DMO和叠前时间偏移的共同起点

DMO和叠前时间偏移对于改善速度分析及叠加效果,最终提高剖面成像质量都是很有用的工具,一般在共偏移距道集中进行。其实现方法有多种,如等价偏移距方法（equivalent offset migration,Bancroft et al,1994)、DMO PSI(prestack imaging)方法（Gardner,1986）和非成像的炮集偏移（non-imaging shot-record migration,Berryhill,1996）等。这些方法的一个共同特点是用一个新定义的偏移距替代原来的偏移距。在每一种方法中,成像过程都归结为以新偏移距定义的共反射点双曲线型时－距关系上的动校正。本文中,我们证明了不同方法的DMO和叠前时间偏移有其共同起点－－双平方根算子,说明它们在原理上是等价的;最后我们提出了基于波动方程的DMO和叠前时间偏移方法。     

LATITUDINAL VARIATION OF DEEP SCATTERING LAYER IN THE WESTERN PACIFIC

The acoustic Echo Intensity (EI) was recorded with 38k shipborne Acoustic Doppler Current Profiler (ADCP) in the Western Pacific in four cruises between Sept. 2001 and Oct. 2002. The main Deep Scattering Layer (DSL) was observed at 400m-600 m depth in the four cruises. The latitudinal variation of the main DSL, which has high level of backscatter strength (BS) at high latitude, is prominent during both nighttime and daytime. The influences of environmental conditions on the DSL are discussed. Since high-oxygen water in the north is a friendly environment of marine animals which form the main DSL, more animals are expected to aggregate in the 400dbars-600dbars layer in the north. Dissolved Oxygen (DO) is the principal factor that causes the main DSL to vary with latitude, and its spatial distributions result from formation and transport of North Pacific Intermediate Water (NPIW).     

Estimation of Separation of Electrolytes and Organic Compounds by Nanofiltration Membranes Using an Irreversible Thermodynamic Modei

Nanofiltration separation has become a popular technique for removing large organic molecules and inorganic substances from water. It is achieved by a combination of three mechanisms: electrostatic repulsion, sieving and diffusion. In the present work, a modei based on irreversible thermodynamics is extended and used to estimate rejection of inorganic salts and organic substances. Binary systems are modeled, where the feed contains an ion that is much less permeable to the membrane as compared with the other ion. The two modei parameters are estimated by fitting the modei to the experimental data. Variation of these parameters with the composition of the feed is described by an empirical correlation. This work attempts to describe transport through the nanofiltration membranes by a simple model.     

杂质Fe对A1-Zn-In牺牲阳极性能的影响

炼制Fe杂质含量不同的6种Al-Zn-In阳极,采用恒电流方去评价了其电化学性能,并通过扫描电镜观察其溶解的微观形貌,探讨了Fe杂质含量对阳极电化学性能的影响规律与机制.结果表明,随着Fe杂质含量的升高,Al-Zn-In阳极的电流效率呈先增加后降低趋势,原因足少量的Fe可增加阳极的活化点,而过量的Fe则作为阴极相引发电偶腐蚀使得阳极呈局部腐蚀溶解.     

模拟深海压力对2种低合金钢腐蚀行为的影响

通过腐蚀失重、电化学测试、锈层分析和微观形貌观察研究了海水压力对不同成分2种低合金钢(X和Y)腐蚀行为的影响.结果表明,X钢更易受到海水压力的影响而被加速腐蚀.深海压力均加速了2种低合金钢的阳极溶解速度;压力对于X钢的氧扩散还原过程影响很小,而海水压力的增加导致Y钢阴极电流密度降低的原因是腐蚀产物直接参与了阴极还原反应...     

Spermine Derivatives of Indole-3-carboxylic Acid,Indole-3-acetic Acid and Indole-3-acrylic Acid as Gram-Negative Antibiotic Adjuvants

The discovery of new antibiotic adjuvants is an attractive option for overcoming antimicrobial resistance. We have previously reported the discovery of a bis-6-bromoindolglyoxylamide derivative of spermine as being able to enhance the action of antibiotics against Gram-negative bacteria but suffers from being cytotoxic and red-blood cell haemolytic. A series of analogues was prepared exploring variation of the indolglyoxylamide unit, to include indole-3-acrylic, indole-3-acetic and indole-3-carboxylate units, and evaluated for antibiotic enhancing properties against a range of Gram-negative bacteria, and for intrinsic antimicrobial, cytotoxic and haemolytic properties. Two spermine derivatives, bearing 5-bromo-indole-3-acetic acid ( 17 ) and 5-methoxy-indole-3-acrylic acid ( 14 ) end groups were found to exhibit good to moderate antibiotic adjuvant activities for doxycycline towards the Gram-negative bacteria Pseudomonas aeruginosa, Escherichia coli and Klebsiella pneumoniae, but with more modest intrinsic antimicrobial activity and greatly reduced cytotoxic and haemolytic properties. The mechanism of action of the latter derivative identified its ability to disrupt the outer membranes of bacteria and to inhibit the AcrAB-TolC efflux pump directly or by inhibiting the proton gradient.     

MicroRNA and Hemostasis Profile of Carotid Atherosclerosis

Carotid atherosclerosis (CA) is an important risk factor for ischemic stroke. We described the miRNA and hemostasis profile of patients with moderate and advanced stages of carotid atherosclerosis and elucidated potential correlations with hemostatic activation. A prospective case-control study included 61 patients with evidence of carotid atherosclerosis (via ultrasound). The study population was divided into groups depending on the degree of carotid artery stenosis: 60% or more (advanced) and <60% (moderate). All patients underwent the following blood tests: general blood test, hemostatic parameters and microRNA. Extraction of microRNA was performed using Leukocyte RNA Purification Kit (NORGEN Biotec Corp., Thorold, ON, Canada); miRNA quantification was performed via RT-PCR. Statistical analysis was performed in R programming language (v. 4.1.0) using RSudio. MicroRNA expression profile was different depending on CA degree. MiR-33a-5p/3p levels were higher in patients with ≥60% carotid stenosis (42.70 and 42.45 versus 38.50 and 38.50, respectively, p < 0.05). Almost complete separation can be visualized with the levels of miR-126-5p: 9.50 in the moderate CA group versus 5.25 in the advanced CA (p < 0.001). MiR-29-5p was higher in the moderate CA group: 28.60 [25.50;33.05] than in advanced CA group: 25.75 [24.38;29.50] (p = 0.086); miR-29-3p was also higher in the moderate CA group: 10.36 [8.60;14.99] than in advanced CA group: 8.46 [7.47;10.3] (p = 0.001). By-group pairwise correlation analyses revealed at least three clusters with significant positive correlations in the moderate CA group: miR-29-3p with factors V and XII (r = 0.53 and r = 0.37, respectively, p < 0.05); miR-21-5p with ADAMTS13, erythrocyte sedimentation rate and D-dimer (r = 0.42, r = 0.36 and r = 0.44, respectively, p < 0.05); stenosis degree with miR-33a-5p/3p and factor VIII levels (r = 0.43 (both) and r = 0.62, respectively, p < 0.05). Hemostasis parameters did not reveal significant changes in CA patients: the only statistically significant differences concerned factor VIII, plasminogen and (marginally significant) ADAMTS-13 and protein C. Down-regulation of miR-126-5p expression has been identified as a promising biomarker of advanced carotid atherosclerosis with high specificity and sensitivity. Correlation cluster analysis showed potential interplay between miRNAs and hemostatic activation in the setting of carotid atherosclerosis.     

A New Manganese Superoxide Dismutase Mimetic Improves Oxaliplatin-Induced Neuropathy and Global Tolerance in Mice

Reactive oxygen species (ROS) are produced by every aerobic cell during mitochondrial oxidative metabolism as well as in cellular response to xenobiotics, cytokines, and bacterial invasion. Superoxide Dismutases (SOD) are antioxidant proteins that convert superoxide anions (O₂^•−) to hydrogen peroxide (H₂O₂) and dioxygen. Using the differential in the level of oxidative stress between normal and cancer cells, SOD mimetics can show an antitumoral effect and prevent oxaliplatin-induced peripheral neuropathy. New Pt(IV) conjugate prodrugs (OxPt-x-Mn1C1A (x = 1, 1-OH, 2)), combining oxaliplatin and a Mn SOD mimic (MnSODm Mn1C1A) with a covalent link, were designed. Their stability in buffer and in the presence of sodium ascorbate was studied. In vitro, their antitumoral activity was assessed by the viability and ROS production of tumor cell lines (CT16, HCT 116, KC) and fibroblasts (primary culture and NIH 3T3). In vivo, a murine model of colorectal cancer was created with subcutaneous injection of CT26 cells in Balb/c mice. Tumor size and volume were measured weekly in four groups: vehicle, oxaliplatin, and oxaliplatin associated with MnSODm Mn1C1A and the bis-conjugate OxPt-2-Mn1C1A. Oxaliplatin-induced peripheral neuropathy (OIPN) was assessed using a Von Frey test reflecting chronic hypoalgesia. Tolerance to treatment was assessed with a clinical score including four items: weight loss, weariness, alopecia, and diarrhea. In vitro, Mn1C1A associated with oxaliplatin and Pt(IV) conjugates treatment induced significantly higher production of H₂O₂ in all cell lines and showed a significant improvement of the antitumoral efficacy compared to oxaliplatin alone. In vivo, the association of Mn1C1A to oxaliplatin did not decrease its antitumoral activity, while OxPt-2-Mn1C1A had lower antitumoral activity than oxaliplatin alone. Mn1C1A associated with oxaliplatin significantly decreased OIPN and also improved global clinical tolerance of oxaliplatin. A neuroprotective effect was observed, associated with a significantly improved tolerance to oxaliplatin without impairing its antitumoral activity.     

Inhibition of Vascular Endothelial Cadherin Cleavage Prevents Elastic Fiber Alterations and Atherosclerosis Induced by Intermittent Hypoxia in the Mouse Aorta

Intermittent hypoxia (IH), the major feature of obstructive sleep apnea syndrome (OSAS), induces atherosclerosis and elastic fiber alterations. VE-cadherin cleavage is increased in OSAS patients and in an IH-cellular model. It is mediated by HIF-1 and Src-tyr-kinases pathways and results in endothelial hyperpermeability. Our aim was to determine whether blocking VE-cadherin cleavage in vivo could be an efficient strategy to inhibit deleterious IH-induced vascular remodeling, elastic fiber defects and atherogenesis. VE-cadherin regulation, aortic remodeling and atherosclerosis were studied in IH-exposed C57Bl/6J or ApoE-/-mice treated or not with Src-tyr-kinases inhibitors (Saracatinib/Pazopanib) or a HIF-1 inhibitor (Acriflavine). Human aortic endothelial cells were exposed to IH and treated with the same inhibitors. LDL and the monocytes transendothelium passage were measured. In vitro, IH increased transendothelium LDL and monocytes passage, and the tested inhibitors prevented these effects. In mice, IH decreased VE-cadherin expression and increased plasmatic sVE level, intima-media thickness, elastic fiber alterations and atherosclerosis, while the inhibitors prevented these in vivo effects. In vivo inhibition of HIF-1 and Src tyr kinase pathways were associated with the prevention of IH-induced elastic fiber/lamella degradation and atherogenesis, which suggests that VE-cadherin could be an important target to limit atherogenesis and progression of arterial stiffness in OSAS.