(Table 2) Ice rafted debris abundance and accumulation rate, sedimentation rate and dry bulk density of bottom sediments from the Sea of Okhotsk

Oxygen isotope records, radiocarbon AMS data, carbonate and opal stratigraphy, sediment magnetic susceptibility, tephrachronology, and paleontological results were used to obtain detailed sediment stratigraphy and an age model for the studied cores. For studying sea-ice sedimentation an analysis of lithogenic grain number in >0.15 mm grain size fraction of bottom sediments was carried out. For quantitative estimation of intensity ice-rafting debris sedimentation number of IRD particles per sq cm per ka was calculated. Obtained results allowed to plot IRD AR distribution for the first oxygen isotope stage (0-12.5 14C ka, 14C) and for the second stage (12.5-24 14C ka). The first stage was subdivided into the latest deglaciation and the beginning of Holocene (6-12.5 14C ka) (transitive period), when the sea level was changing significantly, and the second part of Holocene (0-6 14C ka), when climate conditions and the sea level were similar to modern estimates. Data clearly show strong increase in ice formation in the glacial Sea of Okhotsk and its extent in the middle part of the sea. Average annual duration of ice coverage during glaciation was longer than that for interglaciation. However the sea ice cover was not continuous all the year round and disappeared in summer time except the far northwestern part of the sea.

(Table 1) Detrital modes for sand grains in sediment core CRP-3

Detrital modes determined on 68 sandstone samples from CRP-3 drillcore indicate a continuation of the dynamic history of uplift-related erosion and unroofing previously documented in CRP-1 and CRP-2/2A. The source area is identified very strongly with the Transantarctic Mountains (TAM) Dry Valleys block in southern Victoria Land. Initial unroofing of the TAM comprised removal of much of a former capping sequence of Jurassic Kirkpatrick basalts, which preceded the formation of the Victoria Land Basin. Erosion of Beacon Supergroup outcrops took place during progressive uplift of the TAM in the Oligocene. Earliest CRP-3 Oligocene samples above 788 metres below the sea floor (mbsf) were sourced overwhelmingly in Beacon Supergroup strata, including a recognisable contribution from Triassic volcanogenic Lashly Formation sandstones (uppermost Victoria Group). Moving up-section, by 500 mbsf, the CRP-3 samples are depauperate quartz arenites dominantly derived from the quartzose Devonian Taylor Group. Between c. 500 and 450 mbsf, the modal parameters show a distinctive change indicating that small outcrops of basement granitoids and metamorphic rocks were also being eroded along with the remaining Beacon (mainly Taylor Group) sequence. Apart from enigmatic fluctuations in modal indices above 450 mbsf, similar to those displayed by samples in CRP-2/2A, the CRP-3 modes are essentially constant (within a broad data scatter) to the top of CRP-3. The proportion of exposed basement outcrop remained at < 20 %, indicating negligible uplift (i.e. relative stability) throughout that period.

Final report, June 2, 1916.

"Three maps are submitted accompanying the Final report of the Commission; (1) use district map; (2) height district map; (3) area district map. Each of the above maps is submitted in 35 sections covering the entire city."

Arts companion, or A new assistant for the ingenious, in 3 pts. Pt. 1 containing the art of drawing in perspective ... Pt. II containing the art of drawing and painting in water-colours ... Pt. III containing the art of painting in miniature ... to which are added directions for shadowing, stipling, &c. ... likewise the preparation of an excellent polish and shell: the whole taken from some of the best Italian and other masters.

Includes indexes.

Mesoionic 1,3-oxazinium olates. Rearrangement to acylketenes and 3-azabicyclo[3.1.1]heptanetriones

Metastable but isolable mesoionic 1,3-oxazinium 4-olates 9d-f undergo ring opening to acylketenes 10 at or near room temperature. The ketenes undergo intramolecular criss-cross [2 + 2] cycloaddition to afford 3-azabicyclo[3.1.1]heptanetriones 12. The structure of 12d was established by X-ray crystallography.

Synthesis and characterization of Pd(II) and Pt(II) complexes with triazolopyrimidine derivatives: The crystal structure of [Pd2L2Cl4] where L=5,7-dimethyl-1,2,4-triazolo[1,5-a]pyrimidine

The Pd(II) and Pt(II) complexes with triazolopyrimidine C-nucleosides L-1 (5,7-dimethyl-3-(2',3',5'-tri-O-benzoyl-beta-D-ribofuranosyl-s-triazolo)[4,3-a]pyrimidine), L-2 (5,7-dimethyl-3-beta-D-ribofuranosyl-s-triazolo [4,3-a]pyrimidine) and L-3 (5,7-dimethyl[1,5-a]-s-triazolopyrimidine), [Pd(en)(L-1)](NO3)(2), (Pd(bpy)(L-1)](NO3)(2), cis-Pd(L-3)(2)Cl-2, [Pd-2(L-3)(2)Cl-4]center dot H2O, cis-Pd(L-2)(2)Cl-2 and [Pt-3(L-1)(2)Cl-6] were synthesized and characterized by elemental analysis and NMR spectroscopy. The structure of the [Pd-2(L-3)(2)Cl-4]center dot H2O complex was established by Xray crystallography. The two L-3 ligands are found in a head to tail orientation, with a (PdPd)-Pd-... distance of 3.1254(17) angstrom.L-1 coordinates to Pd(II) through N8 and N1 forming polymeric structures. L-2 coordinates to Pd(II) through N8 in acidic solutions (0.1 M HCl) forming complexes of cis-geometry. The Pd(II) coordination to L-2 does not affect the sugar conformation probably due to the high stability of the C-C glycoside bond. (c) 2006 Elsevier B.V. All rights reserved.

Determinants of visual 2-D echo assessment of left ventricular wall motion: Comparison with myocardial thickening on cardiac magnetic resonance imaging

Background: left ventricular wall motion on 2d echo (2de) is usually scored visually. we sought to examine the determinants of visually assessed wall motion scoring on 2de by comparison with myocardial thickening quantified on MRI. Methods: using a 16 segment model, we studied 287 segments in 30 patients aged 61+/ -11 years (6 female), with ischaemic LV dysfunction (defined by at least 2 segments dysfunctional on 2de). 2de was performed in 5 views and wall motion scores (WMS) assigned: 1 (normal) 103 segments, 2 (hypokinetic) 93 segments, 3 (akinetic) 87 segments. MRI was used to measure end systolic wall thickness (ESWT), end diastolic wall thickness (EDWT) and percentage systolic wall thickening (SWT%) in the plane of the 2de and to assess WMS in the same planes visually. No patient had a clinical ischemic event between the tests. Results: visual assessment of wall motion by 2de and MRI showed moderate agreement (kappa = 0.425). Resting 2de wall motion correlated significantly (p

Phospholipid chlorohydrin induces leukocyte adhesion to Apoe(-/-) mouse arteries via upregulation of P-selectin

HOCl-modified low-density lipoprotein (LDL) has proinflammatory effects, including induction of inflammatory cytokine production, leukocyte adhesion, and ROS generation, but the components responsible for these effects are not completely understood. HOCl and the myeloperoxidase-H2O2-halide system can modify both protein and lipid moieties of LDL and react with unsaturated phospholipids to form chlorohydrins. We investigated the proinflammatory effects of 1-stearoyl-2-oleoyl-sn-3-glycerophosphocholine (SOPC) chlorohydrin on artery segments and spleen-derived leukocytes from ApoE-/- and C57 Bl/6 mice. Treatment of ApoE-/- artery segments with SOPC chlorohydrin, but not unmodified SOPC, caused increased leukocyte-arterial adhesion in a time- and concentration-dependent manner. This could be prevented by pretreatment of the artery with P-selectin or ICAM-1-blocking antibodies, but not anti-VCAM-1 antibody, and immunohistochemistry showed that P-selectin expression was upregulated. However, chlorohydrin treatment of leukocytes did not increase expression of adhesion molecules LFA-1 or PSGL-1, but caused increased release of ROS from PMA-stimulated leukocytes by a CD36-dependent mechanism. The SOPC chlorohydrin-induced adhesion and ROS generation could be abrogated by pretreatment of the ApoE-/- mice with pravastatin or a nitrated derivative, NCX 6550. These findings suggest that phospholipid chlorohydrins formed in HOCl-treated LDL could contribute to the proinflammatory effects observed for this modified lipoprotein in vitro.

Paracellular permeability is increased by basal lipopolysaccharide in a primary culture of colonic epithelial cells; an effect prevented by an activator of Toll-like receptor-2

Lipopolysaccharide (LPS), which generally activates Toll-like receptor 4 (TLR4), is expressed on commensal colonic bacteria. In a number of tissues, LPS can act directly on epithelial cells to increase paracellular permeability. Such an effect in the colon would have an important impact on the understanding of normal homeostasis and of pathology. Our aim was to use a novel primary culture of colonic epithelial cells grown on Transwells to investigate whether LPS, or Pam(3)CSK( 4), an activator of TLR2, affected paracellular permeability. Consequently, [(14)C]-mannitol transfer and transepithelial electrical resistance (TEER) were measured. The preparation consisted primarily of cytokeratin-18 positive epithelial cells that produced superoxide, stained for mucus with periodic acid-Schiff reagent, exhibited alkaline phosphatase activity and expressed TLR2 and TLR4. Tight junctions and desmosomes were visible by transmission electron microscopy. Basally, but not apically, applied LPS from Escherichia coli increased the permeability to mannitol and to a 10-kDa dextran, and reduced TEER. The LPS from Helicobacter pylori increased paracellular permeability of gastric cells when applied either apically or basally, in contrast to colon cells, where this LPS was active only from the basal aspect. A pan-caspase inhibitor prevented the increase in caspase activity caused by basal E. coli LPS, and reduced the effects of LPS on paracellular permeability. Synthetic Pam(3)CSK(4) in the basal compartment prevented all effects of basal E. coli LPS. In conclusion, LPS applied to the base of the colonic epithelial cells increased paracellular permeability by a mechanism involving caspase activation, suggesting a process by which perturbation of the gut barrier could be exacerbated. Moreover, activation of TLR2 ameliorated such effects.