprehensive prevention and control strategy for COPD in China. STUDY DESIGN: An observational study based on the GBDs. METHODS: Based on the GBD 2019 database, we obtained data on incidence, prevalence, mortality, disability-adjusted life years (DALYs) and corresponding age-standardised rates of COPD in China and the global, and analysed and described the changing trends of COPD burden in China and the global from 1990 to 2019. RESULTS: In 2019, the total number of COPD deaths in China was 1.04 (95% uncertainty intervals (95% UI): 0.89-1.27) million cases, the number of patients with COPD was 45.16 (95% UI: 41.13-49.62) million cases, and the number of new cases was 4.0 (95% UI: 3.6-4.4) million cases. DALYs were 74.4 (95% UI: 68.2-80.2) million years. Compared with 1990, the number of new incident cases and the overall prevalence of COPD in China in 2019 increased by 66.20% and 66.76%, respectively, which is lower than the overall global level. CONCLUSION: From 1990 to 2019, the age-standardized prevalence rate (ASPR), the age-standardized incidence rate (ASIR) and the age-standardized death rate (ASDR) in China and the global all showed a downward trend, and the rate of decline in China was much higher than the overall level of the world, indicating that China has made specific achievements in the prevention and treatment of COPD, but overall the disease burden of COPD is still hefty, and the number of affected individuals is still increasing.
Subject(s)
Global Burden of Disease , Pulmonary Disease, Chronic Obstructive , Humans , Cost of Illness , China/epidemiology , Databases, Factual , Pulmonary Disease, Chronic Obstructive/epidemiologyABSTRACT
The main event in the progression of pulmonary fibrosis is the appearance of myofibroblasts. Recent evidence supports pericytes as a major source of myofibroblasts. TGFß/Smad2/3 and PDGF/Erk signaling pathways are important for regulating pericyte activation. Previous studies have demonstrated that PDGFßR and TGFßR are modified by core fucosylation (CF) catalyzed by α-1,6-fucosyltransferase (FUT8). The aim of this study was to compare the effect of inhibiting CF versus the PDGFßR and TGFßR signaling pathways on pericyte activation and lung fibrosis. FUT8shRNA was used to knock down FUT8-mediated CF both in vivo and in isolated lung pericytes. The small molecule receptor antagonists, ST1571 (imatinib) and LY2109761, were used to block the PDGFß/pErk and TGFß/pSmad2/3 signaling pathways, respectively. Pericyte detachment and myofibroblastic transformation were assessed by immunofluorescence and Western blot. Histochemical and immunohistochemical staining were used to evaluate the effect of the intervention on pulmonary fibrosis. Our findings demonstrate that FUT8shRNA significantly blocked pericyte activation and the progression of pulmonary fibrosis, achieving intervention effects superior to the small molecule inhibitors. The PDGFß and TGFß pathways were simultaneously affected by the CF blockade. FUT8 expression was upregulated with the transformation of pericytes into myofibroblasts, and silencing FUT8 expression inhibited this transformation. In addition, there is a causal relationship between CF modification catalyzed by FUT8 and pulmonary fibrosis. Our findings suggest that FUT8 may be a novel therapeutic target for pulmonary fibrosis.
Subject(s)
Fibrosis/genetics , Pericytes/metabolism , Animals , Disease Models, Animal , Humans , Mice , Signal TransductionABSTRACT
Objective To explore the application of medical bottle opener box (authorized patent for utility model) in nurses dispensing operations of opening the plastic bottle cap. Methods Put five self-made medical bottle opener box sample into the hospital emergency department for use. The nurses were divided into control group and experimental group according to the different way of open bottle caps; both groups were 33 nurses who did not turn out of emergency department 2 years nurses for a common object of study. The control group was the 33 nurses adopting the method of unarmed open medicine plastic bottle cap from April 2013 to March 2014. The experimental group was the 33 nurses with medical bottle opener box to open medicine plastic bottle caps from March 2014 to March 2015. The method of comparing two groups was to compare the nurse hands skin wear parts and wear symptoms for opening bottle caps, and make the nurses′satisfaction survey. Results For two groups, the nurse hands skin wear parts were in right hand, index finger and thumb;the number of nurses with finger thick skin in experimental group was lower than that in control group [21.2%(7/33) vs. 78.8%(26/33)], and there was significant difference,χ2=21.87, P<0.05.The number of pain [12.1%(4/33) vs. 54.5%(18/33)] and peeling [15.2%(5/33) vs.69.7%(23/33)] in experimental group were lower than those in control group, and there were significant differences, χ2=13.36, 20.09, P < 0.05. The experimental group eliminated the blisters and scratches, avoided hand bleeding trauma. The nurses′overall satisfaction in experimental group was 93.9% (31/33), and 63.6% (21/33) in control group,and there was significant difference, χ2=9.06, P<0.05. Conclusions Nurses using medical bottle opener box when opening the medicine bottle cap can relieve and reduce occupational injury on the finger skin of nurses, improve the nurse hand skin comfort, provide convenient operation safety, it is worth promoting.
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Objective To examine whether tissue inhibitor of metalloproteinases-1 (TIMP-1) is involved in arterial calcification of chronic renal failure (CRF) rats. Methods CRF model was induced in male Wistar rats by garage daily with 2% adenine 250 mg/kg. The calcification of aorta, femoral artery, renal artery and coronary artery was evaluated histomorphometrically by van Kossa-stained sections at 2-, 4-, 6- and 8-week respectively. RT-PCR and Western blot were used to observe the expressive levels of TIMP-1 mRNA and protein. Expressions of TIMP-1, osteopentin (OPN) and core binding factor α1 (Cbfα-1) protein were analyzed by immunhistochemistry. Results Serum urea nitrogen, creatinine, inorganic phosphate, calcium-phosphorus product and intact parathyroid hormone (iPTH) increased significantly in the model animals compared with control group after 2 weeks (P<0.01). Medial calcification was found in above four arteries of model groups after 6 weeks. RT-PCR and Western blot showed that TIMP-1 expression of model group was significantly higher than that of control group (P< 0.05), and obviously elevated in a time-dependent manner. The expression of TIMP-1 and OPN in calcified aortic smooth muscle cells increased obviously (P<0.05), and positive immunostaining of Cbfα-1 was found. The expression of TIMP-1 was positively correlated with OPN and Cbfα-1 (r=0.317, P=0.000; r=0.485, P=0.000). Conclusions The pathology of arterial calcification in CRF rats induced by adenine is similar to CRF patients, which may serve as a useful model of CRF with arterial calcification. The up-regulation of TIMP-1 seems to participate in the formation and development of vascular calcification in CRF.
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Objective To determine the efficacy of Non-invasive positive pressure ventilation(NPPV)in the management of patients with respiratory failure due to an acute exacerbation of chronic obstructive pulmonary disease(COPD).Methods Forty-two patients were included in the study.Of them,21 were randomly allocated to receive NPPV plus “standard care” and 21 to “standard care”.Both groups had similar characteristics upon their admission in the hospital.Results The use of NPPV significantly decreased the PaCO_2 level and respiratory rates,but significantly increased the PaO_2 level after 2 hours of treatment(P
