Potential of largemouth bass as vectors of 137Cs dispersal.

We conducted a radio telemetry study on the movements of potentially contaminated largemouth bass between Steel Creek, a restricted access (137)Cs contaminated stream on the Savannah River Site (located in South Carolina, USA), and the publicly accessible Savannah River. Largemouth bass were relatively mobile in lower Steel Creek and the portion of the Savannah River near Steel Creek, and there was considerable movement between these two habitats. Largemouth bass had home ranges of about 500 linear meters of shoreline in the Savannah River but sometimes moved long distances. Such movements occurred primarily during the spawning season, largely upstream, and increased when water levels were changing or elevated. However, approximately 90% of the largemouth bass observations were within 10 km of Steel Creek. The total quantity of (137)Cs transported into the Savannah River by largemouth bass was much less than transported by water and suspended sediments discharged from Steel Creek. We conclude that largemouth bass from the Savannah River Site are unlikely to be responsible for long distance dispersal of substantial radiological contamination in the Savannah River.

Specific methods to identify plasma binding abnormalities in euthyroid hyperthyroxinemia.

Methods to identify the plasma T4-binding abnormalities that can cause euthyroid hyperthyroxinemia were evaluated in patients with excess T4-binding globulin, familial dysalbuminemic hyperthyroxinemia, prealbumin-associated hyperthyroxinemia, and autoantibody binding of T4. Familial dysalbuminemic hyperthyroxinemic serum showed a unique persistence of abnormal [125I]T4 binding when diluted 1:100 in phosphate buffer with added 1000-fold excess of unlabeled T4 (10(-6) M T4). Immunoprecipitation of [125I]T4 by antibody to prealbumin, precipitation of [125I]T4 by polyethylene glycol 6000 19%, and in vitro resin uptake of T3 were specific for prealbumin-associated hyperthyroxinemia, autoantibody binding of T4, and T4-binding globulin excess, respectively. These simple methods facilitate investigation of patients with euthyroid hyperthyroxinemia and will identify individuals and families at risk of misdiagnosis by standard methods. Use of these techniques rules out the known binding abnormalities in hyperthyroxinemic patients and may make the diagnosis of generalized hormone resistance more specific.

Relationship between thyrotropin and thyroxine changes during recovery from severe hypothyroxinemia of critical illness.

In a prospective study of critically ill hypothyroxinemic we assessed the relationship between serum TSH and T4 during the return of serum T4 to normal during recovery. In this longitudinal study of 60 patients with a variety of critical illnesses, including burns, septicemia, and acute renal failure, serum T4 fell to less than 2.7 micrograms/dl (35 nmol/liter) in 24 patients, of whom 14 survived with return of T4 to normal. A rise in total T4 of more than 1.9 microgram/dl (25 nmol/liter) within 96 h occurred 13 times in 10 patients, while 4 patients had slower increases in T4. All 13 episodes of rapid T4 rise [1.7 +/- 0.8 (+/- SD) to 5.6 +/- 2.1 micrograms/dl] were associated with a marked increase in serum TSH (1.1 +/- 0.8 to 7.0 +/- 5.2 mU/liter), and TSH was transiently above normal during 8 episodes of T4 recovery. In the 6 episodes with sampling less than 6 h apart, the TSH rise consistently preceded the T4 rise. In the 4 patients who received dopamine, TSH and T4 remained low until cessation of therapy. During the TSH rise, only minor changes, which could not account for the increase in total T4, occurred in T4-binding globulin (12.9 +/- 3.3 to 14.8 +/- 3.3 mg/liter), prealbumin (208 +/- 73 to 234 +/- 82 mg/liter), and albumin (28.3 +/- 2.9 to 31.9 +/- 2.9 g/liter). Mean free T4 increased (0.60 +/- 0.34 to 1.45 +/- 0.56 ng/dl), as did total T3 (16 +/- 14 to 76 +/- 44 ng/dl), during the phase of TSH rise, suggesting that the increase in TSH was not simply a consequence of diminished negative feedback due to increased plasma binding. The very close and consistent temporal relationship between TSH and T4 during the recovery phase suggests that TSH may have an essential role in the return of T4 to normal during recovery from critical nonthyroidal illness.

Monoclonal antibodies against a differentiated retinal cell population.

Two monoclonal antibodies have been isolated which bind preferentially to the plexiform layers of embryonic chick neural retina and to 50-60% of dissociated neural retinal cells in culture as determined by surface binding to cells followed by analysis in a fluorescent activated cell shorter. Each antibody appears to recognize a distinct antigenic determinant on a common cell surface antigen, a protein of approximately 230 kdalton. This antigen increases dramatically in concentration between embryonic days 7 and 11 concomitant with the elaboration of the retinal plexiform layers. The antigen appears first in the central portion of the neural retina and at later times in the periphery, an appearance consistent with the normal pattern of differentiation of the retina.

Identification of sub-populations of chick neural retinal cells by monoclonal antibodies: a fluorescence activated cell sorter screening technique.

An assay was developed which identifies monoclonal antibodies recognizing the cell surfaces of sub-populations of chick retinal cells which survive in culture. Antibodies from hybridoma culture supernatants were bound to monolayers of retina cells followed by a fluorescent secondary antibody. The quantitative fluorescence analysis ability of the fluorescence-activated cell sorter (FACS) was used to determine the fluorescence intensity associated with viable single cells and the frequency with which these cells appear in the total population. Hybridomas were generated which define both overlapping and non-overlapping retina cell populations. The cytotoxic activity of many of the monoclonal antibodies was determined on the FACS by propidium iodide exclusion, and the identity of various sub-populations was demonstrated by immunohistochemical staining of retina sections.

Magnesium levels in alcohol-treated rodents using different consumption paradigms.

To develop an animal model system that examines magnesium (Mg) deficiency associated with chronic alcohol consumption, we tried to reproduce a Mg-deficient state, caused by alcohol consumption, in rats using different alcohol consumption experimental designs. Serum and bone samples were collected from 2-day binge (high BACs achieved by intubating a 5% ethanol solution 2 consecutive days/week), 5-day binge, moderate drinking, and adolescent (4-week-old rats, equivalent to late teen/early adult humans) alcohol consumption projects. Mg content was measured using color spectrophotometry. Alcohol-fed animals consumed a liquid diet containing 0.38 g/kg/day ethanol in the moderate project and 35% ethanol-derived calories in the adolescent drinking project. Animals in the two binge drinking projects were intubated with 12 g/kg/day of ethanol in a 5% solution. When looked at acutely and chronically, no consistent deficiencies in Mg were seen. The lack of a chronic Mg deficiency in rats may indicate a different mechanism of action than observed in humans.

Alcohol consumption inhibits osteoblastic cell proliferation and activity in vivo.

To better understand the effect of alcohol consumption on the bone remodeling process in vivo, we used a rodent animal model system to compare osteoblast activity and number in alcohol-fed, pair-fed, and chow-fed animals. Adult, virgin female Sprague-Dawley rats were assigned to alcohol-fed, pair-fed, and chow groups based on weights. Alcohol animals were fed a liquid diet containing 35% ethanol-derived calories for 6 weeks. Pair-fed animals were matched to test animals on the basis of initial weight and fed an isocaloric diet equivalent to that consumed by the alcohol-matched animals on the previous day with alcohol replaced by maltose-dextrin. Right tibias were fixed and embedded in methyl methacrylate for sectioning. Sections (5 microm) were stained for cement lines and packets were measured using histomorphometric techniques on a BioQuant morphometric system. Alcohol-fed animals exhibited statistically significant decreases in the amount of bone surface containing active osteoblasts and a decrease in mean wall thickness. Osteocalcin values were significantly reduced from pair-fed levels and slightly, but not significantly, reduced from chow-fed animals.

Myocardial tissue characterization using pattern recognition procedures on backscattered ultrasonic signals.

Pattern recognition techniques were applied to backscattered signals obtained in vitro from normal and abnormal canine and human heart samples. Orthogonal transforms, in conjunction with the variance criterion, comprised the feature extractors. The minimum-distance (MD) and nearest-neighbor (NN) rules were used as classification. When the MD rule was used, the magnitude of the DFT gave the best performance for both canine and human samples. When the NN rule was used, all the transforms performed comparably. The classification performances were improved for both species when the NN rule was used with feature extractors containing phase information.

Single dose trimethoprim-sulphamethoxazole treatment of symptomatic urinary infection.

Seventy-nine children with symptoms of urinary tract infections were randomly allocated to treatment with a single dose or a 7-day course of trimethoprim-sulphamethoxazole. Of the 42 patients (39 girls, 3 boys) who fulfilled the criteria for the trial, 23 were given a single-dose regimen and 19 of them a 7-day regimen. Both groups of patients had sterile urine cultures 2 days after starting treatment. Eight patients had underlying structural renal abnormalities (n = 3, single-dose regimen; n = 5, 7-day regimen). One patient in the single dose group had a recurrence of infection on day 7. These results show that single dose trimethoprim-sulphamethoxazole is as effective as the conventional 7-day course in children with symptomatic urinary tract infection. Further investigation of the renal tract is necessary regardless of the fact that the infection has been eradicated by single-dose treatment.

Effect of tetanus toxin on the accumulation of the permeant lipophilic cation tetraphenylphosphonium by guinea pig brain synaptosomes.

Accumulation of the permeant lipophilic cation [(3)H]tetraphenylphosphonium (TPP(+)) by synaptosome preparations from guinea pig brain cerebral cortex is inhibited 1:10 by medium containing 193 mM K(+) and by veratridine. A further 1:10 to 1:15 decrease in TPP(+) uptake occurs under nitrogen and in the presence of mitochondrial inhibitors such as oligomycin, whereas starvation and succinate supplementation have no effect. These data indicate that, in analogy to intact neurons, there is an electrical potential (DeltaPsi, interior negative) of -60 to -80 mV across the synaptosomal membrane that is due primarily to a K(+) diffusion gradient (K(+) (in)-->K(+) (out)). The data also indicate that mitochondria entrapped within the synaptosome but not free mitochondria make a large contribution to the TPP(+) concentration gradients observed. Conditions are defined in which tetanus toxin binds specifically and immediately to synaptosomes in media used to measure TPP(+) uptake. Under these conditions tetanus toxin induces dose-dependent changes in TPP(+) uptake that are blocked by antitoxin and not mimicked by biologically inactivated toxin preparations. The effect of tetanus toxin on TPP(+) uptake is not evident in the presence of 193 mM K(+) or veratridine but remains under conditions known to abolish the mitochondrial DeltaPsi. Moreover, tetanus toxin has no effect on TPP(+) uptake by isolated synaptosomal mitochondria. The results thus define an in vitro action of tetanus toxin on the synaptosomal membrane that can be correlated with biological potency in vivo and is consistent with the in vivo effects of tetanus toxin on neuronal transmission.