Factors affecting fisher decisions: The case of the inshore fishery for European sea bass (Dicentrarchus labrax).

Fishery management relies on forecasts of fish abundance over time and space, on scales of months and kilometres. While much research has focussed on the drivers of fish populations, there has been less investigation of the decisions made day-to-day by fishers and their subsequent impact on fishing pressure. Studies that focus on the fisher decisions of smaller vessels may be particularly important due to the prevalence of smaller vessels in many fisheries and their potential vulnerability to bad weather and economic change. Here we outline a methodology with which to identify the factors affecting fisher decisions and success as well as quantifying their effects. We analyse first the decision of when to leave port, and then the success of the fishing trip. Fisher behaviour is here analysed in terms of the decisions taken by fishers in response to bio-physical and socio-economic changes and to illustrate our method, we describe its application to the under 10-meter fleet targeting sea bass in the UK. We document the effects of wave height and show with increasing wave height fewer vessels left port to go fishing. The decision to leave port was only substantially affected by time of high tide at one of the four ports investigated. We measured the success of fishing trips by the landings of sea bass (kg) per metre of vessel length. Fishing success was lower when wave height was greater and when fish price had increased relative to the previous trip. Fuel price was unimportant, but a large proportion of the variation in success was explained by variation between individual vessels, presumably due to variation in skipper ability or technical restrictions due to vessel characteristics. The results are discussed in the context of management of sea bass and other small-scale inshore fisheries.

Caspase-3 dependent nitrergic neuronal apoptosis following cavernous nerve injury is mediated via RhoA and ROCK activation in major pelvic ganglion.

Axonal injury due to prostatectomy leads to Wallerian degeneration of the cavernous nerve (CN) and erectile dysfunction (ED). Return of potency is dependent on axonal regeneration and reinnervation of the penis. Following CN injury (CNI), RhoA and Rho-associated protein kinase (ROCK) increase in penile endothelial and smooth muscle cells. Previous studies indicate that nerve regeneration is hampered by activation of RhoA/ROCK pathway. We evaluated the role of RhoA/ROCK pathway in CN regulation following CNI using a validated rat model. CNI upregulated gene and protein expression of RhoA/ROCK and caspase-3 mediated apoptosis in the major pelvic ganglion (MPG). ROCK inhibitor (ROCK-I) prevented upregulation of RhoA/ROCK pathway as well as activation of caspase-3 in the MPG. Following CNI, there was decrease in the dimer to monomer ratio of neuronal nitric oxide synthase (nNOS) protein and lowered NOS activity in the MPG, which were prevented by ROCK-I. CNI lowered intracavernous pressure and impaired non-adrenergic non-cholinergic-mediated relaxation in the penis, consistent with ED. ROCK-I maintained the intracavernous pressure and non-adrenergic non-cholinergic-mediated relaxation in the penis following CNI. These results suggest that activation of RhoA/ROCK pathway mediates caspase-3 dependent apoptosis of nitrergic neurons in the MPG following CNI and that ROCK-I can prevent post-prostatectomy ED.

Peptide-derivatized albumins that inhibit fibrin polymerization.

Synthetic peptides patterned on sequences that appear during thrombin proteolysis of fibrinogen are known to influence fibrin formation in very different ways. A-Knob sequences (GPR-) inhibit polymerization, but B-knob sequences (GHR-) can actually enhance the process. We now report that when such peptides are attached to albumin carriers, both knob conjugates inhibit fibrin formation. In contrast, the 2-aminoethylthiol-albumin conjugate control enhances the polymerization to the same degree as albumin. The peptide AHRPam, which is known to bind exclusively to the ßC holes of fibrinogen/fibrin, nullifies the inhibitory effects of the GHRPYGGGCam-albumin conjugate on fibrin polymerization, indicating that the inhibition was exclusively due to interactions with ßC holes. AHRPam was much less effective in countering inhibition by the GPRPGGGGCam-albumin conjugate, suggesting that the observed effects with this conjugate involve mainly the γC holes of fibrin/fibrinogen. This study demonstrates that peptides modeled on fibrin polymerization knobs tethered to albumin retain their capacity to interact with fibrinogen/fibrin and may prove useful as inhibitors of clotting in vivo.