Search

Aiming at the characteristics that the signal noise ratio (SNR) gradually decreases from the near to far range of the swath, an adaptive phase filtering algorithm based on Goldstein filtering and combined with multiple quality-guided graphs was proposed. Firstly, the components used to determine the filtering parameters were obtained through residue density, pseudo-coherence coefficient and pseudo-SNR, the three quality-guided graphs. Then, the filter parameters were calculated by weighting the three components. Finally, the size of filtering window was determined according to the account of residues, and the interferometric phase noise was removed in frequency domain. Simulated data, TSX/TDX data and airborne interferometric imaging radar altimeter data were used to verify the performance of the new algorithm. Compared with the results of Goldstein filtering and its improved algorithms, the results showed that the proposed algorithm can effectively filter out phase noise while maintaining the edge characteristics of interferometric fringe. The section of filtering result can well match with the section of simulated pure interfeometric phase. Moreover, the algorithm proposed in this paper can effectively remove the noise in the interferogram of TSX/TDX sea ice data, and the residues' filtering rate was above 86%, which can effectively remove the phase residues of the sea ice surface while maintaining the characteristics of the sea ice edge. Experimental results showed that the new algorithm provides an effective phase noise filtering method for imaging radar altimeter data processing.

BackgroundWith the widespread use of broad-spectrum antibiotics, the problem of bacterial resistance has become a global crisis. To monitor bacterial resistance in our hospital, the distribution of specimens, the detection of pathogens and their drug resistance from July 2005 to June 2007 (13 years ago) and July 2018 to June 2020 were compared and analyzed.MethodsOrdinary specimens (such as sputum, urine, feces, and secretion) were inoculated in blood AGAR media, MacConkey medium, chocolate medium, double SS medium and selective culture medium. Blood, cerebrospinal fluid, pleural effusion, joint cavity effusion and other sterile body fluid samples were inoculated in aerobic and anaerobic blood culture flasks. Automatic microbial identification, drug sensitivity analysis and mass spectrometry analysis were used to determine their drug sensitivity.ResultsCompared with the results obtained 13 years ago, the number of specimens submitted for inspection in the past two years has increased significantly, exhibiting a growth rate of 283%. The changes in the pathogen species were obvious. Gram-positive cocci were the dominant bacteria 13 years ago, and Gram-negative bacilli were the dominant bacteria in the past two years. In addition, the resistance of several major Gram-negative bacilli to piperacillin/tazobactam, cefoperazone/sulbactam, meropenem and imipenem all showed an increasing trend.ConclusionThe variety of pathogenic bacteria in our hospital has changed significantly in the past two years compared with that 13 years ago, and the clinical isolates of Gram-negative bacilli have increased significantly compared with Gram-positive cocci. In the clinical treatment of anti-infective diseases, antimicrobial agents should be selected according to the bacterial distribution characteristics and drug resistance in each hospital.

Circulating endothelial cells (CECs) are markers of vascular damage that have clinical relevance in many diseases, including acute myocardial infarction (AMI), and may be predictors of treatment responses. Herein, we investigated the diagnostic and prognostic value of CEC monitoring in AMI patients and a murine model.CECs were defined as Hoechst 33342(+)/CD45(-/)CD31(+)/CD146(+)/CD133(-) in human blood samples and Hoechst 33342(+)/CD45(-/)CD31(+)/KDR(+)/CD117(-) in murine samples. To evaluate the validity and variability of our CEC detection system, peripheral blood samples of vascular endothelial growth factor-treated athymic nude mice and AMI patients were collected and subjected to intra-assay analysis. CEC detection by flow cytometry and real-time PCR were compared. Blood samples were obtained from 61 AMI patients, 45 healthy volunteers and 19 samples of the original AMI patients accepted one month treatment, via flow cytometry and expressed as a percentage of peripheral blood mononuclear cells.Our CEC detection method was validated and had limited variability. CEC concentrations were higher in AMI patients compared to healthy controls. One month post-treatment, CECs levels decreased significantly.CEC levels may be useful as a diagnostic and prognostic biomarker in AMI patients.

Hydrogen sulfide, as a novel gaseous mediator, has been suggested to play a key role in atherogenesis. However, the precise mechanisms by which H(2)S affects atherosclerosis remain unclear. Therefore, the present study aimed to investigate the potential role of H(2)S in atherosclerosis and the underlying mechanism with respect to chemokines (CCL2, CCL5 and CX3CL1) and chemokine receptors (CCR2, CCR5, and CX3CR1) in macrophages. Mouse macrophage cell line RAW 264.7 or mouse peritoneal macrophages were pre-incubated with saline or NaHS (50 µM, 100 µM, 200 µM), an H(2)S donor, and then stimulated with interferon-γ (IFN-γ) or lipopolysaccharide (LPS). It was found that NaHS dose-dependently inhibited IFN-γ or LPS-induced CX3CR1 and CX3CL1 expression, as well as CX3CR1-mediated chemotaxis in macrophages. Overexpression of cystathionine γ-lyase (CSE), an enzyme that catalyzes H(2)S biosynthesis resulted in a significant reduction in CX3CR1 and CX3CL1 expression as well as CX3CR1-mediated chemotaxis in stimulated macrophages. The inhibitory effect of H(2)S on CX3CR1 and CX3CL1 expression was mediated by modulation of proliferators-activated receptor-γ (PPAR-γ) and NF-κB pathway. Furthermore, male apoE(-/-) mice were fed a high-fat diet and then randomly given NaHS (1 mg/kg, i.p., daily) or DL-propargylglycine (PAG, 10 mg/kg, i.p., daily). NaHS significantly inhibited aortic CX3CR1 and CX3CL1 expression and impeded aortic plaque development. NaHS had a better anti-atherogenic benefit when it was applied at the early stage of atherosclerosis. However, inhibition of H(2)S formation by PAG increased aortic CX3CR1 and CX3CL1 expression and exacerbated the extent of atherosclerosis. In addition, H(2)S had minimal effect on the expression of CCL2, CCL5, CCR2 and CCR5 in vitro and in vivo. In conclusion, these data indicate that H(2)S hampers the progression of atherosclerosis in fat-fed apoE(-/-) mice and downregulates CX3CR1 and CX3CL1 expression on macrophages and in lesion plaques.

Hydrogen sulfide (H(2)S), as a novel gaseous mediator, plays important roles in mammalian cardiovascular tissues. In the present study, we investigated the cardioprotective effect of S-diclofenac (2-[(2,6-dichlorophenyl)amino] benzeneacetic acid 4-(3H-1,2,dithiol-3-thione-5-yl)phenyl ester), a novel H(2)S-releasing derivative of diclofenac, in a murine model of doxorubicin-induced cardiomyopathy. After a single dose injection of doxorubicin (15 mg/kg, i.p.), male C57BL/6J mice were given daily treatment of S-diclofenac (25 and 50 µmol/kg, i.p.), diclofenac (25 and 50 µmol/kg, i.p.), NaHS (50 µmol/kg, i.p.), or same volume of vehicle. The cardioprotective effect of S-diclofenac was observed after 14 days. It showed that S-diclofenac, but not diclofenac, dose-dependently inhibited the doxorubicin-induced downregulation of cardiac gap junction proteins (connexin 43 and connexin 45) and thus reversed the remodeling of gap junctions in hearts. It also dose-dependently suppressed doxorubicin-induced activation of JNK in hearts. Furthermore, S-diclofenac produced a dose-dependent anti-inflammatory and anti-oxidative effect in this model. As a result, S-diclofenac significantly attenuated doxorubicin-related cardiac injury and cardiac dysfunction, and improved the survival rate of mice with doxorubicin-induced cardiomyopathy. These effects of S-diclofenac were mimicked in large part by NaHS. Therefore, we propose that H(2)S released from S-diclofenac in vivo contributes to the protective effect in doxorubicin-induced cardiomyopathy. These data also provide evidence for a critical role of H(2)S in the pathogenesis of doxorubicin-induced cardiomyopathy.