45, P <  048], CD3+CD69+ [REL: −0 53,

P <  016]) and only

45, P < .048], CD3+CD69+ [REL: −0.53,

P < .016]) and only one negative correlation (with the cell activation marker CD4+CD69+) was significant for the group as a whole. In terms of muscle strength, significant positive correlations were found for several T cell activation markers and memory cell counts: CD3+HLA-DR+, CD3+CD25+HLA-DR+, CD4+CD25+HLA-DR+ and CD8+CD45RA+CD45RO+, although significant relationships were limited to the stronger half of our sample. Data for the group as a whole showed similar (but weaker) positive relationships and also a negative correlation with the CD3+CD4+CD8+ count ( Fig. 1). Neither natural killer cell cytotoxic activity nor lymphocyte proliferation data were significantly correlated with either aerobic power or muscle strength (data not shown). For the purpose of multiple regression analyses, a FITscore was calculated as a half of the sum of [Z aerobic power + Z selleck screening library muscle strength]. Other variables introduced into the equations were the depression, fatigue and quality of life indices and the carbohydrate intake. After appropriate Bonferroni adjustment of probability levels, many of the apparent relationships with the fitness score became non-significant, the only significant items being the numbers of regulatory cells CD3+HLA-DR+ and CD3+CD25+HLA-DR+ (Table 5). The depression score showed a positive association with the relative number of CD3+CD8+

(suppressor) cells, and a negative association with absolute numbers of CD3+CD25+HLA-DR+ EPZ015666 mouse regulatory cells. Fatigue scores showed a strong positive association with the numbers of mature CD56dim cells and with the relative numbers of CD4+CD45RO+ memory cells, and a strong negative relationship with PHA proliferation. A good QOL score also showed Montelukast Sodium positive relationships with the relative number of CD3+CD8+ cells and the relative numbers of CD4+CD45RO+ memory

cells (i.e. the opposite correlations found for depression), and negative associations with activation markers and PHA proliferative response (i.e. the opposite of the correlation that was found for fatigue). Carbohydrate intake showed only one weak positive association with an activation marker. Further regression analyses were calculated, testing a series of immune functions against depression, fatigue, QOL, carbohydrate intake and either aerobic power (Table 6a), muscle strength (Table 6b) or FITscore (Table 6c). The only positive correlations with the fitness variables were for CD3+HLA-DR+ (muscle strength and FITscore) and PHA proliferation (FITscore), although several positive relationships were found for depression, fatigue and QOL. Conclusions were essentially similar on progressively eliminating non-significant beta coefficients from these equations. Our data offer a substantial selection of normative values for lymphocyte subsets in sedentary but otherwise healthy older individuals.

4b; PC1 and PC2 explaining 28% and 23% of the total variance in t

4b; PC1 and PC2 explaining 28% and 23% of the total variance in the fungal community data respectively). In plants inoculated with AM fungi, percent root length colonised was similar in months 1 and 3 (28% and 29% respectively, arcsine square root transformed data) and

in months 5 and 7 (56% and 52% respectively). Harvest time (single factor in ANOVA, F3,16 = 7.24, P = 0.003, MG-132 manufacturer LSD = 16) was the only factor to affect AM colonisation. Percent root length containing arbuscules followed a similar trend (harvest as a single factor, F3,16 = 9.19, P < 0.001). Hyphae and arbuscules were not observed in uninoculated plants. There was a significant positive relationship between percent root length colonised and microbial biomass-C (linear regression, P = 0.014).

Microbial biomass-C was affected by all treatments both as individual factors and as interaction terms. Most of the variation in the ANOVA was accounted for by planting regime as a single factor (F2,40 = 153.03, P < 0001; bare soil, 101 μg C g−1 soil; NM, 258 μg C g−1; AM, 164 μg C g−1; LSD = 18.2) but a planting regime × dilution interaction (F2,40 = 11.65, P < 0.001, LSD = 25.8) and a dilution × month interaction (F3,40 = 32.27, P < 0.001) were evident. Microbial biomass-C was similar in the bare soil at both dilution treatments but in the planted soils, a greater microbial biomass was present in the 10−1 amended soils ( Fig. 5). In months 3 and 5, biomass-C was greatest in the 10−1 treatments relative to the 10−6 treatments but this soil dilution effect had disappeared by month 7 (data not shown). Percentage organic carbon selleck chemical based on loss on ignition was significantly lower in the mycorrhizal planted treatments than in the non-mycorrhizal

Chlormezanone planted, or the bare soil (planting regime as a single factor, F2,57 = 27.90, P < 0.001). The carbon content of the bare soil was reduced in columns amended with the 10−1 dilution relative to those treated with the 10−6 suspension but this trend was not evident in the planted soils (planting regime × dilution interaction, F2,57 = 6.37, P = 0.003, LSD = 0.05, Fig. 5b). Soil aggregate stability (mean weight diameter, MWD) did not differ with planting regime in soils treated with the 10−6 dilution. However, MWD was significantly lower in the bare unplanted and the NM planted soils amended with the 10−1 dilution compared to equivalent planting regimes amended with the 10−6 dilution (Fig. 6a). Soils from mesocosms containing mycorrhizal plants had similar MWD values irrespective of soil dilution treatment (dilution × planting regime interaction in ANOVA, F2,56 = 4.82, LSD = 0.08, P = 0.012, Fig. 6a). Aggregates from the soil with mycorrhizal plants and from soils amended with the 10−6 dilution were more stable than those from the 10−1 bare and NM treatments, although all fall within the accepted classification as ‘stable’. Mean weight diameter (MWD) was greatest in month 3 (1.

Venom was collected according to da Silveira et al (2002), poole

Venom was collected according to da Silveira et al. (2002), pooled and stored at −20 °C until use. Protein concentration was determined by Bradford method ( Bradford, 1976). L. laeta, Loxosceles intermedia and Loxosceles gaucho Brazilian mature spiders were collected in the region of Curitiba, PR, Brazil and maintained at the Centro de Produção e Pesquisa de Imunobiológicos (CPPI) of the State of Paraná, Brazil. The venoms from mature spiders were obtained as described before. Phoneutria nigriventer spiders and Tityus serrulatus scorpions were collected in the region of Belo

Horizonte and maintained at the “Seção de Animais Peçonhentos” of Ezequiel Dias Foundation (FUNED) of Belo Horizonte, Brazil. The crude

venoms were obtained by electric stimulation, lyophilized and stored at −20 °C in the dark until use. Two commercial antivenoms were used for the neutralization assay, the antivenom produced in CPPI, Brazil Dasatinib cell line (Lot. S02100) against BLlv, L. intermedia and L. gaucho venoms and an antivenom produced by Instituto Nacional de Salud del Perú (INS) (Lot. 0300069), containing antibodies against PLlv. The lethality was assessed via intradermal (i.d.) route. Groups of four mice were injected with different doses of venoms (0.4, 0.56, 0.784, 1.098, 1.537, 2.152 mg per kg of body weight) dissolved in 0.1 mL of PBS-BSA 0.5%. Seventy-two hours later deaths were recorded and the LD50 was then calculated by Probit analysis (Finney, 1971). The dermonecrotic, hemorrhagic Selleckchem NVP-LDE225 and edematogenic activities of PLlv and BLlv were determined by intradermal injection of 10 μg of crude venom in 100 μL of PBS pH 7.2 into the shaved back of

five rabbits for each venom, as described by Furlanetto (1962). Injection of PBS alone was used as negative control. The diameters of dermonecrotic, hemorrhagic and edematogenic lesions were measured in the skin areas with a scale meter and caliper rule, 72 h after injection. Three measures of each lesion were made and their arithmetic mean was considered the mean diameter of the lesion. The sphingomyelinase (SMase) activity was measured using the Amplex Red Sphingomyelinase Assay Kit (Invitrogen) as previously described (Gatt et al., 1978; Binford et al., 2009). Briefly, different amounts Sinomenine of the venoms (0.125, 0.25, 0.5, 1.0 μg) were assayed in triplicates. Varion Cary eclipse fluorescence spectrophotometer was used to measure the fluorescence emission from the reactions. Protein profile of PLlv and BLlv was analyzed by two-dimensional electrophoresis using the IPG-SDS-PAGE system ( Gorg, 1993). The venom was solubilized in lysis buffer containing 8 M urea, 2 M thiourea, 4% w/v CHAPS, 65 mM dithioerythritol, 40 mM Tris, 0.002% bromophenol blue, protease inhibitor and 1% of IPG buffer. Nonlinear immobilized pH 3–10 gradient IPG strips were rehydrated with 100 μg of the venom for 4 h (no electric field) and then for 12 h at 30 V.

11 and 12 We have developed a range of statistical models that ad

11 and 12 We have developed a range of statistical models that address these limitations. Our analysis provide estimates of the number of influenza-associated health care outcomes in different age groups in those with and without high-risk conditions in England under the existing influenza vaccination selleck screening library programme. Measuring the effect of being in a high-risk group on the age-related burden of influenza was

essential for the modelling and cost effectiveness analyses that underpinned the recent decision in the United Kingdom to extend the existing age and risk-based vaccination policy to healthy children. 3 Data were obtained for the eight years immediately preceding the A(H1N1)v pandemic (2000/1 to 2007/8) and arranged into epidemiological years April to March to encompass the annual influenza season. Laboratory reports: Public Health

England receives weekly computerised reports of clinically significant infections confirmed by microbiology laboratories in England and Wales. The United Kingdom Standards Z-VAD-FMK nmr for Microbiology Investigations recommend the diagnostic algorithms that should be applied to patients presenting with different clinical syndromes in order to promote consistency in testing over time and between laboratories. 13 Weekly numbers of reports PD-1 antibody by date of test and age group were obtained from the national database for the following pathogens: influenza A, influenza B, respiratory syncytial virus, parainfluenza, adenovirus, rhinovirus, S. pneumoniae, Mycoplasma pneumoniae and Haemophilus influenzae. Only invasive specimens of S. pneumoniae, M. pneumoniae and H. influenzae were included due to lack of consistency in reporting non-invasive isolates. The increasing use of genomic detection methods for rhinovirus and parainfluenza resulted in a spurious temporal increase in these respiratory viruses. Reports for these pathogens where the method of

detection was either “genomic detection” or “antibody detection” were therefore omitted from the analysis. The proportion of influenza A cases that are either H1 or H3 subtypes was obtained from the results of routine surveillance specimens taken by general practices in the United Kingdom participating in the Royal College of General Practitioners Weekly Returns Service. 14 Inpatient admissions: Weekly inpatient admissions to National Health Service hospitals in England were obtained from the Hospital Episode Statistics database. 15 Patients were included in the analysis if they had an acute respiratory illness code (ICD-10 codes J0*, J1*, J2*, J3*, J40*, J41*, J42*, J43*, J44*, J47*) in any diagnosis field.

33 and 34 Moreover, these groups may have different expectations

33 and 34 Moreover, these groups may have different expectations concerning RTW, which could lead to a higher dropout rate from rehabilitative interventions.35 In this study, they represented 50% of patients. Although, studies about the role of the mother language are scarce, 1 study36 reported that the mother language, among others, was a predictor for non-RTW. Additionally, a non-Swiss mother language is related to a low health literacy, which may cause a substantial burden to society and the injured person.37 Understanding the role of language in the development of chronic WADs may be crucial for developing effective work disability

prevention programs for patients with WADs. Predicting RTW in patients with chronic pain is difficult. Lifting tests explain 10% to 20% of the variance in RTW in patients with musculoskeletal disorders.38 Some authors reported an explained variance up to 27%,39 while others suggested that adding FCE tests find more to self-reported data would increase the explained variance from 9% to 16%.40 However, others reported a 10% explained variance, questioning the predictive value of FCE tests for RTW in patients with chronic musculoskeletal pain.41 and 42 These differences may be explained by differences in study design (eg, cross-sectional vs prospective) or sample size ranging from 5 to 20 events per prognostic association tested. Follow-up times may range from 1 to 12 months, statistical

models may use uni- or multivariate analysis that corrects for confounders.8 Moreover, buy PR-171 results between studies may Vasopressin Receptor differ based on the definition of RTW used, which can be measured by self-report or insurance data. Also social security systems between different countries may lead to different results. This study shows that the strength of the correlation between WC and FCE tests is related to the time point after the whiplash injury. Most of the patients in this study reached full WC within the 12-month follow-up period. This is in contrast to other studies1 and 2 showing that a substantial proportion of patients with WADs (40%–60%) still have varying levels of pain and self-reported disability after 1 year.

We hypothesized that WC over 12 months may not be indicative of perceived disability. In a post hoc analysis, we evaluated the correlation between WC and the available NDI scores at 3 and 12 months (50% of the study sample). The correlations were low (r<0.3; WC accounts for 9% of the explained variance of NDI), indicating that disability and WC are related but distinct constructs. While it may be methodologically correct to study FCE tests separately, in clinical work, FCE tests are used in conjunction with medical records, patient interviews, musculoskeletal evaluation, and job-specific observations.11 One may argue that predictive values would be higher if RTW can be predicted based on the full clinical package, including FCE tests. Results of this strategy are indeed positive.

Na maioria dos doentes com CU a doença localiza‐se à esquerda (67

Na maioria dos doentes com CU a doença localiza‐se à esquerda (67,6%) (tabela 1). A duração média de tratamento com AZA foi de 35,1 ± 30,6 meses. A duração mínima de utilização do fármaco foi 3 meses e a duração máxima foi 136 meses. Em um doente a AZA foi utilizada apenas por 3 meses por mielotoxicidade e selleck kinase inhibitor em 3 doentes

foi usada por 4 meses (em 2 dos quais por mielotoxicidade e em outro por hepatotoxicidade). Os restantes doentes estiveram medicados com a AZA por períodos superiores a 6 meses. A taxa global de efeitos secundários foi de 30,6% (em 11 doentes os efeitos secundários surgiram antes dos 3 meses de tratamento e em 4 doentes surgiram após esse período). Nenhum doente havia sido tratado previamente com biológicos ou metotrexato. A maioria dos doentes (83,3%) estava medicada concomitantemente com 5‐ASA. Na altura da introdução da AZA, a mesma percentagem selleck chemical de doentes (83,3%) estava também medicada com corticoides, com uma duração média de 6,8 ± 10,0 meses. A AZA foi eficaz em 48 doentes (66,7%). Na CU a AZA foi eficaz em 70,6% dos doentes e na DC em 60%. A tabela 2 caracteriza de forma discriminada a população estudada, de acordo com a eficácia do tratamento a longo prazo. O sexo, o

tipo de doença (DC/CU/DII) e a idade de diagnóstico da DII não têm relação com a eficácia da AZA a longo prazo. Existe relação entre through a idade de introdução da AZA e a resposta a longo prazo do fármaco, embora esta relação seja sustentada estatisticamente por

uma significância marginal (r = 0,228, p = 0,054). Quanto mais avançada a idade do doente na altura da introdução da AZA, maior a eficácia do fármaco a longo prazo. No que respeita ao tempo de evolução da doença, não se verificou correlação com a eficácia sustentada da AZA (r = 0,097, p = 0,416). Utilizando a regressão linear, pelo método stepwise, verificou‐se que a única variável que prediz o sucesso a longo prazo da AZA aquando do início da terapêutica é a idade mais avançada na altura da introdução do fármaco (R = 0,303, p = 0,019) (fig. 1). Neste modelo utilizaram‐se como variáveis o sexo, o tipo de doença, os PL antes do início da terapêutica, o tempo de evolução da doença e a idade do doente na altura da introdução da AZA. Além disso, avaliando o subgrupo de doentes com CU, verificou‐se também associação entre a localização da doença e a eficácia da AZA a longo prazo, sendo que os doentes com colite esquerda respondem de forma mais favorável do que os doentes com pancolite (r = –0,381, p = 0,026). Já nos doentes com DC, não se observou relação com a eficácia da AZA no que respeita ao fenótipo, à localização e à presença de doença perianal, tal como se verifica na tabela 2.

15 (Table 2) (Gundersen et al , 1999) The estimation of DG micro

15 (Table 2) (Gundersen et al., 1999). The estimation of DG microglia mean body cell volume, microglia mean body cell number, and DG volume, was assisted by Stereologer™ software (Stereology Resource Center, Chester, MD). The software was installed on a Dell Optiplex tower computer and connected to a Nikon Eclipse E600 microscope

(Nikon, Melville, NY) fitted with an X–Y–Z motorized stage controller (Prior Scientific, Rockland, MA), linear encoder microcator (z-axis gauge) (Heidenhain, Schaumburg, IL), high resolution color video camera (IMI Tech, Inc., Encinitas, CA) selleck chemical and .50 C-mount (Nikon, Melville, NY). DG volume was estimated at 4× (Nikon Plan 4× 0.10); GSK2118436 manufacturer DG microglia mean cell volume and mean cell number were estimated at 60× (Nikon Plan APO 1.40 Oil). The camera image was processed with a high resolution video card and displayed on a 21 in. high resolution Dell monitor. One experimenter (C.S.) collected all of the stereological data without knowledge of the blood Pb level of each subject;

the experimenter was not blind to treatment group. An unbiased estimate of the number of microglia in the DG was obtained using the optical fractionator method (West et al., 1991) as reported previously for quantification of total number of microglia in mouse models of aging and neuropathology (Mouton et al., 2002). For each section the software randomly sampled virtual 3-D counting frames (disector) at 60× magnification with a 2 μm guard area. Using thin-focal

plane optical scanning, microglia were counted when they fell within the central depth of the counting frame and/or touched the inclusion lines. The total number of microglia was estimated with the following selleck kinase inhibitor formula: Nobj = ΣQ− × 1/SSF × 1/ASF × 1/TSF; where ΣQ− = sum of the objects sampled; SSF = sampling interval; ASF = total area sampled/total area on all sampled sections; and TSF = the height of the sample/total section thickness. For each frame, mean cell volume was quantified on microglia counted with the disector probe. The dentate gyrus reference volume (V(ref)) was determined at 4× magnification using the Cavalieri-point counting approach ( Gundersen and Jensen, 1987): V(ref) = ([k × t] × ∑P × [a(p)/M2]); where: k = sampling interval; t = post-processing section average thickness; and thus [k × t] = distance between planes; ∑P = sum of points counted; [a(p)/M2] = test grid area per point (μm2) divided by the magnification factor squared. Examples of microglia images are provided in Fig. 4. SAS Version 9.2 statistical software was used for all analyses. All data were entered and checked for accuracy and distribution properties prior to analysis. No extreme outliers were identified, and all data were included for analysis.

Samples of soil were air dried for 7–14 days after which aggregat

Samples of soil were air dried for 7–14 days after which aggregate size distribution was determined by gently sieving a 25 g homogenised GDC-0199 supplier sub-sample through nine sieves: 4000, 2000, 1000, 500, 425, 300, 212, 106 and 53 μm. The mass retained on each sieve was weighed, recorded and the percentage mass in each fraction calculated. From aggregate size distributions, the coefficient of uniformity (Kézdi 1974) was used to numerically illustrate the differences in distributions where large and small aggregates co-existed. Aggregate stability was determined by the fast wetting (slaking) technique developed by Le Bissonnais (1996) and expressed

as mean weight diameter (MWD). Aggregate hydraulic properties were measured by a miniaturised infiltrometer (Leeds-Harrison et al., 1994 and Hallett and Young, 1999). Further sub-samples of the air dried soil Inhibitor Library in vivo were sieved to 2–5 mm,

prior to oven drying at 40 °C for 24 h. The infiltration device was constructed with capillary tubing, glass tubing (3.5 mm internal diameter) and a 200 μl pipette tip. In order to assess the hydraulic conductivity, the sorptivity of water flowing into soil aggregates at five different heads of water was measured (0, −10, −20, −30 and −40 mm). Water repellency (R) was determined through measurements of the ethanol (Se) and water sorptivity (Sw) at the −20 mm head. Ethanol infiltration is not affected by hydrophobic substances and hence isolates the influence of the pore structure on wetability. Non-specific serine/threonine protein kinase The repellency index (R) of individual aggregates was calculated from: R=1.95SeSwwith the constant accounting for the differences in surface

tension and viscosity. Soil structural analysis was undertaken non-destructively using a Venlo H series, X-ray CT Scanner (H 350/225 CT; X-TEK, Tring, Hertfordshire, UK). A 2 mm primary copper filter was placed near the X-ray source to eliminate X-ray scatter, in addition to a 4 mm secondary copper filter placed at the detector to prevent detector saturation (i.e. when the input to the detector exceeds the total capacity) and beam hardening (Taina et al. 2008). Gain and offset correction was applied to all of the diodes within the detector by applying a black (offset) and white (gain) reference to adjust for exposure variations. Macrocosms were scanned at 175 kV and 3 μA, with an exposure time of 90 ms. The samples were placed 145 mm away from the detector and scanned to collect a single image at 6 pre-determined depths according to each particular experimental layout. Images were processed using AnalySIS® (Soft Imaging Systems (SIS), Münster, Germany) to segment pore space. The image resolution was 65.4 μm pixel−1. Initial images were cropped to 52.97 mm × 50.69 mm (810 pixel × 775 pixel), to remove the sides of the macrocosm from the image, in addition to boundary effects such as cracks that occasionally ran down the edges of the macrocosm.

The intent of prime-boost vaccination is to induce different type

The intent of prime-boost vaccination is to induce different types of immune responses and enhance the overall immune response, a result that may not occur if only one type of vaccine were to be given for all doses. This approach has been employed in trials with,

for example, TB, CMV, malaria and HIV candidate vaccines. For example, in studies on new TB vaccines, subjects already primed with the live, attenuated BCG vaccine have been boosted with a subunit adjuvanted vaccine (see Tuberculosis). Respiratory syncytial virus is a common cause of bronchiolitis and pneumonia in infants, and exacerbations of chronic obstructive pulmonary disease in the elderly. The development of an effective vaccine has been challenging; natural immunity to RSV infection is incomplete and re-infections occur in all age groups. Moreover, the primary target population for vaccination is newborns and young infants, and they are this website a challenging population selleckchem as they have relatively immature immune systems and the presence of maternal antibodies may interfere with vaccination of the young

infant (see Chapter 2 – Vaccine immunology). The initial efforts to develop a formalin-inactivated cell culture-derived RSV vaccine resulted in an unanticipated enhancement of natural RSV disease in some of the RSV-naïve infants who received the vaccine in a clinical trial and subsequently were exposed to RSV. The exacerbated disease is thought to be due to an exaggerated T helper type 2 cell immune response (see Chapter 2 – Vaccine immunology). Safety STK38 concerns regarding the potential of vaccines to trigger or prime for immunopathological responses has resulted in a cautious approach to the development of RSV vaccines. The vaccine candidates most advanced in clinical development use two different approaches – one uses a live, attenuated virus with a gene deletion deliberately targeted to minimise

immunopathological responses. The other approach uses a live viral vector to deliver only a key RSV surface antigen, thereby avoiding the risk of an immunopathological response arising from exposure to the RSV virus itself. Infectious illnesses exert a major burden of disease in developing countries. The greatest burden is caused by diseases for which we currently have no vaccines, eg taeniid cestode parasites are associated with high human morbidity and losses in livestock. Global efforts to reduce these infections in humans are ongoing through the use of antihelminthics and the implementation of lifestyle changes, but this is having little effect. However, substantial progress has been made towards developing veterinary vaccines which encourages investigation of the potential use of similar vaccines in humans to prevent, for example, hydatid disease (arising from infection with Echinococcus granulosus) and cysticercosis (from infection with Taenia solium).

The number of individuals of razor clams and other bivalves were

The number of individuals of razor clams and other bivalves were counted at each sampling station and the density was estimated using the area of the sampling frame. Sediment samples were collected with a 30 cm corer. Then they were dried in an oven at 80 °C for two days and apportioned using a 1000 μm analytical sieve (Retsch, Düsseldorf, Germany). Their size distribution was estimated with a laser granulometer (LS200, Beckman Coulter Inc, Brea, CA, USA) and classified according to the Folk classification ( Folk, 1954 and Jackson and Richardson, 2007). All this information is summarised in Table 1. The acoustic survey was carried

out on 12 July 2009, using a small fishing boat (6.25 m long). A Simrad EK60 scientific echosounder with an ES200-7C split-beam 200 kHz transducer was mounted find more on a steel pole attached to the hull rail of the boat. The transducer was operated with maximum emitting power (1 kW), minimum pulse length (64 μs) and a sampling rate of 10 pings s− 1 to obtain the maximum vertical and horizontal resolution. The acoustic survey was carried out under good weather conditions and keeping

the boat’s speed between 1.5 and 3.5 knots. This speed permits the oversampling of every bottom point in at least 4 consecutive pings (the split beam angle is 7° and the survey area depth ranges from 5–11 m), thereby ensuring spatial continuity. Positions were recorded into the sounder files using a GPS (Simrad GN33) signal input. To define the acoustic transects, an imaginary line, parallel to the coast, was defined over each sandbar. Transects were sailed along these lines repeatedly, each one at least three Lumacaftor research buy times (see Figure 3, p. 507), switching the course in between, i.e. leaving the coast to the left and right sides; this was later used to assess the differences due to the ship’s course. In total,

14 acoustic transects were recorded: five along the Raxó sandbar, five along Aguete and four along A Cova, with respective mean lengths of 550 m, 250 m and 285 m. Angular information from the seabed. The phase distribution of the backscattered signal is due to the bottom surface roughness and the sub-bottom scatterers (razor shells in our study case) within the insonified seabed area. In Alanine-glyoxylate transaminase previous works split-beam characterisation of bottom roughness has been used to discriminate fish aggregations near the seabed (MacLennan et al. 2004) or to improve 3-D bathymetry resolution and seabed classification (Demer et al., 2009 and Cutter and Demer, 2010). This technique uses multifrequency transducer assemblies to overcome the baseline decorrelation problem. Our hypothesis is that a similar mechanism in the sub-bottom volume, where impedance fluctuations are due to the presence of benthic biomass, local variations of granulometry, or seabed composition, should give us angular information about the presence of razor clam patches (angle φ in Figure 2a and alongship and athwartship angles in Figure 2b).