Derby Fisheries, Individual Quotas, and Transition in the Fish Processing Industry

Processors adapt to the pulse of landings in derby fisheries by investing in large-scale facilities capable of preserving and storing fish products. In fisheries where the pulse of landings suppresses the ability of processors to meet consumer demand for fresh product, the imposition of individual quota (IQ) systems transforms the associated fish processing industry. The cost of fresh fish processing is generally lower and more malleable than that for preserved fish, and consumers may pay a price premium for fresh product, which creates an opportunity for entry by fresh-fish processors and results in higher equilibrium ex-vessel prices. Incumbent firms are likely to experience an economic dislocation due to a diminished value of nonmalleable capital used to preserve and store fish products. Our paper generalizes and provides a modeling framework for the observed changes in the British Columbian halibut harvester/processor industry complex following the introduction of an IQ system.Derby fishery, individual quotas, pulse of landings, fish processing, fresh fish, preserved fish, product forms, ex-vessel price, wholesale fish price, processing capital, malleability, Resource /Energy Economics and Policy, Q13, Q22,

Self-regulation and social welfare: The political economy of corporate environmentalism

We extend the economic theory of regulation to allow for strategic self-regulation that preempts political action. When political "entry" is costly for consumer, firms can deter it through voluntary restraints. Unlike standard entry models, deterrence is achieved by over-investing to raise the rival's welfare in the event of entry. Empirical evidence on releases of toxic chemicals shows that an increased threat of regulation (as proxied by increased membership in conservation groups) indeed induces firms to reduce toxic releases. We establish conditions under which self-regulation, if it occurs, is a Pareto improvement once costs of influencing policy are included

Una perspectiva Social Cognitiva de la transición entre la escuela y el trabajo

Este artículo propone a la Teoría Social Cognitiva del Desarrollo de Carrera (SCCT; Lent, Brown, & Hackett, 1994) como una ventajosa perspectiva para comprender el proceso de transición entre la escuela y el trabajo. En lugar de enfatizar solo el período inmediatamente precedente al egreso de la escuela media, la perspectiva SCCT del proceso de transición entre la escuela y el trabajo se concentra en seis aspectos relacionados evolutivamente que se manifiestan a través de los años escolares. El énfasis en estos seis temas (formación de autoeficacia y expectativas de resultados, desarrollo de los intereses, relaciones entre intereses y metas, traducción de metas en acciones, ejecución de  destrezas; negociación de apoyos y obstáculos de transición) sugiere múltiples metas e intervenciones tendientes a facilitar el desarrollo de carrera de los estudiantes durante los años de escuela y después del ingreso al trabajo

Intramembrane proteolysis mediates shedding of a key adhesin during erythrocyte invasion by the malaria parasite.

Apicomplexan pathogens are obligate intracellular parasites. To enter cells, they must bind with high affinity to host cell receptors and then uncouple these interactions to complete invasion. Merozoites of Plasmodium falciparum, the parasite responsible for the most dangerous form of malaria, invade erythrocytes using a family of adhesins called Duffy binding ligand-erythrocyte binding proteins (DBL-EBPs). The best-characterized P. falciparum DBL-EBP is erythrocyte binding antigen 175 (EBA-175), which binds erythrocyte surface glycophorin A. We report that EBA-175 is shed from the merozoite at around the point of invasion. Shedding occurs by proteolytic cleavage within the transmembrane domain (TMD) at a site that is conserved across the DBL-EBP family. We show that EBA-175 is cleaved by PfROM4, a rhomboid protease that localizes to the merozoite plasma membrane, but not by other rhomboids tested. Mutations within the EBA-175 TMD that abolish cleavage by PfROM4 prevent parasite growth. Our results identify a crucial role for intramembrane proteolysis in the life cycle of this pathogen

The malaria parasite egress protease SUB1 is a calcium-dependent redox switch subtilisin.

Malaria is caused by a protozoan parasite that replicates within an intraerythrocytic parasitophorous vacuole. Release (egress) of malaria merozoites from the host erythrocyte is a highly regulated and calcium-dependent event that is critical for disease progression. Minutes before egress, an essential parasite serine protease called SUB1 is discharged into the parasitophorous vacuole, where it proteolytically processes a subset of parasite proteins that play indispensable roles in egress and invasion. Here we report the first crystallographic structure of Plasmodium falciparum SUB1 at 2.25 Å, in complex with its cognate prodomain. The structure highlights the basis of the calcium dependence of SUB1, as well as its unusual requirement for interactions with substrate residues on both prime and non-prime sides of the scissile bond. Importantly, the structure also reveals the presence of a solvent-exposed redox-sensitive disulphide bridge, unique among the subtilisin family, that likely acts as a regulator of protease activity in the parasite

Living clinical guidelines for stroke: Updates, challenges and opportunities

Continued growth in the number of published clinical studies has necessitated changes to the way evidence-based resources such as clinical guidelines are developed and updated. The Australian and New Zealand Clinical Guidelines for Stroke Management (https://informme.org.au/guidelines/clinical-guidelines-for-stroke-management) are based on continual evidence surveillance and timely updates to recommendations as new research is published. In this article, we outline the main updates to recommendations since the guidelines moved into a living mode in 2018, and discuss key challenges and benefits of living guidelines

The malaria parasite sheddase SUB2 governs host red blood cell membrane sealing at invasion.

Red blood cell (RBC) invasion by malaria merozoites involves formation of a parasitophorous vacuole into which the parasite moves. The vacuole membrane seals and pinches off behind the parasite through an unknown mechanism, enclosing the parasite within the RBC. During invasion, several parasite surface proteins are shed by a membrane-bound protease called SUB2. Here we show that genetic depletion of SUB2 abolishes shedding of a range of parasite proteins, identifying previously unrecognized SUB2 substrates. Interaction of SUB2-null merozoites with RBCs leads to either abortive invasion with rapid RBC lysis, or successful entry but developmental arrest. Selective failure to shed the most abundant SUB2 substrate, MSP1, reduces intracellular replication, whilst conditional ablation of the substrate AMA1 produces host RBC lysis. We conclude that SUB2 activity is critical for host RBC membrane sealing following parasite internalisation and for correct functioning of merozoite surface proteins