Can vertical migrations of dinoflagellates explain observed bioluminescence patterns during an upwelling event in Monterey Bay, California?

Extensive AUVs surveys showed that during the development of upwelling, bioluminescent dinoflagellates from the northern part of the Monterey Bay, California (called the upwelling shadow area), were able to avoid advection by southward flowing currents along the entrance to the Bay, while non-bioluminescent phytoplankton were advected by currents. It is known that vertical swimming of dinoflagellates to deeper layers helps them avoid losses due to advection. In the present paper, we investigate if modeling dinoflagellates’ vertical swimming can explain the observed dinoflagellates’ ability to avoid advection during the upwelling development. The dynamics of a dinoflagellate population is modeled with the tracer model with introduced vertical swimming velocity. Three swimming behaviors are considered: sinking, swimming to the target depth and diel vertical migration. Velocities in all swimming cases are considered in the ranges of documented velocities for the observed dinoflagellates species during the upwelling development in the Monterey Bay. Our modeling confirmed that observed bioluminescent dinoflagellates’ avoidance of advection during the upwelling development can be explained by their vertical swimming ability. In the case of swimming with 20 m/day (which is half of observed maximum swimming velocity), around 40% of dinoflagellates population from the northern part of the Bay were advected along the entrance to the Bay in comparison to the case without swimming. This is in agreement with the ratio of around 45% of observed mean bioluminescence intensity at the entrance to the Bay to the observed mean intensity in the northern part of the Bay. This mechanism also helps explain the general persistence of dinoflagellates in this part of the coastline

Structural Evaluation of Full-Depth Flexible Pavement Using APT

The fundamentals of rutting behavior for thin full-depth flexible pavements (i.e., asphalt thickness less than 12 inches) are investigated in this study. The scope incorporates an experimental study using full-scale Accelerated Pavement Tests (APTs) to monitor the evolution of each pavement structural layer\u27s transverse profiles. The findings were then employed to verify the local rutting model coefficients used in the current pavement design method, the Mechanistic-Empirical Pavement Design Guide (MEPDG). Four APT sections were constructed using two thin typical pavement structures (seven-and ten-inches thick) and two types of surface course material (dense-graded and SMA). A mid-depth rut monitoring and automated laser profile systems were designed to reconstruct the transverse profiles at each pavement layer interface throughout the process of accelerated pavement deterioration that is produced during the APT. The contributions of each pavement structural layer to rutting and the evolution of layer deformation were derived. This study found that the permanent deformation within full-depth asphalt concrete significantly depends upon the pavement thickness. However, once the pavement reaches sufficient thickness (more than 12.5 inches), increasing the thickness does not significantly affect the permanent deformation. Additionally, for thin full-depth asphalt pavements with a dense-graded Hot Mix Asphalt (HMA) surface course, most pavement rutting is caused by the deformation of the asphalt concrete, with about half the rutting amount observed within the top four inches of the pavement layers. However, for thin full-depth asphalt pavements with an SMA surface course, most pavement rutting comes from the closet sublayer to the surface, i.e., the intermediate layer. The accuracy of the MEPDG’s prediction models for thin full-depth asphalt pavement was evaluated using some statistical parameters, including bias, the sum of squared error, and the standard error of estimates between the predicted and actual measurements. Based on the statistical analysis (at the 95% confidence level), no significant difference was found between the version 2.3-predicted and measured rutting of total asphalt concrete layer and subgrade for thick and thin pavements

Kidney oxygenation, perfusion and blood flow in people with and without type 1 diabetes

Background We used magnetic resonance imaging (MRI) to study kidney energetics in persons with and without type 1 diabetes (T1D). Methods In a cross-sectional study, 15 persons with T1D and albuminuria and 15 non-diabetic controls (CONs) underwent multiparametric MRI (3 Tesla Philips Scanner) to quantify renal cortical and medullary oxygenation (R-2*, higher values correspond to higher deoxyhaemoglobin concentration), renal perfusion (arterial spin labelling) and renal artery blood flow (phase contrast). Analyses were adjusted for age, sex, systolic blood pressure, plasma haemoglobin, body mass index and estimated glomerular filtration rate (eGFR). Results Participants with T1D had a higher median (Q1; Q3) urine albumin creatinine ratio (UACR) than CONs [46 (21; 58) versus 4 (3; 6) mg/g; P < .0001] and a lower mean +/- SD eGFR (73 +/- 32 mL/min/1.73 m(2) versus 88 +/- 15 mL/min/1.73 m(2); P = .12), although not significantly. Mean medullary R-2* was lower in T1D (34 +/- 6/s versus 38 +/- 5/s; P < .01) corresponding to a higher oxygenation. R-2* was not different in the cortex. Cortical perfusion was lower in T1D (163 +/- 40 versus 224 +/- 49 mL/100 g/min; P < .001). Renal artery blood flow was lower in T1D than in CONs (360 +/- 130 versus 430 +/- 113 mL/min; P = .05). In T1D, lower cortical oxygenation and renal artery blood flow were both associated with higher UACR and lower eGFR (P < .05). Conclusions Participants with T1D and albuminuria exhibited higher medullary oxygenation than CONs, despite lower cortical perfusion and renal artery blood flow. This might reflect perturbed kidney energetics leading to a higher setpoint of medullary oxygenation in T1D. Lower cortical oxygenation and renal artery blood flow were associated with higher UACR and lower eGFR in T1D.Peer reviewe

British Lung Foundation/United Kingdom primary immunodeficiency network consensus statement on the definition, diagnosis, and management of granulomatous-lymphocytic interstitial lung disease in common variable immunodeficiency disorders

A proportion of people living with common variable immunodeficiency disorders develop granulomatous-lymphocytic interstitial lung disease (GLILD). We aimed to develop a consensus statement on the definition, diagnosis, and management of GLILD. All UK specialist centers were contacted and relevant physicians were invited to take part in a 3-round online Delphi process. Responses were graded as Strongly Agree, Tend to Agree, Neither Agree nor Disagree, Tend to Disagree, and Strongly Disagree, scored +1, +0.5, 0, −0.5, and −1, respectively. Agreement was defined as greater than or equal to 80% consensus. Scores are reported as mean ± SD. There was 100% agreement (score, 0.92 ± 0.19) for the following definition: “GLILD is a distinct clinico-radio-pathological ILD occurring in patients with [common variable immunodeficiency disorders], associated with a lymphocytic infiltrate and/or granuloma in the lung, and in whom other conditions have been considered and where possible excluded.” There was consensus that the workup of suspected GLILD requires chest computed tomography (CT) (0.98 ± 0.01), lung function tests (eg, gas transfer, 0.94 ± 0.17), bronchoscopy to exclude infection (0.63 ± 0.50), and lung biopsy (0.58 ± 0.40). There was no consensus on whether expectant management following optimization of immunoglobulin therapy was acceptable: 67% agreed, 25% disagreed, score 0.38 ± 0.59; 90% agreed that when treatment was required, first-line treatment should be with corticosteroids alone (score, 0.55 ± 0.51)

A randomised controlled trial of positive memory training for the treatment of depression within schizophrenia

Abstract Background: Depression is highly prevalent within individuals diagnosed with schizophrenia, and is associated with an increased risk of suicide. There are no current evidence based treatments for low mood within this group. The specific targeting of co-morbid conditions within complex mental health problems lends itself to the development of short-term structured interventions which are relatively easy to disseminate within health services. A brief cognitive intervention based on a competitive memory theory of depression, is being evaluated in terms of its effectiveness in reducing depression within this group. Methods/Design: This is a single blind, intention-to-treat, multi-site, randomized controlled trial comparing Positive Memory Training plus Treatment as Usual with Treatment as Usual alone. Participants will be recruited from two NHS Trusts in Southern England. In order to be eligible, participants must have a DSM-V diagnosis of schizophrenia or schizo-affective disorder and exhibit at least a mild level of depression. Following baseline assessment eligible participants will be randomly allocated to either the Positive Memory Training plus Treatment as Usual group or the Treatment as Usual group. Outcome will be assessed at the end of treatment (3-months) and at 6-month and 9-month post randomization by assessors blind to group allocation. The primary outcome will be levels of depression and secondary outcomes will be severity of psychotic symptoms and cost-effectiveness. Semi-structured interviews will be conducted with all participants who are allocated to the treatment group so as to explore the acceptability of the intervention. Discussion: Cognitive behaviour therapy is recommended for individuals diagnosed with schizophrenia. However, the number of sessions and length of training required to deliver this intervention has caused a limit in availability. The current trial will evaluate a short-term structured protocol which targets a co-morbid condition often considered of primary importance by service users. If successful the intervention will be an important addition to current initiatives aimed at increasing access to psychological therapies for people diagnosed with severe mental health problems. Trial registration: Current Controlled Trials. ISRCTN99485756. Registered 13 March 2014

Imaging of bronchial pathology in antibody deficiency: Data from the European Chest CT Group

Studies of chest computed tomography (CT) in patients with primary antibody deficiency syndromes (ADS) suggest a broad range of bronchial pathology. However, there are as yet no multicentre studies to assess the variety of bronchial pathology in this patient group. One of the underlying reasons is the lack of a consensus methodology, a prerequisite to jointly document chest CT findings. We aimed to establish an international platform for the evaluation of bronchial pathology as assessed by chest CT and to describe the range of bronchial pathologies in patients with antibody deficiency. Ffteen immunodeficiency centres from 9 countries evaluated chest CT scans of patients with ADS using a predefined list of potential findings including an extent score for bronchiectasis. Data of 282 patients with ADS were collected. Patients with common variable immunodeficiency disorders (CVID) comprised the largest subgroup (232 patients, 82.3%). Eighty percent of CVID patients had radiological evidence of bronchial pathology including bronchiectasis in 61%, bronchial wall thickening in 44% and mucus plugging in 29%. Bronchiectasis was detected in 44% of CVID patients aged less than 20 years. Cough was a better predictor for bronchiectasis than spirometry values. Delay of diagnosis as well as duration of disease correlated positively with presence of bronchiectasis. The use of consensus diagnostic criteria and a pre-defined list of bronchial pathologies allows for comparison of chest CT data in multicentre studies. Our data suggest a high prevalence of bronchial pathology in CVID due to late diagnosis or duration of disease