An Examination of the Variability of Migratory Timing Statistics Estimated From Catch and Effort Observations

The estimate of the mean arrival time based on catch or CPUE of fishes migrating into a fixed harvest area is a function of the number of days fished. Simulation studies using chinook salmon catch and effort data from the Yukon River delta, Alaska indicate that fishing effort concentrated at the tails of the migratory distribution which would tend to erroneously weigh the estimated mean arrival time in the direction of the sample, away from the true mean, is only a significant problem when the number of days open to fishing is small, covering less than 12% of the total duration of the migration. At sampling rates of the time domain greater than 12%, estimated mean arrival times are usually within 50% of the true mean. The variance of the ratio estimator and the mean square error (biased MSE) for the ratio estimator both allow for the construction of confidence limits for an estimated arrival time based on commercial catch and CPUE data. Arrival time estimates for migrations with large variances and with fewer than 12% of the time domain of the migration sampled have narrower 95% confidence intervals than the same methods produced for arrival time estimates for migrations of small variances. The variance of the ratio estimator is more conservative with sampling rates below 12%, however, it closely matches the biased MSE when sampling greater than 12% of the time domain of the migration. Once about a quarter of the migratory time span is fished, the confidence interval is greatly reduced. This is particularly true for migrations of small variance where the proportions of the population sampled tend to be quite concentrated about the central mass of the time distribution of abundance. Sampling from the average empirical proportion of catch yields a narrower confidence interval on the mean arrival time than does sampling from CPUE data. However, samples from annual daily proportions of CPUE with broader variances yield stronger confidence in arrival time estimates than do samples from migrations of average to small variances

mGluR5 protect astrocytes from ischemic damage in postnatal CNS white matter

AbstractAstrocytes perform essential neuron-supporting functions in the central nervous system (CNS) and their disruption has devastating effects on neuronal integrity in multiple neuropathologies. Although astrocytes are considered resistant to most pathological insults, ischemia can result in astrocyte injury and astrocytes in postnatal white matter are particularly vulnerable. Metabotropic glutamate receptors (mGluR) are neuroprotective in ischemia and are widely expressed by astrocytes throughout CNS grey matter, but their potential cytoprotective role in astrocytes had not been determined. Here, we identify functional expression of group I mGluR in white matter astrocytes and demonstrate their activation protects astrocytes from ischemic damage in the postnatal mouse optic nerve. Optic nerve astrocytes are shown to express mGluR5 using immunolabelling of sections and explant cultures from transgenic reporter mice in which GFAP drives expression of EGFP. In addition, using Fluo-4 calcium imaging in isolated intact optic nerves, we show that the group I/II mGluR agonist ACPD and the specific group I mGluR agonist DHPG evoke glial Ca2+ signals that were significantly inhibited by the group I mGluR antagonist AIDA. A key finding is that activation of group I mGluR protects astrocytes against oxygen-glucose deprivation (OGD) in situ, in isolated intact optic nerves from GFAP-EGFP mice. This study identifies a role for group I mGluR in protecting astrocytes against ischemia in postnatal white matter and suggests this may be a strategy for limiting damage in neuropathologies involving excitotoxity

Field Studies in the Lynnhaven River for Calibration of a Tidal Prism Water Quality Model

Under the Virginia Coastal Resources Management Program Grants (VCRMPG) for FY \u2793, a tidal prism water quality model has been developed for small coastal basins and tidal creeks. The rationale of the model development is provided and the model is described in detail in Kuo & Park ( 1994). The tidal prism model uses the concept of tidal flushing for physical transport processes. The nutrient and phytoplankton kinetics are mostly from the Chesapeake Bay three-dimensional water quality model (Cereo & Cole 1994), and the model also includes the sediment process model of the main Bay (DiToro & Fitzpatrick 1993). The model has twenty four water column and twenty seven sediment state variables (Table 1-1). The model, being a generic model applicable to any small coastal basins and tidal creeks, and operational on a personal computer, should provide a tool to state and local agencies for water quality management of Virginia\u27s small coastal basins

Persistent Wnt/β-catenin signaling determines dorsalization of the postnatal subventricular zone and neural Stem cell specification into oligodendrocytes and glutamatergic neurons

In the postnatal and adult central nervous system (CNS), the subventricular zone (SVZ) of the forebrain is the main source of neural stem cells (NSCs) that generate olfactory neurons and oligodendrocytes (OLs), the myelinating cells of the CNS. Here, we provide evidence of a primary role for canonical Wnt/β-catenin signaling in regulating NSC fate along neuronal and oligodendroglial lineages in the postnatal SVZ. Our findings demonstrate that glutamatergic neuronal precursors (NPs) and oligodendrocyte precursors (OPs) are derived strictly from the dorsal SVZ (dSVZ) microdomain under the control of Wnt/β-catenin, whereas GABAergic NPs are derived mainly from the lateral SVZ (lSVZ) microdomain independent of Wnt/β-catenin. Transcript analysis of microdissected SVZ microdomains revealed that canonical Wnt/β-catenin signaling was more pronounced in the dSVZ microdomain. This was confirmed using the β-catenin-activated Wnt-reporter mouse and by pharmacological stimulation of Wnt/β-catenin by infusion of the specific glycogen synthase kinase 3β inhibitor, AR-A014418, which profoundly increased the generation of cycling cells. In vivo genetic/pharmacological stimulation or inhibition of Wnt/β-catenin, respectively, increased and decreased the differentiation of dSVZ-NSCs into glutamatergic NPs, and had a converse effect on GABAergic NPs. Activation of Wnt/β-catenin dramatically stimulated the generation of OPs, but its inhibition had no effect, indicating other factors act in concert with Wnt/β-catenin to fine tune oligodendrogliogenesis in the postnatal dSVZ. These results demonstrate a role for Wnt/β-catenin signaling within the dorsal microdomain of the postnatal SVZ, in regulating the genesis of glutamatergic neurons and OLs