Modeling the effect of ozone loss on photobleaching of chromophoric dissolved organic matter in the St. Lawrence estuary

Temporal trends in total ozone for the St. Lawrence estuary were estimated from ground-based measurements at the NOAA/CMDL station in Caribou, Maine. Linear regression analysis showed that from 1979 to 1999 total ozone has decreased by about 3.3% per decade on an annual basis and ≤6.2% per decade on a monthly basis relative to unperturbed (pre-CFC) levels. The influence of increased ultraviolet-B (280–320 nm) radiation associated with ozone depletion on water column photochemical processes was evaluated by modeling the photobleaching of chromophoric dissolved organic material (CDOM). Linear regression analysis showed small (<0.5% per decade), but statistically significant upward trends in maximum noontime photobleaching rates. Most notably, positive trends in relative rates for May, June, and July, when maximum absolute rates are expected, were predicted. A global model based on TOMS ozone data revealed increases in photobleaching of ≤3% per decade at high latitudes in the Southern Hemisphere. Radiation amplification factors for increases in photochemically weighted UV (280–400 nm) in response to ozone depletion were estimated at 0.1 and 0.08 for photobleaching of CDOM absorbance at 300 and 350 nm, respectively. Application of the laboratory-based model to conditions that more closely resembled those in situ were variable with both overestimation and underestimation of measured rates. The differences between modeled rates and observed rates under quasi-natural conditions were as large or larger than the predicted increases due to ozone depletion. These comparisons suggest that biological activity and mixing play an important, but as yet ill-defined, role in modifying photochemical processes.

Twin and grain boundary in InP: A synchrotron radiation study

Experimentally observed X-ray reflectivity curves show bi-crystal(twin) characteristics. The study revealed that there was defect segregation at the twin boundary. Stress was relaxed at the edge of the boundary. Relaxation of the stress resulted in formation of twin and other defects. As a result of formation of such defects, a defect-free and stress-free zone or low defect density and small stress zone is created around the defects. So a twin model was proposed to explain the experimental results. Stress(mainly thermal stress), chemical stoichiometry deviation and impurities nonhomogeneous distributions are the key factors that cause twins in LEC InP crystal growth. Twins on (111) face in LEC InP crystal were studied. Experimental evidence of above mentioned twin model and suggestions on how to get twin-free LEC InP single crystals will be discussed.

Delta-resonance effective mass in medium

Based on the relativistic chiral effective field theory, we study the effective mass of the Delta-resonance in medium by investigating the self-energy of the Delta-resonance related to the pi N decay channel in symmetric nuclear matter. We find that the effective mass of Delta-resonance decreases evidently with increasing nuclear density rho. In our calculation, we also consider the influence of the shifts of the nucleon mass, pion mass and its decay constant due to the restoration of chiral symmetry in medium. The results are roughly consistent with the data given by Lawrence Berkeley National Laboratory.

强子的介质效应

本论文简述了强子介质效应的研究现状，理论方法以及实验探测技术。系统的介绍了相对论平均场理论和手征有效场论。利用相对论平均场研究了Pentaquark的介质效应，利用手征有效场论研究了△(1232)共振态的介质效应。 在密度相关的平均场理论基础上，计算出的Pentaquark的有效质量随核物质密度的增加而减小。一定的Pentaquark含量导致每核子的结合能减小，这使得核物质系统更加稳定。 在手征有效场论的框架下，利用泡利不相容原理对核子传播子的修正，以及核子有效质量在核物质中的改变，通过计算△共振态一阶自能，讨论了△共振态的有效质量和衰变宽度对核物质密度的依赖关系。结果表明：△共振态的有效质量随核物质密度的增加而减小，在正常核密度下为1221MeV，而在3倍正常核密度时为1186MeV，其减小幅度与美国Lawrence Berkeley国家实验室上做的58Ni+Cu（能量为1.97GeV/u）碰撞实验给出的结果大致相符；△粒子的衰变宽度在核物质中的变化主要决定于核子以及△粒子的有效质量的变化

Endothelial microparticles released in thrombotic thrombocytopenic purpura express von Willebrand factor and markers of endothelial activation

It has been suggested that endothelial apoptosis is a primary lesion in the pathogenesis of thrombotic thrombocytopenic purpura (TTP). We tested this hypothesis by examining the phenotypic signatures of endothelial microparticles (EMP) in TTP patients. In addition, the effect of TTP plasma on microvascular endothelial cells (MVEC) in culture was further delineated. EMP released by endothelial cells (EC) express markers of the parent EC; EMP released in activation carry predominantly CD54 and CD62E, while those in apoptosis CD31 and CD105. We investigated EMP release in vitro and in TTP patients. Following incubation of MVEC with TTP plasma, EMP and EC were analysed by flow cytometry for the expression of CD31, CD51, CD54, CD62E, CD105, CD106 and von Willebrand factor (VWF) antigen. EMP were also analysed in 12 TTP patients. In both EC and EMP, CD62E and CD54 expression were increased 3- to 10-fold and 8- to 10-fold respectively. However, CD31 and CD105 were reduced 40-60% in EC but increased twofold in EMP. VWF expression was found in 55 +/- 15% of CD62E(+) EMP. Markers of apoptosis were negative. In TTP patients, CD62E(+) and CD31(+)/CD42b(-) EMP were markedly elevated, and preceded and correlated well with a rise in platelet counts and a fall in lactate dehydrogenase. CD62E(+) EMP (60 +/- 20%) co-expressed VWF and CD62E. The ratio of CD31(+)/42b(-) to CD62E(+) EMP exhibited a pattern consistent with activation. In conclusion, our studies indicate endothelial activation in TTP. EMP that co-express VWF and CD62E could play a role in the pathogenesis of TTP.

Endothelial cells release phenotypically and quantitatively distinct microparticles in activation and apoptosis

Background: Endothelial cells (EC) shed endothelial microparticles (EMP) in activation and apoptosis. Objectives: We compared the antigenic expression of EMP species released during activation as compared to apoptosis, in three cell lines. Methods: EC from renal and brain microvascular (MiVEC) and coronary macrovascular (MaVEC) origin were incubated with TNF-alpha to induce activation, or deprived of growth factors to induce apoptosis. Antigens expressed on EMP and EC were assayed flow cytometrically and included constitutive markers (CD31, CD51/61, CD105), inducible markers (CD54, CD62E and CD106), and annexin V binding. Results: It was found that in apoptosis, constitutive markers in EMP were markedly increased (CD31>CD105), with a concomitant decrease in expression in EC. Annexin V EC surface binding and annexin V+ EMP were more sharply increased in apoptosis than in activation. In contrast, in activation, inducible markers in EMP were markedly increased in both EMP and EC (CD62E>CD54>CD 106). Coronary MaVEC released significantly less EMP than MiVEC. Conclusion: EC release qualitatively and quantitatively distinct EMP during activation compared to apoptosis. Analysis of EMP phenotypic signatures may provide clinically useful information on the status of the endothelium. (C) 2003 Elsevier Science Ltd. All rights reserved.