Snowpack-runoff relationships for mid-elevation snowpacks on the Workman Creek Watersheds of central Arizona /

"July 2002."

School-house architecture : illustrated in seventeen designs in various styles : with full descriptive drawings in plan, elevation, section, and detail /

Mode of access: Internet.

Surface Elevation Change Processes in the Snohomish River Estuary, Washington

Estuaries provide crucial ecosystem functions and contain significant socio-economic value. Within Washington State, estuaries supply rearing habitat for juvenile salmon during their transition period from freshwater to open sea. In order to properly manage wetland resources and restore salmon habitat, the mechanisms through which estuaries evolve and adapt to pressures from climate change, most notably eustatic sea level rise, must be understood. Estuaries maintain elevation relative to sea level rise through vertical accretion of sediment. This report investigates the processes that contribute to local surface elevation change in the Snohomish Estuary, conveys preliminary surface elevation change results from RTK GPS monitoring, and describes how surface elevation change will be monitored with a network of RSET-MH’s. Part of the tidal wetlands within the Snohomish River Estuary were converted for agricultural and industrial purposes in the 1800’s, which resulted in subsidence of organic soils and loss of habitat. The Tulalip Tribes, the National Oceanic and Atmospheric Administration (NOAA), Northwest Indian Fisheries Commission (NWIFC), and the Environmental Protection Agency (EPA) are conducting a large-scale restoration project to improve ecosystem health and restore juvenile salmon habitat. A study by Crooks et al. (2014) used 210Pb and carbon densities within sediment cores to estimate wetland re-building capacities, sediment accretion rates, and carbon sequestration potential within the Snohomish Estuary. This report uses the aforementioned study in combination with research on crustal movement, tidal patterns, sediment supply, and sea level rise predictions in the Puget Sound to project how surface elevation will change in the Snohomish Estuary with respect to sea level rise. Anthropogenic modification of the floodplain has reduced the quantity of vegetation and functional connectivity within the Snohomish Estuary. There have been losses up to 99% in vegetation coverage from historic extents within the estuary in both freshwater and mesohaline environments. Hydrographic monitoring conducted by NOAA and the Tulalip Tribe shows that 85% of the historic wetland area is not connected to the main stem of the Snohomish (Jason Hall 2014, unpublished data, NOAA). As vegetation colonization and functional connectivity of the floodplains of the Snohomish estuary is re-established through passive and active restoration, sediment transport and accretion is expected to increase. Under the Intergovernmental Panel on Climate Change (IPCC) “medium- probability” scenario sea level is projected to rise at a rate of 4.28 mm/year in the Puget Sound. Sea level rise in the Snohomish Estuary will be exacerbated from crustal deformation from subsidence and post-glacial rebound, which are measured to be -1.4 mm/year and -0.02 mm/year, respectively. Sediment accretion rates calculated by Crooks et al. (2014) and RTK GPS monitoring of surface elevation change of the Marysville Mitigation site from 2011-2014 measured vertical accretion rates that range from -48-19 mm/year and have high spatial variability. Sediment supply is estimated at 490 thousand tons/year, which may be an under-estimate because of the exclusion of tidal transport in this value. The higher rates of sediment accretion measured in the Snohomish Estuary suggest that the Snohomish will likely match or exceed the pace of sea level rise under “medium-probability” projections. The network of RSET-MH instruments will track surface elevation change within the estuary, and provide a more robust dataset on rates of surface elevation change to quantify how vertical accretion and subsidence are contributing to surface elevation change on a landscape scale.

Local thrombolysis or rapid transfer for primary angioplasty for patients presenting with ST segment elevation myocardial infarction to hospitals without angioplasty facilities

No Abstract

Integrating JERS-1 imaging radar and elevation models for mapping tropical rainforest communities in far North Queensland, Australia

The Wet Tropics World Heritage Area in Far North Queens- land, Australia consists predominantly of tropical rainforest and wet sclerophyll forest in areas of variable relief. Previous maps of vegetation communities in the area were produced by a labor-intensive combination of field survey and air-photo interpretation. Thus,. the aim of this work was to develop a new vegetation mapping method based on imaging radar that incorporates topographical corrections, which could be repeated frequently, and which would reduce the need for detailed field assessments and associated costs. The method employed G topographic correction and mapping procedure that was developed to enable vegetation structural classes to be mapped from satellite imaging radar. Eight JERS-1 scenes covering the Wet Tropics area for 1996 were acquired from NASDA under the auspices of the Global Rainforest Mapping Project. JERS scenes were geometrically corrected for topographic distortion using an 80 m DEM and a combination of polynomial warping and radar viewing geometry modeling. An image mosaic was created to cover the Wet Tropics region, and a new technique for image smoothing was applied to the JERS texture bonds and DEM before a Maximum Likelihood classification was applied to identify major land-cover and vegetation communities. Despite these efforts, dominant vegetation community classes could only be classified to low levels of accuracy (57.5 percent) which were partly explained by the significantly larger pixel size of the DEM in comparison to the JERS image (12.5 m). In addition, the spatial and floristic detail contained in the classes of the original validation maps were much finer than the JERS classification product was able to distinguish. In comparison to field and aerial photo-based approaches for mapping the vegetation of the Wet Tropics, appropriately corrected SAR data provides a more regional scale, all-weather mapping technique for broader vegetation classes. Further work is required to establish an appropriate combination of imaging radar with elevation data and other environmental surrogates to accurately map vegetation communities across the entire Wet Tropics.

Street elevation, Lahz House, Spring Hill

Winner of the Robin Dods Award RAIA Queensland Chapter 1990

North-East elevation, Ocean View Farmhouse, Mt. Mee

As seen from north-east with timber shutters to the living room in the open position.

View along North-East elevation, Ocean View Farmhouse, Mount Mee

As seen from timber entrance ramp.

The elevation in circulating anti-angiogenic factors is independent of markers of neutrophil activation in preeclampsia

Background - Severe preeclampsia is associated with increased neutrophil activation and elevated serum soluble endoglin (sEng) and soluble Flt-1 (sFlt-1) in the maternal circulation. To dissect the contribution of systemic inflammation and anti-angiogenic factors in preeclampsia, we investigated the relationships between the circulating markers of neutrophil activation and anti-angiogenic factors in severe preeclampsia or systemic inflammatory state during pregnancy. Methods and results - Serum sEng, sFlt-1, placenta growth factor, interleukin-6 (IL-6), calprotectin, and plasma a-defensins concentrations were measured by ELISA in 88 women of similar gestational age stratified as: severe preeclampsia (sPE, n = 45), maternal systemic inflammatory response (SIR, n = 16) secondary to chorioamnionitis, pyelonephritis or appendicitis; and normotensive controls (CRL, n = 27). Neutrophil activation occurred in sPE and SIR, as a-defensins and calprotectin concentrations were two-fold higher in both groups compared to CRL (P < 0.05 for each). IL-6 concentrations were highest in SIR (P < 0.001), but were higher in sPE than in CRL (P < 0.01). sFlt-1 (P < 0.001) and sEng (P < 0.001) were ˜20-fold higher in sPE compared to CRL, but were not elevated in SIR. In women with sPE, anti-angiogenic factors were not correlated with markers of neutrophil activation (a-defensins, calprotectin) or inflammation (IL-6). Conclusions - Increased systemic inflammation in sPE and SIR does not correlate with increased anti-angiogenic factors, which were specifically elevated in sPE indicating that excessive systemic inflammation is unlikely to be the main contributor to severe preeclampsia.

36 monocyte subpopulations counts and associations with global longitudinal strain in st-elevation myocardial infarction patients with normal ejection fraction

Introduction - Monocytes, with 3 different subsets, are implicated in the initiation and progression of the atherosclerotic plaque contributing to plaque instability and rupture. Mon1 are the “classical” monocytes with inflammatory action, whilst Mon3 are considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. In PCI era, fewer patients have globally reduced left ventricular ejection fraction post infarction, hence the importance of studying regional wall motion abnormalities and deformation at segmental levels using longitudinal strain. Little is known of the role for the 3 monocyte subpopulations in determining global strain in ST elevation myocardial infarction patients (STEMI). Conclusion In patients with normal or mildly impaired EF post infarction, higher counts of Mon1 and Mon2 are correlated with GLS within 7 days and at 6 months of remodelling post infarction. Adverse clinical outcomes in patients with reduced convalescent GLS were predicted with Mon1 and Mon2 suggestive of an inflammatory role for the newly identified Mon2 subpopulation. These results imply an important role for monocytes in myocardial healing when assessed by subclinical ventricular function indices. Methodology - STEMI patients (n = 101, mean age 64 ± 13 years; 69% male) treated with percutaneous revascularisation were recruited within 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2- (Mon3). Phagocytic activity of monocytes was measured using flow cytometry and Ecoli commercial kit. Transthoracic 2D echocardiography was performed within 7 days and at 6 months post infarct to assess global longitudinal strain (GLS) via speckle tracking. MACE was defined as recurrent acute coronary syndrome and death. Results - STEMI patients with EF ≥50% by Simpson’s biplane (n = 52) had GLS assessed. Using multivariate regression analysis higher counts of Mon1 and Mon 2 and phagocytic activity of Mon2 were significantly associated with GLS (after adjusting for age, time to hospital presentation, and peak troponin levels) (Table 1). At 6 months, the convalescent GLS remained associated with higher counts of Mon1, Mon 2. At one year follow up, using multivariate Cox regression analysis, Mon1 and Mon2 counts were an independent predictor of MACE in patients with a reduced GLS (n = 21)

Monocyte subpopulation counts and associations with left ventricular ejection fraction post ST elevation myocardial infarction

Background: Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to plaque instability and rupture. Little is known about the role of the three phenotypically and functionally different monocyte subpopulations in determining ventricular remodelling following ST elevation myocardial infarction (STEMI). Mon1 are the ‘classical’ monocytes with inflammatory action, whilst Mon3 are considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited within the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Transthoracic 2D echocardiography was performed within 7 days and at 6 months post infarct to assess ventricular volumes, mass, systolic, and diastolic functions as well as strain and strain rate. Results: Using linear regression analysis higher counts for Mon1, and lower counts for Mon2 and Mon3 were significantly associated with the baseline left ventricular ejection fraction (LVEF) within 7 days post infarct (table 1). At 6 months post STEMI lower counts of Mon2 remained positively associated with a decrease in LVEF at completion of remodelling (p=0.002). Conclusion: Peripheral monocytes of all three subsets correlate with LVEF after a myocardial infarction. High counts of the inflammatory Mon1 are associated with the reduced baseline ejection fraction post infarction. After remodelling, the convalescent ejection fraction was independently predicted by monocyte subpopulation 2. As lower counts depicted negative ventricular remodelling, this suggests a possible myofibroblast deposition and angiogenesis role for the newly described intermediate monocyte subpopulation Mon2 as opposed to the previously anticipated inflammatory role.

Monocyte subpopulation counts and TNF alpha associations with clinical outcome post ST elevation myocardial infarction

Background Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to its instability and rupture. Although peripheral monocytosis has been related to poor clinical outcome post ST elevation myocardial infarction (STEMI), only scarce information is available of mechanisms of this association. Tumour necrosis factor alpha (TNFα) is a key cytokine in the acute phase inflammatory response, and it is predominantly produced by inflammatory macrophages. Little is known about TNFα association with circulating monocyte subpopulations post STEMI. Method A total of 142 STEMI patients (mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited with blood samples obtained within first 24 hours from the onset and on day 10-14. Peripheral blood monocyte subpopulations were enumerated and characterized using flow cytometry after staining for CD14, CD16 and CCR2 and were defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Plasma levels of TNFα were measured by enzyme-linked immunosorbent assay (ELISA, Peprotec system, UK). Major adverse cardiac events (MACE), defined as recurrent STEMI, new diagnosis of heart failure and death were recorded at follow up, mean of 164±134 days. Results TNFα levels were significantly higher 24 hours post STEMI, compared to day 14 (paired t-test, p <0.001) with day 1 levels weakly correlated with total monocyte count as well as Mon1 (Spearman’s correlation, r=0.19, p=0.02 and r=0.22, p=0.01, respectively). There was no correlation between TNFα and Mon2 or Mon3 subpopulations. TNFα levels were significantly higher in patients with a recorded MACE (n=28, Mann-Whitney test, p<0.001) (figure 1).⇓

Monocyte subset counts associations with left ventricular systolic function post ST elevation myocardial infarction

Background: Monocytes are implicated in the initiation and progression of theatherosclerotic plaque contributing to plaque instability and rupture. Little is knownof the role played by the 3 phenotypically and functionally different monocytesubpopulations in determining ventricular remodeling following ST elevation my-ocardial infarction (STEMI). Mon1 are "classical" inflammatory monocytes, whilstMon3 are considered reparative with fibroblast deposition ability. The function ofthe newly described Mon2 is yet to be elucidated. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treatedwith percutaneous revascularization were recruited within the first 24 hours. Pe-ripheral blood monocyte subpopulations were enumerated and characterizedusing flow cytometry after staining for CD14, CD16 and CCR2. Phenotypi-cally, monocyte subpopulations are defined as: CD14+CD16-CCR2+ (Mon1),CD14+CD16+CCR+ (Mon2) and CD14lowCD16+CCR2- (Mon3) cells. Transtho-racic 2D echocardiography was performed within 7 days and 6 months post infarctto assess ventricular volumes, mass, systolic, and diastolic functions. Results: Using linear regression analysis higher counts for Mon1, and lowercounts for Mon2 and Mon3 were significantly associated with the baseline leftventricular ejection fraction (LVEF) within seven days post infarction. At 6 monthspost STEMI lower counts of Mon2 remained positively associated with decreasedLVEF (p value= 0.002).Monocyte subsets correlation with LVEFMonocytes mean florescence Baseline left ventricular Left ventricular ejectionintensity (cells/μl) ejection fraction (%) fraction (%) at 6 months post infarctβ-value P-valueβ-value P-valueTotal Mon0.31 P<0.001 0.360.009Mon 10.019 0.020.070.62Mon 2−0.28 0.001 −0.420.002Mon 3−0.27 0.001 −0.180.21 Conclusion: Peripheral monocytes of all three subsets correlate with LVEF af-ter a myocardial infarction. High counts of the inflammatory Mon1 are associatedwith reduction in the baseline LVEF. Post remodelling, the convalescent EF wasindependently predicted by monocyte subpopulation 2. As lower counts depictednegative ventricular remodeling, this suggests a reparative role for the newly de-scribed Mon2, possibly via myofibroblast deposition and angiogenesis, in contrastto an anticipated inflammatory role.

Construction and experimental study of an elevation linear Fresnel reflector

This paper outlines a novel elevation linear Fresnel reflector (ELFR) and presents and validates theoretical models defining its thermal performance. To validate the models, a series of experiments were carried out for receiver temperatures in the range of 30-100 °C to measure the heat loss coefficient, gain in heat transfer fluid (HTF) temperature, thermal efficiency, and stagnation temperature. The heat loss coefficient was underestimated due to the model exclusion of collector end heat losses. The measured HTF temperature gains were found to have a good correlation to the model predictions - less than a 5% difference. In comparison to model predictions for the thermal efficiency and stagnation temperature, measured values had a difference of -39% to +31% and 22-38%, respectively. The difference between the measured and predicted values was attributed to the low-temperature region for the experiments. It was concluded that the theoretical models are suitable for examining linear Fresnel reflector (LFR) systems and can be adopted by other researchers.