938 resultados para Copepoda -- migration -- British Columbia -- Muchalat Inlet


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Senior thesis written for Oceanography 445

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Senior thesis written for Oceanography 445

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Senior thesis written for Oceanography 445

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Senior thesis written for Oceanography 445

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Sediment traps were deployed inside the anoxic inner basin of Effingham Inlet and at the oxygenated mouth of the inlet from May 1999 to September 2000 in a pilot study to determine the annual depositional cycle and impact of the 1999-2000 La Niña event within a western Canadian inlet facing the open Pacific Ocean. Total mass flux, geochemical parameters (carbon, nitrogen, opal, major and minor element contents, and stable isotope ratios) and diatom assemblages were determined and compared with meteorological and oceanographic data. Deposition was seasonal, with coarser grained terrestrial components and benthic diatoms settling in the autumn and winter, coincident with the rainy season. Marine sedimentary components and abundant pelagic diatoms were coincident with coastal upwelling in the spring and summer. Despite the seasonal differences in deposition, the typical temperate-zone Thalassiosira-Skeletonema-Chaetoceros bloom succession was muted. A July 1999 total mass flux peak and an increase in biogenous components coincided with a rare bottom-water oxygen renewal event in the inlet. Likewise, there were cooler-than-average sea surface temperatures (SSTs) just outside the inlet, and unusually high abundances of a previously undescribed cool-water marine diatom (Fragilariopsis pacifica sp. nov.) within the inlet. Each of these occurrences likely reflects a response to the strong La Niña that followed the year after the strongest-ever recorded El Niño event of 1997-1998. By the autumn of 1999, SSTs had returned to average, and F. pacifica had all but disappeared from the remaining trap record, indicating that oceanographic conditions had returned to normal. Oxygenation events were not witnessed in the inlet in the years before or after 1999, suggesting that a rare oceanographic and climatic event was captured by this sediment trap time series. The data from this record can therefore be used as a benchmark for identifying anomalous environmental conditions on this coast.

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Manganese-iron oxide concretions are presently forming on Patrick Sill in upper Jervis Inlet. The marine geology of Patrick Sill and the adjoining basins (Queen's Reach and Princess Royal Reach) was studied to define the environment in which the concretions form. The river at the inlet head is the principal source of sediment to the upper basin. The average grain size of surficial bottom sediments within this basin decreases uniformly with distance from the source. Patrick Sill separates the upper from the lower basin. The sediment distribution pattern within the lower basin differs markedly from the upper basin as there is no dominant source of material but rather many localized sources. Abundant shallow marine faunal remains recovered in deep water sediment samples indicate that sediments deposited as deltas off river and stream mouths periodically slump to the basin floors. Geologic and optical turbidity information for the upper basin can best be explained by slumping from the delta at the inlet head with the initiation of turbidity or density currents. Patrick Sill appears to create a downstream barrier to this flow. The mineralogy of the bottom sediments indicates derivation from a granitic terrain. If this is so, the sediments presently being deposited in both basins are reworked glacial materials initially derived by glacial action outside the present watershed. Upper Jervis Inlet is mapped as lying within a roof pendant of pre-batholithic rocks, principally slates. Patrick Sill is thought to be a bedrock feature mantled with Pleistocene glacial material. The accumulation rate of recent sediments on the sill is low especially in the V-notch or medial depression. The manganese-iron oxide concretions are forming within the depression and apparently nowhere else in the study area. Also forming within the depression are crusts of iron oxide and what are tentatively identified as glauconite-montmorillonoid pellets. The concretions are thought to form by precipitation of manganese-iron oxides on pebbles and cobbles lying at the sediment water interface. The oxide materials are mobile in the reducing environment of the underlying clayey-sand sediment but precipitate on contact with the oxygenating environment of the surficial sediments. The iron crusts are thought to be forming on extensive rocky surfaces above the sediment water interface. The overall appearance and evidence of rapid formation of the crusts suggests they formed from a gel in sea water. Reserves of manganese-iron concretions on Patrick Sill were estimated to be 117 metric tons. Other deposits of concretions have recently been found in other inlets and in the Strait of Georgia but, to date, the extent of these has not been determined.

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Senior thesis written for Oceanography 445

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Senior thesis written for Oceanography 445

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Thesis (Ph.D.)--University of Washington, 2016-08

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Background: Epidermogenesis and epidermal wound healing are tightly regulated processes during which keratinocytes must migrate, proliferate and differentiate. Cell to cell adhesion is crucial to the initiation and regulation of these processes. CUB domain containing protein 1 (CDCP1) is a transmembrane glycoprotein that is differentially tyrosine phosphorylated during changes in cell adhesion and survival signalling and is expressed by keratinocytes in native human skin, as well as in primary cultures. Objectives: To investigate the expression of CDCP1 during epidermogenesis and its role in keratinocyte migration. Methods: We examined both human skin tissue and an in vitro three-dimensional human skin equivalent model to examine the expression of CDCP1 during epidermogenesis. To examine the role of CDCP1 in keratinocyte migration we used a function blocking anti-CDCP1 antibody and a real-time Transwell™ cell migration assay. Results: Immunohistochemical analysis indicated that in native human skin CDCP1 is expressed in the stratum basale and stratum spinosum. In contrast, during epidermogenesis in a 3-dimensional human skin equivalent model CDCP1 was expressed only in the stratum basale, with localization restricted to the cell-cell membrane. No expression was detected in basal keratinocytes that were in contact with the basement membrane. Further, an anti-CDCP1 function blocking antibody was shown to disrupt keratinocyte chemotactic migration in vitro. Conclusions: These findings delineate the expression of CDCP1 in human epidermal keratinocytes during epidermogenesis and demonstrate that CDCP1 is involved in keratinocyte migration.

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Background The level of plasma-derived naturally circulating anti-glycan antibodies (AGA) to P1 trisaccharide has previously been shown to significantly discriminate between ovarian cancer patients and healthy women. Here we aim to identify the Ig class that causes this discrimination, to identify on cancer cells the corresponding P1 antigen recognised by circulating anti-P1 antibodies and to shed light into the possible function of this glycosphingolipid. Method An independent Australian cohort was assessed for the presence of anti-P1 IgG and IgM class antibodies using suspension array. Monoclonal and human derived anti-glycan antibodies were verified using three independent glycan-based immunoassays and flow cytometry-based inhibition assay. The P1 antigen was detected by LC-MS/MS and flow cytometry. FACS-sorted cell lines were studied on the cellular migration by colorimetric assay and real-time measurement using xCELLigence system. Results Here we show in a second independent cohort (n=155) that the discrimination of cancer patients is mediated by the IgM class of anti-P1 antibodies (P=0.0002). The presence of corresponding antigen P1 and structurally related epitopes in fresh tissue specimens and cultured cancer cells is demonstrated. We further link the antibody and antigen (P1) by showing that human naturally circulating and affinity-purified anti-P1 IgM isolated from patients ascites can bind to naturally expressed P1 on the cell surface of ovarian cancer cells. Cell-sorted IGROV1 was used to obtain two study subpopulations (P1-high, 66.1%; and P1-low, 33.3%) and observed that cells expressing high P1-levels migrate significantly faster than those with low P1-levels. Conclusions This is the first report showing that P1 antigen, known to be expressed on erythrocytes only, is also present on ovarian cancer cells. This suggests that P1 is a novel tumour-associated carbohydrate antigen recognised by the immune system in patients and may have a role in cell migration. The clinical value of our data may be both diagnostic and prognostic; patients with low anti-P1 IgM antibodies present with a more aggressive phenotype and earlier relapse.

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Rupture of vulnerable atheromatous plaque in the carotid and coronary arteries often leads to stroke and heart attack respectively. The mechanism of blood flow and plaque rupture in stenotic arteries is still not fully understood. A three dimensional rigid wall model was solved under steady state conditions and unsteady conditions by assuming a time-varying inlet velocity profile to investigate the relative importance of axial forces and pressure drops in arteries with asymmetric stenosis. Flow-structure interactions were investigated for the same geometry and the results were compared with those retrieved with the corresponding 2D cross-section structural models. The Navier-Stokes equations were used as the governing equations for the fluid. The tube wall was assumed hyperelastic, homogeneous, isotropic and incompressible. The analysis showed that the three dimensional behavior of velocity, pressure and wall shear stress is in general very different from that predicted by cross-section models. Pressure drop across the stenosis was found to be much higher than shear stress. Therefore, pressure may be the more important mechanical trigger for plaque rupture other than shear stress, although shear stress is closely related to plaque formation and progression.