Abundance and exploitation rate of the blue crab (Callinectes sapidus) in Chesapeake Bay

We estimated absolute abundance of the blue crab stock in Chesapeake Bay during winter from stratified random surveys conducted baywide from 1990 to 1999, using the swept-area method. We estimated catching efficiency of the survey gear from multiple depletion experiments to correct for temporal and vessel/area differences in catchability. The survey was conducted during the winter, when crabs are dormant and buried in the bottom. Analysis of crab carapace width (CW) frequency distributions revealed two size modes: CW less or equal 60 mm and CW greater than 60 mm, corresponding to age-0 (recruits) and age-1+ (one year and older), respectively. Absolute density of blue crab recruits varied from 10 to 55 crabs per 1,000 m(2) across years (95 million to 540 million baywide), with no significant trends over time. Abundance of age-1 + crabs declined significantly from 35 to 38 crabs per I 000 m(2) in 1990-1991 (342 million to 371 million crabs baywide) to 8.3 in 1999 (92 million crabs baywide). A stronger decline in the number of males indicates that males were exploited more intensively than females. A three-year moving average of spawning stock abundance (age- 1+ females) declined twofold from the early to the late 1990s. The absolute abundance of the blue crab population in Chesapeake Bay varied from 241 million to 867 million. Over-wintering mortality was usually less than 2%, but substantially higher mortality occurred in 1994 (7.3%) and 1996 (11.9%). High correlation between January water temperature and the percentage of dead crabs provides strong evidence of the adverse effect of cold winter on survival of crabs. Large crabs were affected most by cold winter temperatures. We estimated exploitation rates for the commercial fishery by comparing abundance with total landings. The estimated exploitation rates varied from 40% to 52% from 1990 to 1998 and increased to a record high of 70% in 1999. Fishing mortality rates varied from 0.6 to 0.9 year(-1) ill most years and were above the level providing maximum yield per recruit (F-max = 0.64 year(-1)) in nearly all years. The record fishing mortality in 1999 (F-1999, = 1.6 year(-1)) exceeded the overfishing threshold (F-10% = 1.0 year(-1)). Despite evidence of growth overfishing, the blue crab population supported large harvests throughout the 1990s. Increase of fishing mortality above the F-10% in 1999, indicates that the population was overfished and is at risk of recruitment overfishing if fishing mortality remains at this level

Quantification of the effects of an alpha-2 adrenergic agonist on reflex properties in spinal cord injury using a system identification technique

<p>Abstract</p> <p>Background</p> <p>Despite numerous investigations, the impact of tizanidine, an anti-spastic medication, on changes in reflex and muscle mechanical properties in spasticity remains unclear. This study was designed to help us understand the mechanisms of action of tizanidine on spasticity in spinal cord injured subjects with incomplete injury, by quantifying the effects of a single dose of tizanidine on ankle muscle intrinsic and reflex components.</p> <p>Methods</p> <p>A series of perturbations was applied to the spastic ankle joint of twenty-one spinal cord injured subjects, and the resulting torques were recorded. A parallel-cascade system identification method was used to separate intrinsic and reflex torques, and to identify the contribution of these components to dynamic ankle stiffness at different ankle positions, while subjects remained relaxed.</p> <p>Results</p> <p>Following administration of a single oral dose of Tizanidine, stretch evoked joint torque at the ankle decreased significantly (p < 0.001) The peak-torque was reduced between 15% and 60% among the spinal cord injured subjects, and the average reduction was 25%. Using systems identification techniques, we found that this reduced torque could be attributed largely to a reduced reflex response, without measurable change in the muscle contribution. Reflex stiffness decreased significantly across a range of joint angles (p < 0.001) after using tizanidine. In contrast, there were no significant changes in intrinsic muscle stiffness after the administration of tizanidine.</p> <p>Conclusions</p> <p>Our findings demonstrate that tizanidine acts to reduce reflex mechanical responses substantially, without inducing comparable changes in intrinsic muscle properties in individuals with spinal cord injury. Thus, the pre-post difference in joint mechanical properties can be attributed to reflex changes alone. From a practical standpoint, use of a single "test" dose of Tizanidine may help clinicians decide whether the drug can helpful in controlling symptoms in particular subjects.</p