Negative refraction in hyperbolic hetero-bicrystals.

We visualized negative refraction of phonon polaritons, which occurs at the interface between two natural crystals. The polaritons-hybrids of infrared photons and lattice vibrations-form collimated rays that display negative refraction when passing through a planar interface between the two hyperbolic van der Waals materials: molybdenum oxide (MoO3) and isotopically pure hexagonal boron nitride (h11BN). At a special frequency ω0, these rays can circulate along closed diamond-shaped trajectories. We have shown that polariton eigenmodes display regions of both positive and negative dispersion interrupted by multiple gaps that result from polaritonic-level repulsion and strong coupling.

Fizeau drag in graphene plasmonics.

Dragging of light by moving media was predicted by Fresnel1 and verified by Fizeau's celebrated experiments2 with flowing water. This momentous discovery is among the experimental cornerstones of Einstein's special relativity theory and is well understood3,4 in the context of relativistic kinematics. By contrast, experiments on dragging photons by an electron flow in solids are riddled with inconsistencies and have so far eluded agreement with the theory5-7. Here we report on the electron flow dragging surface plasmon polaritons8,9 (SPPs): hybrid quasiparticles of infrared photons and electrons in graphene. The drag is visualized directly through infrared nano-imaging of propagating plasmonic waves in the presence of a high-density current. The polaritons in graphene shorten their wavelength when propagating against the drifting carriers. Unlike the Fizeau effect for light, the SPP drag by electrical currents defies explanation by simple kinematics and is linked to the nonlinear electrodynamics of Dirac electrons in graphene. The observed plasmonic Fizeau drag enables breaking of time-reversal symmetry and reciprocity10 at infrared frequencies without resorting to magnetic fields11,12 or chiral optical pumping13,14. The Fizeau drag also provides a tool with which to study interactions and nonequilibrium effects in electron liquids.

[The application status of optimal medical therapy after percutaneous coronary intervention and its influence on prognosis].

Objective: To investigate the application status of optimal medical therapy (OMT) in patients with coronary heart disease after percutaneous coronary intervention (PCI) and its influence on the 1-year prognosis of patients after surgery. Methods: Data of 3 812 patients diagnosed with coronary heart disease by coronary angiography and successfully completed PCI in the Department of Cardiology, TEDA International Cardiovascular Hospital from October 2016 to September 2017 were prospectively collected. The OMT status and the occurrence of major adverse cardiovascular and cerebrovascular events (MACCE) during the hospitalization and 1, 6, and 12 months after discharge were recorded. Patients were divided into OMT group (n=1 299) and non-OMT group (n=2 289) according to their adherence to OMT after PCI. Chi-square test was used to compare the differences of MACCE between groups, and to screen for significant differences and clinically significant variables between groups. Cox regression model was used to analyze the influencing factors of MACCE after PCI. Results: Among 3 588 patients (224 cases lost to follow-up), 58.8% (2 110/3 588) used OMT during hospitalization after PCI, and 36.0% (1 293/3 588) still adhered to OMT after 12 months of follow-up. The utilization rates of OMT showed a decreasing trend, among which till the 12th month, ß-blockers and ACEI/ARB showed the greatest decreasing degree, from 75.3%(2 701/3 588) and 75.1%(2 692/3 588) to 59.1%(2 122/3 588) and 53.0%(1 903/3 588). Pearson χ2 analysis showed that elderly patients, the number of amalgamative diseases, history of PCI, history of chronic myocardial infarction, history of chronic renal insufficiency, the lesion counts, lesion type, the Gensini score, adhere to the OMT and smoking during the follow-up were related to postoperative MACCE, the difference was statistically significant (P<0.05). Cox regression model showed that OMT adherence after PCI was an independent protective factor for postoperative MACCE events (HR=0.471,95%CI: 0.300-0.734, P=0.001). Conclusion: The application of OMT after PCI was suboptimal, and the application rate decreased with the lengthening of the discharge time, among which the use of ACEI/ARB and ß-blockers deserved more attention. Adherence to OMT after PCI was an independent protective factor, which could reduce the incidence of postoperative MACCE and improve the prognosis of patients.

MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-ß1 signaling pathway.

OBJECTIVE: To investigate the effects of micro ribonucleic acid (miR)-808 on cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction (MI) by regulating the transforming growth factor-ß1 (TGF-ß1) signaling pathway. MATERIALS AND METHODS: A total of 24 specific pathogen-free female Sprague-Dawley rats were enrolled and randomly divided into normal group, model group, and miR-808 group, 8 rats in each group. In the model group and miR-808 group, MI model was prepared by ligation of the left anterior descending coronary artery in the rats. The miR-808 group was transfected with miR-808 lentivirus after the model was established. After one week of intervention, the expression of TGF-ß1 was detected by reverse transcription-polymerase chain reaction (RT-PCR). The cardiac function of rats was determined by echocardiography. The myocardium of rats was observed by Masson staining. The cardiomyocyte apoptosis of rats was examined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The expression levels of caspase-3 and caspase-9 were detected by Western blotting. RESULTS: The expression of TGF-ß1 mRNA was higher in the model group than that in the normal group (p<0.05), but compared with that in the model group, it was lower in the miR-808 group. The myocardial function and cardiomyocyte survival rate in the miR-808 group was better and higher than those in the model group (p<0.05). The expression levels of caspase-3 and caspase-9 in the miR-808 group were lower than those in the model group (p<0.05). CONCLUSIONS: MiR-808 can inhibit cardiomyocyte apoptosis in rats with MI by down-regulating TGF-ß1 expression and inhibiting the expressions of caspase-3 and caspase-9.

STRAP reduces endoplasmic reticulum stress and apoptosis in cardiomyocytes and attenuates myocardial ischemia-reperfusion injury by activating PI3K/PDK1/Akt signaling pathway.

OBJECTIVE: Myocardial ischemia-reperfusion injury (MIRI) is a common problem in heart-related diseases. The aim of this study was to explore the protective effects of STRAP on cardiomyocytes in the MIRI process and its mechanisms. MATERIALS AND METHODS: We used SD rats to construct a MIRI model and increased the expression of STRAP in myocardial tissue by Entranster to detect the effect of STRAP on rat myocardial tissue. In addition, we cultured rat cardiomyocyte cell line H9c2 cells and constructed a hypoxia-reoxygenation model to detect the protective effect of STRAP on H9c2 cells. LY294002, an inhibitor of the PI3K/PDK1/Akt signaling pathway, was used to validate the mechanism by which STRAP protects cardiomyocytes. RESULTS: Overexpression of STRAP significantly reduced the activity of MDA in myocardial tissue and increased the activity of SOD. STRAP also substantially lowered CK and LDH levels in rat serum and increased Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity. In addition, overexpression of STRAP considerably reduced endoplasmic reticulum stress (ERS) and apoptosis levels in H9c2 cells. However, LY294002 attenuated the protective effect of STRAP on cardiomyocytes. CONCLUSIONS: STRAP reduces ERS and apoptosis in cardiomyocytes by activating the PI3K/PDK1/Akt signaling pathway, thereby reducing myocardial MIRI.

[The predictive value of epicardial adipose tissue and inflammatory factors for in-stent restenosis].

Objective: To investigate the predictive value of epicardial adipose tissue volume (EATV) and inflammatory factors on in-stent restenosis (ISR) after percutaneous coronary implantation (PCI) in patients with coronary heart disease (CAD). Methods: A total of 407 patients with CAD who were treated with drug-eluting stents in TEDA international cardiovascular disease hospital were enrolled from November 2016 to October 2017. Levels of inflammatory cytokines such as high sensitive c-reactive protein (Hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α) were detected. EATV was measured preoperatively by multi-sliced CT. Patients were divided into ISR group (n=52) and N-ISR group (n=355) according to ISR occurred within 1 year after procedure. The relationship between EATV and inflammatory factors and ISR after PCI was analyzed. Results: The differences between ISR group (n=52) and N-ISR group (n=355) were statistically significant in terms of diabetes history, IL-6, TNF-α, EATV ((150±36) cm(3)vs(120±40) cm(3),P=0.001)), bifurcation lesions, stent length and Gensini score (P<0.05). Multivariate Logistic regression analysis results showed that diabetes history,bifurcation lesions, TNF-α, EATV, and Gensini score were risk factors for in-stent restenosis.The area under the ROC curve (AUC) of EATV, TNF-α, and IL-6 in patients with CAD after PCI was 0.712, 0.752 and 0.675 (95%CI 0.648-0.776, 0.686-0.819, 0.584-0.766, respectively, all P<0.001), with a sensitivity of 86.5%, 67.3% and 69.2%, a specificity of 53.8%, 74.4% and 70.1% and a cut-off value of 116.61 cm(3),138.40 µg/L and 126.4 µg/L, respectively. Conclusion: EATV, TNF-α, and IL-6 have certain predictive values for in-stent restenosis, and can be used as clinical indicators to predict in-stent restenosis.

IL-6 knockout ameliorates myocardial remodeling after myocardial infarction by regulating activation of M2 macrophages and fibroblast cells.

OBJECTIVE: To investigate the effects of interleukin-6 (IL-6) gene knockout on myocardial remodeling after myocardial infarction (MI) in mice and the potential mechanism, to provide certain references for the prevention and treatment of MI in clinic. MATERIALS AND METHODS: A total of 40 male C57 mice were divided into two groups, namely Sham group (n=20) and MI group (n=20), using a random number table. Another 20 mice with IL-6 gene knockout were enrolled into the MI + IL-6 KO group. The MI model was established by means of ligating the left anterior descending coronary artery of the mice. 28 d later, the survival status of the three groups of mice was recorded. In addition, the cardiac functions of each group of mice, including two-dimensional echocardiography, ejection fraction (EF%) and fractional shortening (FS%), were measured. The cross-sectional area and pathological change of the myocardial cells in cardiac tissues of each group of mice were detected via hematoxylin and eosin (H&E) staining. Immunohistochemistry was applied to determine the expression of tumor necrosis factor-alpha (TNF-α) in each group of mouse cardiac tissues. Moreover, immunofluorescent staining was utilized to measure the content of M2 macrophages in each group of mouse cardiac tissues. RESULTS: The 28-d survival rate of the mice with IL-6 gene knockout was remarkably higher than that of the wild-type mice (p<0.05). Furthermore, the cardiac functions of the mice in the MI + IL-6 KO group were superior to those in the MI group, with markedly improved FS% and EF% (p<0.05). According to the H&E staining results, the cross-sectional areas of the heart and myocardial cells were decreased notably in MI + IL-6 KO group compared with those in the MI group (p<0.05). The immunohistochemical staining results showed that IL-6 knockout could lower the MI-induced high expression of TNF-α (p<0.05), and Masson's trichrome staining indicated that IL-6 knockout could also repress the degree of cardiac fibrosis. Moreover, it was discovered through immunofluorescent staining that the mice in the MI + IL-6 KO group had markedly elevated content of M2 macrophages in cardiac tissues than those in the MI group (p<0.05). CONCLUSIONS: Inhibiting IL-6 gene expression can prominently ameliorate the MI-induced myocardial remodeling, whose mechanism is possibly associated with the activation of M2 macrophages and reduced collagen production in fibroblast cells.

Downregulated miRNA-26a-5p induces the apoptosis of endothelial cells in coronary heart disease by inhibiting PI3K/AKT pathway.

OBJECTIVE: Multiple microRNAs (miRNAs) are abnormally expressed in endothelial cells during the occurrence of coronary artery disease (CAD). Previous researches have demonstrated that miRNA-26a-5p participates in regulating the proliferation of vascular smooth muscle cells and angiogenesis. The aim of this study was to clarify the role of miRNA-26a-5p in regulating cellular performances of endothelial cells in the progression of CAD. PATIENTS AND METHODS: In vivo CAD model was successfully established by feeding high-fat diet in 8-week-old female ApoE/LDLR-/- mice. CAD mice were administered with miRNA-26a-5p NC or miRNA-26a-5p inhibitor, respectively. Meanwhile, coronary endothelial cells were isolated from CAD mice and normal controls. Relative levels of miRNA-26a-5p, the gene of phosphate and tension homology deleted on chromosome ten (PTEN) and vascular endothelial growth factor (VEGF) in CAD patients and coronary endothelial cells isolated from CAD mice were examined. The regulatory effect of miRNA-26a-5p on atherosclerosis-related genes in primary endothelial cells and HUVECs were detected as well. Moreover, the viability and apoptosis of primary endothelial cells with miRNA-26a-5p knockdown were assessed by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Dual-luciferase reporter gene assay was conducted to identify the relationship between miRNA-26a-5p and PTEN. Furthermore, the regulatory role of miRNA-26a-5p in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway was examined in endothelial cells. RESULTS: MiRNA-26a-5p and VEGF were significantly downregulated in CAD patients and primary endothelial cells isolated from CAD mice. However, PTEN was significantly upregulated. CAD mice administrated with miRNA-26a-5p inhibitor exhibited remarkably upregulated ET-1, TxA2, and ANG II, as well as downregulated eNOS and PGI2. Conversely, transfection of miRNA-26a-5p mimics in HUVECs obtained the opposite trends. PTEN was identified as the direct target gene of miRNA-26a-5p. Moreover, significantly reduced viability and enhanced apoptotic rate were observed in endothelial cells isolated from CAD mice administrated with miRNA-26a-5p inhibitor. In addition, the protein level of p-AKT in endothelial cells with miRNA-26a-5p knockdown was significantly down-regulated. CONCLUSIONS: MiRNA-26a-5p influences the proliferative and apoptotic abilities of endothelial cells isolated from CAD mice by targeting PTEN to activate PI3K/AKT pathway.

Imaging the nanoscale phase separation in vanadium dioxide thin films at terahertz frequencies.

Vanadium dioxide (VO2) is a material that undergoes an insulator-metal transition upon heating above 340 K. It remains debated as to whether this electronic transition is driven by a corresponding structural transition or by strong electron-electron correlations. Here, we use apertureless scattering near-field optical microscopy to compare nanoscale images of the transition in VO2 thin films acquired at both mid-infrared and terahertz frequencies, using a home-built terahertz near-field microscope. We observe a much more gradual transition when THz frequencies are utilized as a probe, in contrast to the assumptions of a classical first-order phase transition. We discuss these results in light of dynamical mean-field theory calculations of the dimer Hubbard model recently applied to VO2, which account for a continuous temperature dependence of the optical response of the VO2 in the insulating state.

[Effects of epicardial adipose tissue and inflammatory factors on left ventricular diastolic function in patients with coronary heart disease].

Objective: To investigate the effects ofepicardial adipose tissue volume (EATV) and inflammatory factors on left ventricular diastolic function in patients with coronary heart disease(CHD). Methods: The clinical data of patients with coronary heart disease receiving coronary artery intervention therapy from January 2014 to October 2015 in TEDA international cardiovascular hospital were preoperatively collected.We measured the indexes of EATV and left ventricular diastolic function. Results: The difference of age (F=7.76, P=0.01), IL-6 (F=14.34, P<0.01), Hs-CRP (F=4.08, P=0.04), adiponect-in (F=4.50, P=0.04) and EATV (F=71.29, P<0.01) between the diastolicdysfunction group (n=156) and the normal group (n=76) was statistically significant.Multivariate logistic regression analysis showed that EATV was a risk factor for left ventricular diastolic dysfunction in patients with coronary artery disease (P<0.05), OR=1.05, 95%CI (1.03-1.06). The AUC value of EATV in the diagnosis of left ventriculardiastolic function in patients with coronary heart disease was 0.79, 95%CI (0.73-0.85) P<0.01. Conclusions: EATV can be used as an independent risk factor for left ventricular diastolic dysfunction.It has some non-invasive diagnosis and predictive value, and it can be used as a new therapeutic target.

[Study on the efficiency of tertiary public hospitals and its influencing factors in Beijing].

OBJECTIVE: To evaluate the comprehensive technical efficiency of the tertiary public hospitals in Beijing between 2006 and 2015 and explore its influencing factors, so as to propose corresponding policy suggestions. METHODS: The data envelopment analysis was employed to evaluate the comprehensive technical efficiency, pure technical efficiency and scale efficiency of the tertiary public hospitals in Beijing. Malmquist index model was used to analyze the changes of the above three dynamic efficiencies. Finally, randomeffect panel tobit model was utilized to analyze the influencing factors of the comprehensive technical efficiency. RESULTS: The average comprehensive technical efficiency and pure technical efficiency of the tertiary public hospitals in Beijing were relatively high, and they had respectively increased from 0.44 and 0.51 in 2006 to 0.62 and 0.68 in 2015, and the highest proportion of two kinds of efficiency values was between 0.5 and 0.8. Most of the scale efficiency values distributed between 0.8 and 1.0, and the majority of hospitals were in a state of decreasing returns to scale. The total factor productivity of hospitals had been increasing at an average rate of 5.78% per year due to the double progress of technical efficiency and technology at annual rates of 3.77% and 1.94% respectively, further decomposing technological efficiency change, and the pure technical efficiency change increased at the speed of 3.21% per year, and the annual average rate of progress in scale efficiency was only 0.53%. The comprehensive technical efficiency was positively correlated with the turnover rate of beds, annual visits per doctor, the ratio of doctors to nurses, and negatively correlated with the number of beds, the ratio of outpatients to inpatients, the proportion of medical technical personnel, and the proportion of drugs. CONCLUSION: Future health policies should strictly control the scale of tertiary public hospitals, pay attention to the innovation and application of hospital technology, change the hospital internal management level and management model, promote refined management, and achieve sustainable development.

[Relationship between epicardial adipose tissue and clinical prognosis of patients with coronary heart disease after percutaneous coronary intervention].

Objective: To further evaluate the clinical value of epicardial adipose tissue volume (EATV) in predicting the prognosis of coronary heart disease (CHD) after percutaneous coronary intervention (PCI). Methods: From July 2013 to July 2016 in TEDA International Cardiovascular Disease Hospital, a total of 474 patients diagnosed with CHD were included in this study.According to the result of EATV, patients were divided into three groups, group A (EATV≤75 ml), group B (75 ml120.39 ml can be used as an independent risk factor for predicting the occurrence of MACE. Conclusion: The level of EATV is closely related to the occurrence of MACE events, and EATV>120.39 ml is an independent risk factor for MACE in patients with CHD after PCI.

[Exploratory study of circulating tumor DNA detection in early breast cancer: an analysis of 75 next-generation sequencing results].

Objective: To explore the utility of circulating tumor DNA detection in early breast cancer by using next-generation sequencing. Methods: This exploratory study of circulating tumor DNA detection is for early invasive breast cancer patients treated in Breast Disease Center, Peking University First Hospital from December 2015 to July 2016. Plasma samples were collected and were used to isolate plasma cell-free DNA.Exons or hotspots of 247 cancer related genes were sequenced by next-generation sequencing. Mutations and their correlation with clinic-pathological factors were analyzed. The correlation between mutations and clinic-pathological factors was evaluated by χ(2) test or Fisher's exact test. Results: Seventy-five patients were enrolled in this study. All patients were female and aged from 31 to 88 years with median age of 58 years. All patients' clinic-pathological records were complete. Sixty-four mutations in 18 genes (ALK, BCR, ERBB2, ROS1, PDGFRA, EGFR, FGFR2, CYP1B1, CALR, CASP7, BRAF, FGFR1, FGFR3, MET, NRAS, PTEN, KIT, SOD2) were detected in 47 (62.7%) among all 75 patients.Exons were captured in 10 genes, and mutations in 2 of 3 genes analyzed were clustered. Gene mutations were not correlated with menopausal status, histological type, primary tumor (T), regional lymph nodes (N), TNM stage, histological grade, estrogen receptor status, progesterone receptor status, human epidermal growth factor receptor 2 status, Ki-67 and molecular subtype (all P>0.05). Conclusion: Circulating tumor DNA sequencing by next-generation sequencing was useful for detecting breast cancer-related mutations.

CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.

Myocardial ischemia is a major cause of death and remains a disease with extremely deficient clinical therapies and a major problem worldwide. Cold inducible RNA-binding protein (CIRBP) is reported to be involved in multiple pathological processes, including myocardial ischemia. However, the molecular mechanisms of myocardial ischemia remain elusive. Here, we first overexpressed CIRBP by transfection of pc-CIRBP (pcDNA3.1 containing coding sequenced for CIRBP) and silenced CIRBP by transfection of small interfering RNA targeting CIRBP (siCIRBP). pcDNA3.1 and the negative control of siCIRBP (siNC) were transfected into H9C2 cells to act as controls. We then constructed a cell model of myocardial ischemia through culturing cells in serum-free medium with hypoxia in H9C2 cells. Subsequently, AlamarBlue assay, flow cytometry and western blot analysis were used, respectively, to assess cell viability, reactive oxygen species (ROS) level and apoptosis, and expression levels of IκBα, p65 and Bcl-3. We demonstrated that CIRBP overexpression promoted cell proliferation (P<0.001), inhibited cell apoptosis (P<0.05), reduced ROS level (P<0.001), down-regulated phosphorylated levels of IκBα and p65 (P<0.01 or P<0.001), and up-regulated expression of Bcl-3 (P<0.001) in H9C2 cells with myocardial ischemia. The influence of CIRBP knockdown yielded opposite results. Our study revealed that CIRBP could protect H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.

CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-kappaB pathway

Myocardial ischemia is a major cause of death and remains a disease with extremely deficient clinical therapies and a major problem worldwide. Cold inducible RNA-binding protein (CIRBP) is reported to be involved in multiple pathological processes, including myocardial ischemia. However, the molecular mechanisms of myocardial ischemia remain elusive. Here, we first overexpressed CIRBP by transfection of pc-CIRBP (pcDNA3.1 containing coding sequenced for CIRBP) and silenced CIRBP by transfection of small interfering RNA targeting CIRBP (siCIRBP). pcDNA3.1 and the negative control of siCIRBP (siNC) were transfected into H9C2 cells to act as controls. We then constructed a cell model of myocardial ischemia through culturing cells in serum-free medium with hypoxia in H9C2 cells. Subsequently, AlamarBlue assay, flow cytometry and western blot analysis were used, respectively, to assess cell viability, reactive oxygen species (ROS) level and apoptosis, and expression levels of IκBα, p65 and Bcl-3. We demonstrated that CIRBP overexpression promoted cell proliferation (P<0.001), inhibited cell apoptosis (P<0.05), reduced ROS level (P<0.001), down-regulated phosphorylated levels of IκBα and p65 (P<0.01 or P<0.001), and up-regulated expression of Bcl-3 (P<0.001) in H9C2 cells with myocardial ischemia. The influence of CIRBP knockdown yielded opposite results. Our study revealed that CIRBP could protect H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.

[Situation of long-term use of oral anticoagulation among atrial fibrillation patients with stroke in different level hospital].

OBJECTIVE: To investigate the current situation, time trends and factors associated with long-term use of oral anticoagulation (OAC) among atrial fibrillation (AF) patients with ischemic stroke. METHODS: We used the dataset from the CAFR (Chinese Atrial Fibrillation Registry), a prospective, multicenter, hospital-based registry study involving 20 tertiary and 12 nontertiary hospitals in Beijing. In brief, 380 consecutive AF patients with following ischemic stroke were enrolled from 2003 to 2014.Patients with valvular AF, radiofrequency catheter ablation history or contraindications of OAC were excluded. We divided the patients into two groups according to hospital level, and investigated the rate of OAC use and its change over time in patients who had indication, the factors including patient characteristics and hospital level associated with OAC use were also analyzed. RESULTS: Overall oral anticoagulation use rate was 27.71%, which dropped to 22.11% and 15.26% at 6 months and 12 months, respectively.A total of 298 participates were enrolled from tertiary hospitals (78.42%), and 82 were enrolled from nontertiary hospitals. The status of OAC use in tertiary hospitals was better than nontertiary hospitals (32.66% vs 7.32%, P<0.001). Multivariable analysis showed better oral anticoagulation use was independently associated with higher-level hospitals (odds ratio 1.785, 95% confidence interval 1.026-3.106, P=0.040), and history of heart failure (odds ratio 2.247, 95% confidence interval 1.235-4.090, P=0.008). CONCLUSIONS: These data indicates oral anticoagulation use has improved in atrial fibrillation patients with stroke in Beijing. The use of anticoagulation among the patients from tertiary hospitals is significantly better than those from nontertiary hospitals, and the history of heart failure may have effect on the use of oral anticoagulation.

The incidence and economic burden of injuries in Jiangxi, China.

OBJECTIVES: This study estimated the incidence, direct medical and non-medical costs, and productivity losses due to morbidity and mortality across multiple strata for injuries that occurred in Jiangxi, China. STUDY DESIGN: Cross-sectional study. METHODS: Data came from the Jiangxi injury survey, a provincially-representative, population-based sample of 100,010 households. The major economic costs of injuries were divided into direct costs and indirect costs. Direct costs encompass medical costs and direct non-medical costs. Indirect costs refer to the productivity losses due to injury-related morbidity and mortality. RESULTS: In 2005, about one of 18 residents in Jiangxi, China, experienced an injury. Overall, fall, animal bite, and road traffic crash (RTC) injuries accounted for more than 66% of all injuries, while fall, RTC, drowning, and self-harm injuries accounted for 80% of fatal injuries. Average cost per case for a fatal injury was 163,389 RMB ($20,171) for lost productivity and 2800 RMB ($346) in direct medical & non-medical costs. A non-fatal injury resulting in hospitalisation or permanent disability on average caused 5221 RMB ($643) in direct costs and 18,437 RMB ($2276) in lost productivity and, an additional loss of three school days. A non-hospitalised non-fatal injury on average caused 303 ($37) RMB in direct costs and 491 RMB ($61) in lost productivity and, an additional loss of 0.5 school days. CONCLUSIONS: The unequivocal evidence of the substantial health and financial burden of injuries indicates to Chinese policy makers that more research and efforts are needed to find efficacious and cost-effective interventions targeting injury.

Insights on Flow Behavior of Foam in Unsaturated Porous Media during Soil Flushing.

One-dimensional column and two-dimensional tank experiments were carried out to determine (1) the physics of foam flow and propagation of foaming gas, foaming liquid, and foam; (2) the pressure distribution along foam flow and the effect of media permeability, foam flow rate and foam quality on foam injection pressure; and (3) the migration and distribution property of foam flow in homogeneous and heterogeneous sediments. The results demonstrated that: (1) gas and liquid front were formed ahead of the foam flow front, the transport speed order is foaming gas > foaming liquid > foam flowing; (2) injection pressure mainly comes from the resistance to bubble migration. Effect of media permeability on foam injection pressure mainly depends on the physics and behavior of foam flow; (3) foam has a stronger capacity of lateral spreading, besides, foam flow was uniformly distributed across the foam-occupied region, regardless of the heterogeneity of porous media.

Genetic diversity in European Pisum germplasm collections.

The distinctness of, and overlap between, pea genotypes held in several Pisum germplasm collections has been used to determine their relatedness and to test previous ideas about the genetic diversity of Pisum. Our characterisation of genetic diversity among 4,538 Pisum accessions held in 7 European Genebanks has identified sources of novel genetic variation, and both reinforces and refines previous interpretations of the overall structure of genetic diversity in Pisum. Molecular marker analysis was based upon the presence/absence of polymorphism of retrotransposon insertions scored by a high-throughput microarray and SSAP approaches. We conclude that the diversity of Pisum constitutes a broad continuum, with graded differentiation into sub-populations which display various degrees of distinctness. The most distinct genetic groups correspond to the named taxa while the cultivars and landraces of Pisum sativum can be divided into two broad types, one of which is strongly enriched for modern cultivars. The addition of germplasm sets from six European Genebanks, chosen to represent high diversity, to a single collection previously studied with these markers resulted in modest additions to the overall diversity observed, suggesting that the great majority of the total genetic diversity collected for the Pisum genus has now been described. Two interesting sources of novel genetic variation have been identified. Finally, we have proposed reference sets of core accessions with a range of sample sizes to represent Pisum diversity for the future study and exploitation by researchers and breeders.

Identification of microRNA-target interaction in APRIL-knockdown colorectal cancer cells.

MicroRNAs (miRNAs) regulate mammalian gene expression by targeting mRNAs and have key roles in several cellular processes, including differentiation, development, apoptosis and cancer pathomechanisms. Our previous studies have confirmed that a proliferation-inducing ligand (APRIL) gene is overexpressed in colorectal cancer (CRC) tumors and SW480 cells. To study the potential mechanisms of APRIL gene in the occurrence and development of the CRC, herein, we investigated whether APRIL-knockdown had the inhibitory effect on the growth of SW480 cells and had the simultaneous expression changes of miRNAs and mRNAs by microarrays. Our results suggest that siRNA-APRIL can effectively inhibit the growth of SW480 cells in vitro and in vivo and several miRNAs via specific pathways might be involved in regulating the phenotype of loss-of-function in APRIL-knockdown SW480 cells. Thus, our study highlights the possible mechanisms of miRNA-target regulating the function of APRIL gene in CRC cells, moreover, siRNA-APRIL holds great promise as a novel gene therapy approach for APRIL- positive CRC treatment.