Characterizing fishing effort and spatial extent of coastal fisheries

Biodiverse coastal zones are often areas of intense fishing pressure due to the high relative density of fishing capacity in these nearshore regions. Although overcapacity is one of the central challenges to fisheries sustainability in coastal zones, accurate estimates of fishing pressure in coastal zones are limited, hampering the assessment of the direct and collateral impacts (e.g., habitat degradation, bycatch) of fishing. We compiled a comprehensive database of fishing effort metrics and the corresponding spatial limits of fisheries and used a spatial analysis program (FEET) to map fishing effort density (measured as boat-meters per km2) in the coastal zones of six ocean regions. We also considered the utility of a number of socioeconomic variables as indicators of fishing pressure at the national level; fishing density increased as a function of population size and decreased as a function of coastline length. Our mapping exercise points to intra and interregional 'hotspots' of coastal fishing pressure. The significant and intuitive relationships we found between fishing density and population size and coastline length may help with coarse regional characterizations of fishing pressure. However, spatially-delimited fishing effort data are needed to accurately map fishing hotspots, i.e., areas of intense fishing activity. We suggest that estimates of fishing effort, not just target catch or yield, serve as a necessary measure of fishing activity, which is a key link to evaluating sustainability and environmental impacts of coastal fisheries.     

A cluster randomized controlled trial comparing three methods of disseminating practice guidelines for children with croup [ISRCTN73394937]

Background

The optimal management of croup – a common respiratory illness in young children – is well established. In particular, treatment with corticosteroids has been shown to significantly reduce the rate and duration of intubation, hospitalization, and return to care for on-going croup symptoms. Furthermore treatment with a single dose of corticosteroids does not appear to result in any significant adverse outcomes, and yields overall cost-savings for both families and the health care system. However, as has been shown with many other diseases, there is a significant gap between what we know and what we do. The overall aim of this study is to identify, from a societal perspective, the costs and associated benefits of three strategies for implementing a practice guideline that addresses the management of croup.

Methods/designs

We propose to use a matched pair cluster trial in 24 Alberta hospitals randomized into three intervention groups. We will use mixed methods to assess outcomes including linkage and analysis of administrative databases obtained from Alberta Health and Wellness, retrospective medical chart audit, and prospective telephone surveys of the parents of children diagnosed to have croup. The intervention strategies to be compared will be mailing of printed educational materials (low intensity intervention), mailing plus a combination of interactive educational meetings, educational outreach visits, and reminders (intermediate intensity intervention), and a combination of mailing, interactive sessions, outreach visits, reminders plus identification of local opinion leaders and establishment of local consensus processes (high intensity intervention). The primary objective is to determine which of the three intervention strategies are most effective at lowering the rate of hospital days per 1,000 disease episodes. Secondary objectives are to determine which of the three dissemination strategies are most effective at increasing the use of therapies of known benefit. An economic analysis will be conducted to determine which of the three intervention strategies will most effectively reduce total societal costs including all health care costs, costs borne by the family, and costs stemming from the strategies for disseminating guidelines.     

Quantification of six herbicide metabolites in human urine

We developed a sensitive, selective and precise method for measuring herbicide metabolites in human urine. Our method uses automated liquid delivery of internal standards and acetate buffer and a mixed polarity polymeric phase solid phase extraction of a 2 mL urine sample. The concentrated eluate is analyzed using high-performance liquid chromatography-tandem mass spectrometry. Isotope dilution calibration is used for quantification of all analytes. The limits of detection of our method range from 0.036 to 0.075 ng/mL. The within- and between-day variation in pooled quality control samples range from 2.5 to 9.0% and from 3.2 to 16%, respectively, for all analytes at concentrations ranging from 0.6 to 12 ng/mL. Precision was similar with samples fortified with 0.1 and 0.25 ng/mL that were analyzed in each run. We validated our selective method against a less selective method used previously in our laboratory by analyzing human specimens using both methods. The methods produced results that were in agreement, with no significant bias observed.     

The Fanconi anemia pathway limits the severity of mutagenesis

Fanconi anemia (FA) is a developmental and cancer predisposition disorder in which key, yet unknown, physiological events promoting chromosome stability are compromised. FA cells exhibit excess metaphase chromatid breaks and are universally hypersensitive to DNA interstrand crosslinking agents. Published mutagenesis data from single-gene mutation assays show both increased and decreased mutation frequencies in FA cells. In this review we discuss the data from the literature and from our isogenic fancg knockout hamster CHO cells, and interpret these data within the framework of a molecular model that accommodates these seemingly divergent observations. In FA cells, reduced rates of recovery of viable X-linked hypoxanthine phosphoribosyltransferase (hprt) mutants are characteristically observed for diverse mutagenic agents, but also in untreated cultures, indicating the relevance of the FA pathway for processing assorted DNA lesions. We ascribe these reductions to: (1) impaired mutagenic translesion synthesis within hprt during DNA replication and (2) lethality of mutant cells following replication fork breakage on the X chromosome, caused by unrepaired double-strand breaks or large deletions/translocations encompassing essential genes flanking hprt. These findings, along with studies showing increased spontaneous mutability of FA cells at two autosomal loci, support a model in which FA proteins promote both translesion synthesis at replication-blocking lesions and repair of broken replication forks by homologous recombination and DNA end joining. The essence of this model is that the FANC protein pathway serves to restrict the severity of mutational outcome by favoring base substitutions and small deletions over larger deletions and chromosomal rearrangements.     

Looking for Thom's biomarkers with proteomics

In recent years, large numbers of putative disease biomarkers have been identified. Combinations of protein biomarkers have been proposed to overcome the lack of single, magic-bullet identifiers of disease conditions. The number of biomarkers in a panel must be kept small to avoid the combinatorial explosion that requires very large, uneconomical sample cohorts for validation. Recent results on high sensitivity blood-based diagnostic proteomics (Godovac-Zimmermann, J et al., J. Proteome Res. 2006) suggest that the keys to identifying useful panels include judicious application of physiological knowledge to choose appropriate combinations of local, tissue/disease markers and global, systemic markers and to use very high sensitivity protein detection. Biomarkers that show non-Gaussian landscapes reminiscent of Rene Thom's multiple, stable-state landscapes seem to have the greatest predictive value for breast cancer (Godovac-Zimmermann, J. et al., J. Proteome Res. 2006).     

Estimation and interpretation of egg provisioning in marine invertebrates

Per-offspring maternal investment is an integral part of life-historytheory. To understand the evolution of per-offspring maternalinvestment in marine invertebrates, a number of mathematicalmodels have been developed. These models examine how selectionaffects the proportion of maternally derived egg energy usedto produce a newly metamorphosed juvenile (s) and make predictionsabout the distribution of s in nature. However, there are veryfew published values of s and therefore it is difficult to evaluatehow well these models match nature. We present several equationsto empirically estimate values of s for any group of marineinvertebrate, and use data from echinoderms to compare the differentequations. The calculations that directly estimate s requireinformation on the amount of egg energy, juvenile energy, andenergy metabolized during development. Currently, there arefew data available for directly estimating s, and thus generatingdistributions of s derived from direct estimates is not possible.Furthermore, the direct estimations of s are informative forplanktotrophy but not for lecithotrophy. We have developed anequation that can be used to directly estimate s for lecithotrophs.The calculations to indirectly estimate s only require egg energyor egg size for the species in question and the value of s andegg energy or size for a reference species. This reference speciesreplaces the need to measure juvenile energy and energy metabolizedduring larval development. Because egg energy or size is currentlyavailable for many species, the indirect estimates will be usefulfor generating distributions of s, and will allow comparisonswith models. Although these indirect methods are good for generatingdistributions of s, they do not provide reliable estimates ofs for any particular species. Estimating values of s to comparemodels is a critical gap in our current evaluations of marineinvertebrate life-history models.     

Spatial regulation and the rate of signal transduction activation

Of the many important signaling events that take place on the surface of a mammalian cell, activation of signal transduction pathways via interactions of cell surface receptors is one of the most important. Evidence suggests that cell surface proteins are not as freely diffusible as implied by the classic fluid mosaic model and that their confinement to membrane domains is regulated. It is unknown whether these dynamic localization mechanisms function to enhance signal transduction activation rate or to minimize cross talk among pathways that share common intermediates. To determine which of these two possibilities is more likely, we derive an explicit equation for the rate at which cell surface membrane proteins interact based on a Brownian motion model in the presence of endocytosis and exocytosis. We find that in the absence of any diffusion constraints, cell surface protein interaction rate is extremely high relative to cytoplasmic protein interaction rate even in a large mammalian cell with a receptor abundance of a mere two hundred molecules. Since a larger number of downstream signaling events needs to take place, each occurring at a much slower rate than the initial activation via association of cell surface proteins, we conclude that the role of co-localization is most likely that of cross-talk reduction rather than coupling efficiency enhancement.