Status of the Instream Flow Issue in Arkansas, 1987

Expansion of Arkansas\u27 population with concurrent increases in the state\u27s domestic, industrial, and agricultural water uses and possible out-of-state diversion are placing substantial demands on the state\u27s water resources. In an attempt to address this growing concern, Act 1051 (1985) of the Arkansas legislature was passed requiring the determination of present and future state water needs. A specific area of this mandate was the quantification of instream flow requirements. Basic instream flow needs are maintenance of the aquatic ecosystem and dependent riparian environment. Flow reservation may compliment other instream uses such as recreation, navigation, water quality, and groundwater recharge. However, offstream uses (e.g. irrigation and industry) may compete for these same flows and often at the most critical time of year. In order to answer questions concerning instream flow requirements, over 40 methods of instream flow determination have been developed, the majority in the semi-arid western United States. These individual procedures may be classified into four major methodologies: (1) discharge, (2) single transect, (3)multiple transect, and (4) regression analysis of historical data. Requirements of these four types vary according to necessary level of expertise, time and effort expended, and monetary outlay. In one year, requests for fish and wildlife instream flow needs for approximately 60 stream reaches throughout Arkansas limited the possible options. Modification and further development of a well-known method is outlined as an initial step in the process of quantifying Arkansas\u27 instream flow needs. Examples are given for some of the major river basins throughout the state

Response of Fish Communities to Habitat Alteration in a Small Ozark Stream

From 1984 to 1986, the Arkansas Highway and Transportation Department reconstructed and upgraded a portion of St. Hwy. 123 west of St. Hwy.7 at Pelsor, Arkansas. As a result of the construction, portions of Haw Creek, Johnson County, Arkansas, a third order stream in the Boston Mountains Ecoregion, were straightened and channelized. In reconstructing specific stream reaches, stream banks were riprapped and vegetated, gabions constructed and positioned, stream substrates and pool-riffle ratios altered. Instream and riparian habitat and fish biomass and diversity in altered reaches were radically altered. Channelized reaches became wide and shallow, lacking overstory cover and pools. Substrate particle size changed from boulder/rubble to rubble/gravel/sand and velocity increased. Fish communities in channeled reaches simple; Campostoma anomalum, Notropis boops, and Etheostoma spectabile accounted for more than 80 percent of all fish captured. This represented a shift from piscivore and insectivorepiscivore to herbivore and insectivore dominated feeding guilds. Natural channel reaches had more complex fish communities and greater abundance of centrarchids and ictalurids, primarily deeper water groups. Immediately after channelization, altered reaches had a larger biomass than natural reaches (0.43-0.26 g/m^2 ). The summer following alteration, channeled segments were basically dewatered, and biomass decreased dramatically (0.06-0.1 1 g/m^2). One year post channelization, altered reaches had eroded, scoured and deepened at their headwaters, and embedded. Fish community composition in altered reaches s stabilizing to a riffle-type assemblage dominated by the herbivore Campostoma anomalum

Mice with a D190N Mutation in the Gene Encoding Rhodopsin: A Model for Human Autosomal-Dominant Retinitis Pigmentosa

Rhodopsin is the G protein–coupled receptor in charge of initiating signal transduction in rod photoreceptor cells upon the arrival of the photon. D190N (RhoD190n), a missense mutation in rhodopsin, causes autosomal-dominant retinitis pigmentosa (adRP) in humans. Affected patients present hyperfluorescent retinal rings and progressive rod photoreceptor degeneration. Studies in humans cannot reveal the molecular processes causing the earliest stages of the condition, thus necessitating the creation of an appropriate animal model. A knock-in mouse model with the D190N mutation was engineered to study the pathogenesis of the disease. Electrophysiological and histological findings in the mouse were similar to those observed in human patients, and the hyperfluorescence pattern was analogous to that seen in humans, confirming that the D190N mouse is an accurate model for the study of adRP