The northeastern Black Sea redox zone: Hydrochemical structure and its temporal variability

Detailed studies of the vertical structure of hydrochemical parameters in the northeastern Black Sea near Gelendzhik are presented and discussed. This work is based on a set of systematic observations carried out in this region during R/V Akvanavt and R/V Ashamba cruises from 1997 to 2005 and also on data from previous studies from 1984 to 1997. The Black Sea region near Gelendzhik is far from the influences of the Bosporus input and Danube River inflow. Therefore, the vertical structure in this region is more stable compared to the western Black Sea and reflects integrated, rather than local, changes of the Black Sea. Seasonal variations in the distribution of chemical parameters at the redox interface are connected to seasonal variations in hydrophysical processes and organic matter production. In winter, maxima of organic phosphorus and urea were absent in the vicinity of the onset of hydrogen sulfide. The concentrations of nitrate were lower in winter than in summer. Winter mixing in the anticyclone eddies led to reduced vertical gradients in the redox layer and to the disappearance of an upper phosphate minimum. Study of the interannual dynamics of oxygen concentrations in the Cold Intermediate Layer and anoxic waters boundary in the density field position revealed climatic-scale changes that may be connected with changes in the North Atlantic Oscillation (NAO) index. © 2006 Elsevier Ltd. All rights reserved

Molecular signatures for CCN1, p21 and p27 in progressive mantle cell lymphoma

Mantle cell lymphoma (MCL) is a comparatively rare non-Hodgkin’s lymphoma characterised by overexpression of cyclin D1.Many patients present with or progress to advanced stage disease within 3 years. MCL is considered an incurable disease withmedian survival between 3 and 4 years. We have investigated the role(s) of CCN1 (CYR61) and cell cycle regulators inprogressive MCL. We have used the human MCL cell lines REC1 G519 > JVM2 cells by RQ-PCR, depicting a decrease in CCN1expression with disease progression. Investigation of CCN1 isoform expression by western blotting showed that whilst expres-sion of full-length CCN1 was barely altered in the cell lines, expression of truncated forms (18–20 and 28–30 kDa) decreasedwith disease progression. We have then demonstrated that cyclin D1 and cyclin dependent kinase inhibitors (p21CIP1and p27KIP1)are also involved in disease progression. Cyclin D1 was highly expressed in REC1 cells (OD: 1.0), reduced to one fifth in G519cells (OD: 0.2) and not detected by western blotting in JVM2 cells. p27KIP1followed a similar profile of expression as cyclin D1.Conversely, p21CIP1was absent in the REC1 cells and showed increasing expression in G519 and JVM2 cells. Subcellularlocalization detected p21CIP1/p27KIP1primarily within the cytoplasm and absent from the nucleus, consistent with altered roles in treatment resistance. Dysregulation of the CCN1 truncated forms are associated with MCL progression. In conjunction withreduced expression of cyclin D1 and increased expression of p21, this molecular signature may depict aggressive disease andtreatment resistance

Eleven papers in analysis

This collection of eleven papers covers a broad spectrum of topics in analysis, from the study of certain classes of analytic functions to the solvability of singular problems for differential and integral equations to computational schemes for the partial differential equations and singular integral equations

Anticyclonic eddies in the deep eastern Black Sea in summer-autumn 1999 (satellite and ship-borne observations

peer reviewe

Oxidative Modifications of Extracellular Matrix Promote the Second Wave of Inflammation via B\u3csub\u3e2\u3c/sub\u3e Integrins

Early stages of inflammation are characterized by extensive oxidative insult by recruited and activated neutrophils. Secretion of peroxidases, including the main enzyme, myeloperoxidase, leads to the generation of reactive oxygen species. We show that this oxidative insult leads to polyunsaturated fatty acid (eg, docosahexaenoate), oxidation, and accumulation of its product 2-(v-carboxyethyl)pyrrole (CEP), which, in turn, is capable of protein modifications. In vivo CEP is generated predominantly at the inflammatory sites in macrophage-rich areas. During thioglycollate-induced inflammation, neutralization of CEP adducts dramatically reduced macrophage accumulation in the inflamed peritoneal cavity while exhibiting no effect on the early recruitment of neutrophils, suggesting a role in the second wave of inflammation. CEP modifications were abundantly deposited along the path of neutrophils migrating through the 3-dimensional fibrin matrix in vitro. Neutrophil-mediated CEP formation was markedly inhibited by the myeloperoxidase inhibitor, 4-ABH, and significantly reduced in myeloperoxidase-deficient mice. On macrophages, CEP adducts were recognized by cell adhesion receptors, integrin aMb2 and aDb2. Macrophage migration through CEP-fibrin gel was dramatically augmented when compared with fibrin alone, and was reduced by b2-integrin deficiency. Thus, neutrophil-mediated oxidation of abundant polyunsaturated fatty acids leads to the transformation of existing proteins into stronger adhesive ligands for aMb2- and aDb2-dependent macrophage migration. The presence of a carboxyl group rather than a pyrrole moiety on these adducts, resembling characteristics of bacterial and/or immobilized ligands, is critical for recognition by macrophages. Therefore, specific oxidation-dependent modification of extracellular matrix, aided by neutrophils, promotes subsequent aMb2- and aDb2-mediated migration/retention of macrophages during inflammation