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ABSTRACT: The Extended leak-off test, XLOT, is a main tool for obtaining minimum stress data during drilling operations. If performed according to a proper protocol, it is perhaps the most cost-effective and robust method for determining the minimum stress. The low cost of the test means that a lot of data can be collected, allowing for efficient regional analysis. A widely reproduced figure by Gaarenstrom et al. (1993) has become a classic in the industry. It shows the pump-in phase as two distinct linear segments. The point of change in slope is denoted the Leak-off Point or the Leak-off Pressure (LOP). It is sometimes argued that the LOP is a good measure of the in-situ stress, and it is sometimes argued the LOP marks the initiation of a fracture. We analyze this hypothesis and show by basic theoretical considerations and several examples of high quality field data that this is not necessarily the case. The nonlinear behavior during initial pump-in may be due to leak-off to a permeable formation or through a poorly cemented casing shoe. 1. INTRODUCTION The importance of knowing the in-situ stress has been realized for a long time in the petroleum industry, see e.g., Hubbert and Willis (1957), Fairhurst (1965), Haimson and Fairhurst (1967), Nolte and Smith (1981), and many others. The minimum stress is of direct use in hydraulic fracturing, where proper stress data are essential for the design of a successful job. Therefore, most conventional fracturing jobs are preceded with datafracs or minifracs, aiming to determine the parameters for designing the main job, with the minimum horizontal stress being of central importance in addition to calibrating fluid leak-off behavior during fracture propagation. More recently the Diagnostic Fracture Injection Test has gained prominence in very tight and unconventional plays where it is possible to estimate the same main parameters but also analyze for pore pressure and permeability.

Corn (Zea mays) grown in the southern Piedmont requires 200 to 280 kg nitrogen (N) ha−1 annually and requires up to 0.87 cm of water per day, making groundwater systems susceptible to nitrate (NO3−) leaching. A perennial white clover (Trifolium repens L.) living mulch (LM) system may reduce NO3-N leaching by using legume N to replace mineral N, though little information is available on such a system in the southern Piedmont. Therefore, a HYDRUS-1D model was used to simulate water and NO3-N flux in three cover crop systems. Cereal rye (Secale cereal L.) (CR), crimson clover (Trifolium incarnatum L.) (CC), and a white clover LM were fertilized with 280, 168, and 56 kg N ha−1. The HYDRUS-1D model was calibrated and validated with observed water contents and NO3-N data that were collected over two years. Water and NO3-N flux models were created for each treatment and evaluated using coefficient of determination, percentage bias, and index of agreement, and showed good agreement to observed data. Nitrate leaching below 1 m in 2015/2016 was 23.5, 12.7, and 21.4 kg ha−1 for the CC, LM, and CR treatments, respectively, but was less than 1 kg ha−1 for all treatments in 2016/2017 due to prolonged drought. Differences in leached NO3-N among treatments were attributed to variation in mineral N application rate and NO3-N uptake by cover crops. Overall, results suggest that the use of a perennial LM system may reduce NO3-N leaching when compared to annual CC and CR cover crop systems.

Rabbits were immunized with two synthetic peptides based on hydrophilic regions of selenoprotein W from rat muscle. The resulting polyclonal antibodies were used in Western blots to determine the compartmentation and tissue distribution of selenoprotein W, and to determine the influence of selenium on the levels of this selenoprotein in rat muscle. Selenoprotein W exists mainly in cytosol, but very small amounts were associated with membranes. Western blots revealed selenoprotein W in muscle, spleen, testis, and brain of rats. Rats were fed diets of either no addition of selenium (0 ppm Se) or additions of 0.1 and 4.0 mg selenium/g (0.1 ppm Se and 4.0 ppm Se) diet for 6 wk. Selenoprotein W was undetectable in skeletal muscle of rats fed the basal diet, detectable in those fed 0.1 ppm selenium in the diet, and much higher in muscle from rats fed 4 ppm selenium diet. In a species comparison, Western blots indicated the presence of selenoprotein W in muscle of rabbits, sheep, and cattle.

Results from sand retention tests (SRT) performed with different screens and test sands can show significant differences in perceived production performance given by the permeability of the retained sand layer as well as sand control behavior. However, this paper presents a new sand retention test set up that exhibits no plugging tendencies for various screen designs when using non-uniform test sands with high content of fines material (Uc=7.5, fines = 18%).13 screen designs, 12 metal mesh and one wire wrapped screen, with screen gauges varying from 200 to 275 microns were tested. The results show insignificant differences when it comes to sand control as well as the permeability of the sand layer calculated from the pressure drop across the screen and the sand layer retained by the screen. This work supports critical reviews made by other authors of the various laboratory testing procedures used in the industry and confirms that interpretation of screen performance is often incorrect with these set-ups. The new test set up was developed to enable screen testing under more realistic conditions. Emphasis was placed on low velocities to avoid turbulent, non Darcy effects as well as avoiding the use of fluids containing polymers. High flow rates tend to cause rapid and efficient localization of the sand grains around the sand screen filter openings prior to the establishment of the sand layer. A set up where the total pressure drop is dominated by the turbulent part can readily lead to inaccurate determination of the true permeability and consequently erroneous comparison of screen behavior. With the low approach velocities used in this setup, sand layers of measureable thickness can develop before the pressure rating of the cell is reached. The sand layer permeability is calculated by using Darcy ’ law based on the thickness, flow rate, fluid viscosity and pressure drop. The measured volume of sand produced through the screens in relation to the total volume pumped was used to define their sand control behavior. The flow rate used in this study was 160 ml/min which gives an approach velocity of 0.00053 m/s. Although this is sufficiently low to ensure the absence of non Darcy effects in the resulting sand packs around the screens, it still equates to relatively high rates in the field. For instance, this test rate represents a production rate of 36000 Sm3/d through a 2000 m long 6 5/8" screen section which is a normal length on some fields in the North Sea. In the storage cell where the test sand slurry is kept prior to injection into the sand screen test cell, the sand is suspended in brine with a matching density. In this way, a viscous carrier fluid is not required, thus eliminating any possible test artifacts based on undesired polymer effects. The results show that screen plugging with porous test sands is not an issue for any screens given that sensible apertures are chosen that give retention whilst allowing the production of any mobile fines present. The test results confirm that other SRT set-ups with inherently high approach velocities will often misinterpret the pressure response as plugging and thereby rank the various screens incorrectly. Based on these results, and providing that the various screen designs give sand control, the choice of optimum sand screen for a given application should be based more on mechanical properties, cost and contractual issues, other functionality (such as ICD or shroud) rather than "plugging" potential that is erroneously ascribed to different screens in standard SRTs. Screen plugging from other factors during installation and service in the field is, however, possible and should be minimized by good design and operational practice.

Rats were trained to stable performance in a conditional brightness discrimination task and then received infusions of ibotenic acid or vehicle into the basal forebrain. Following 2 weeks of recovery, animals were retested in the original discrimination. Lesioned rats tended to performed badly on the first day of testing as measured by all parameters (percent correct responding, latency to respond, and missed trials) but thereafter, most rats recovered quickly to prelesion levels. In keeping with previous reports, an approximately 30% reduction in choline acetyltransferase activity was observed in the lesioned animals. Four rats showed no recovery over a period of several months; however, an analysis of the choline acetyltransferase in several brain regions revealed no obvious differences to those animals in which performance recovered. Postlesion testing with the putative nootropic β-carboline ZK 93426 showed no major differences to the effects observed in control animals. Scopolamine had similar negative effects in both groups tested. These data indicate that deficits induced by lesions of the basal forebrain do not correlate with reductions in cholinergic activity.

TNF-alpha and lymphotoxin (LT or TNF-beta) are structurally related cytokines that share several proinflammatory and immunomodulatory activities. The shared biologic activities of TNF and LT have been attributed to their binding to a common cell surface receptor(s). We observed that rTNF enhanced the expression of MHC class I proteins on the human T cell hybridoma, II-23.D7, however LT was largely unable to regulate MHC expression. To determine the molecular basis of this disparity between LT and TNF the receptor binding characteristics of rTNF and rLT were investigated by direct and competitive radioligand assays on the II-23.D7 T hybridoma, and for comparison, anti-CD3 activated human T lymphocytes. Specific 125I-rTNF binding to the II-23.D7 line revealed a single class of sites with a Kd = 175 pM and 3000 sites/cell; anti-CD3 activated T cells exhibited specific TNF binding with similar properties. The relationship of receptor occupancy to the induction of MHC class I Ag yielded a hyperbolic curve indicating a complex relationship between rTNF binding and biologic response. LT appeared to function like a partial agonist in that rLT was 10- to 20-fold less effective than rTNF in competitively inhibiting 125I-rTNF binding on the II-23.D7 line. Scatchard type analysis revealed a single class of low affinity binding sites for 125I-rLT. No differences in the competitive binding activity of rTNF and rLT were observed on the anti-CD3-activated T cells. Receptors for rTNF and rLT were immunoprecipitated from the II-23.D7 and activated T cells with anticytokine antibodies after cross-linking of radioiodinated rTNF or rLT to intact cells by using chemical cross-linking reagents. Analysis of the cross-linked adducts by SDS-PAGE and autoradiography indicated a major adduct of 92 kDa for rTNF and 104 kDa for rLT. Enzymatic digestion with neuraminidase or V8 protease revealed a unique structure to these adducts consistent with the cross-linking of a single chain of cytokine to a cell surface glycoprotein. rTNF inhibited the formation of the 104-kDa adduct formed with 125I-rLT on the II-23.D7 line, indicating these two cytokines bind to the same receptor of approximately 80 kDa. These results suggest that the disparate activities of LT and TNF to induce MHC class I proteins on the II-23.D7 cells are, in part, associated with a modified state of a common receptor.

All atypical antipsychotics avoid extrapyramidal side-effects yet differ in their propensity to cause other side-effects, like prolactin elevation. We proposed that the atypical antipsychotics with a propensity for prolactin elevation would show a higher pituitary versus striatal D2 receptor occupancy. To investigate this hypothesis, we tested four atypical antipsychotics, two that are commonly associated with prolactin elevation (amisulpride and risperidone) and two that are less frequently associated (quetiapine and olanzapine). In particular, we calculated their ED(50) values to increase plasma prolactin and block peripheral pituitary D2 receptors to their ED(50) values to antagonize apomorphine-induced stereotypy and occupy central striatal D2 receptors. All antipsychotics dose dependently increased prolactin levels and antagonized apomorphine-induced stereotypy. However, the central to peripheral potency (ED(50) for apomorphine antagonism to ED(50) for prolactin elevation) differed remarkably across these drugs: amisulpride (21764), risperidone (14), quetiapine (10), and olanzapine (1.7). Compounds displaying a higher peripheral potency brought about higher prolactin levels for a given level of functional central antagonism. This dissociation between central and peripheral effects was explained by the differential occupancy of D2 receptors in the striatum versus in the pituitary [ratio of striatal/pituitary ED(50) values (milligram per kilogram) for D2 occupancy): amisulpride (17/0.026 = 654), risperidone (0.89/0.081 = 14), quetiapine (24/4.1 = 6), olanzapine (0.30/0.43 = 0.7). These results indicate that dissociation between central and peripheral D2 receptor occupancy is a major determinant of the degree of prolactin elevation observed at therapeutic doses.

In vitro, (S)-2-(chloro-5-fluoro-indol-1-yl)-1-methylethylamine 1:1 C4H4O4 and (S)-2-(4,4,7-trimethyl-1,4-dihydro-indeno[1, 2-b]pyrrol-1-yl)-1-methylethylamine 1:1 C4H4O4 exhibited high-affinity binding to the serotonin2C (5HT2C) receptors and stimulated turnover of inositol 1,4,5-triphosphate. Affinity to several of the other 5-HT receptor subtypes and to numerous nonserotonergic receptors was much lower. In rats, both compounds elicited behavioral signs of 5-HT2C receptor agonism but not 5-HT2A receptor agonism. Hypomotility induced in rats by high doses of these compounds was reversed by the 5-HT2C receptor antagonist N-(2-naphthyl)-N'-(3-pyridyl)-urea 1:1 HCI. In addition, these compounds were active in tests used to demonstrate anticompulsive effects: reducing schedule-induced polydipsia in rats (prevented by the 5-HT2C/2B receptor antagonist N-(1-methyl-5'-indolyl)-(3-pyridyl)urea 1:1 HCl, reversing increased scratching induced with 8-hydroxy-dipropylaminotetralin 1:1 HCl in squirrel monkeys (no tolerance developed), decreasing responding in the marble-burying task in mice, and decreasing excessive eating of palatable food in rats. In contrast to these compounds, fluoxetine was much less potent, and in some tasks less efficacious, in reducing excessive behavior in these models. These two 5-HT2C receptor agonists do not show anxiogenic effects in the plus-maze in rats. (S)-2-(4,4,7-trimethyl-1,4-dihydro-indeno[1, 2-b]pyrrol-1-yl)-1-methylethylamine 1:1 C4H4O4 reduced the olfactory bulbectomy-induced passive avoidance impairment in rats, a result that indicates antidepressant potential. Similarly, in the differential-reinforcement-of-low rate 72-s operant schedule task in rats, (S)-2-(chloro-5-fluoro-indol-1-yl)-1-methylethylamine 1:1 C4H4O4 increased (and (S)-2-(4,4,7-trimethyl-1,4-dihydro-indeno[1, 2-b]pyrrol-1-yl)-1-methylethylamine 1:1 C4H4O4 showed a tendency to increase) total reinforcements received, which is suggestive of antidepressant activity. The electroencephalography defined sleep-waking pattern in rats produced by these two 5-HT2C agonists, as well as fluoxetine, included increased quiet-waking and decreased rapid-eye-movement sleep, which is characteristic of antidepressant drugs. These results suggest that 5-HT2C receptor agonism is associated with therapeutic potential in obsessive compulsive disorder and depression.

To evaluate a quantitative system to measure the early lesions of diabetic retinopathy seen in stereoscopic fundus photographs.Using a quantitative classification system, photographs of 4657 eyes (7 stereo pairs of 35-mm slides per eye) were scored for 16 diabetic lesions. A single severity level (identical to the ETDRS Interim Scale) was calculated for each eye. The reliability of this technique, and its reproducibility by independent examiners, was evaluated for individual lesions and severity levels using percent agreement, kappa, and weighted kappa statistics.This quantitative technique demonstrated an "almost perfect" agreement (weighted kappaor = 0.810) on all but one lesion by independent observers. For the severity levels, there was a 95.7% perfect agreement (kappa = 0.9428). The reproducibility of agreement over time was "almost perfect" on all but four lesions; with 88% perfect agreement (kappa = 0.8394) for severity levels.When used to evaluate the early lesions of diabetic retinopathy, the Vanderbilt Classification System is highly reliable between graders and over time. This system can gather quantitative data and evaluate incremental changes in an accurate, reproducible manner.

Four groups of Wistar rats received either vehicle, quisqualate, or one of two different ibotenic acid infusions into the basal forebrain. Following recovery from surgery, all rats were tested in three distinct behavioral paradigms: the Battig radial arm maze, the Barnes circular platform, and autoshaping in an operant chamber. The results showed that the size and site of the ibotenic acid lesion had a profound effect on acquisition performance in some, but not all, procedures. Performance in the Battig maze and acquisition of a food-rewarded lever press were in particular disrupted by ibotenic acid lesions. The severity of the reduction in cortical choline acetyltransferase (ChAT) did not correlate with performance in the tests. Quisqualate produced the largest reduction in ChAT levels but had no significant effect on performance in any of the three procedures used. Anatomic analysis revealed severe nonspecific damage to the striatum following ibotenic acid that was more pronounced in the group receiving a highly concentrated solution of ibotenic acid as compared to rats infused with a greater volume but less concentrated solution of the neurotoxin. Striatal damage was much less severe following quisqualic acid infusions. However, both types of neurotoxins produced equivalent nonspecific degeneration of the reticular thalamic nucleus. These data confirm reports that nonspecific damage appears to define the severity of ibotenic acid lesions on subsequent behavioral performance.

The effects of several centrally active drugs were investigated using two visual discrimination tasks: a two-lever food-rewarded conditional brightness discrimination, and a similar conditional brightness discrimination where a delay was introduced between the disappearance of the stimulus and the opportunity to respond on the levers for food. The substances tested (amphetamine, scopolamine, methylscopolamine, physostigmine, diazepam and beta-carboline benzodiazepine receptor antagonist, ZK 93426), all produced differing profiles of action on the performance parameters recorded. In the simple conditional visual discrimination, amphetamine increased omissions without significant effects on accuracy or response latency. Physostigmine enhanced response latencies and failures to respond without significant effects on accuracy. ZK 93426 had no consistent effects on accuracy although at higher doses, some increase in response latency was seen in the delayed responding version of the visual discrimination task. Diazepam had negative effects on all parameters in both discrimination procedures. Scopolamine disrupted responding, but not accuracy in the simple discrimination, whereas accuracy was reduced in a dose, but not delay dependent manner in the delayed discrimination. A similar effect to that observed with scopolamine was observed following methylscopolamine in the delayed discrimination procedure. In the simple visual discrimination small increases in accuracy were recorded, accompanied by increased response latencies.

Excitatory amino acids are employed as neurotransmitters in the majority of excitatory synapses in the brain (Watkins and Evans, 1981). At present, four subtypes of receptor are recognized, and defined on the basis of their preferred agonists as being N-methyl-D-aspartate (NMDA), quisqualate (Quis), kainate (K) or metabolotropic receptors. Of these, only the NMDA receptor is at all well characterized, largely as a consequence of the availability of specific antagonists acting at a number of apparently different sites on the receptor complex. This receptor gates a channel in neuronal membranes which is permeable to sodium and to calcium. The classical antagonists for NMDA receptors are 2-amino-5-phosphono-alkane carbonic acid derivatives such as 2-amino-5-phosphonopentanoic acid (AP5), which compete with excitatory amino acids for their binding sites at this receptor (e.g. Foster and Fagg, 1984). Additionally, however, a number of well-known pharmacological agents act as non-competitive antagonists, acting at a site apparently within the ion channel; among these are the dissociative anaesthetics such as ketamine (Honey et al., 1985), the hallucinogenic phencyclidine (Anis et al., 1983) and the experimental anticonvulsant, MK 801 (Wong et al., 1986).

The cholinergic agonist pilocarpine triggers sustained limbic seizures in rodents. Pilocarpine seizures were blocked by systemic administration of benzodiazepines, barbiturates, valproate and trimethadione, while diphenylhydantoin did not affect, and ethosuximide increased the susceptibility of rats to such seizures. This pattern of action antiepileptic drugs is characteristic for pilocarpine seizures and different from other rodent models of epilepsy. Although the anatomical substrates in the forebrain involved in the expression of anticonvulsant activity are unknown, the basal ganglia are believed to be essential for the motor expression of pilocarpine seizures. Bilateral microinjections into the substantia nigra, a major output station of the basal ganglia, of midazolam (ED 50 38.5 nmol; range 29–52 nmol), phenobarbital (ED 50 16 nmol; range 7–39 nmol) and trimethadione (ED 50 30 nmol; range 16–56 nmol) protected rats against pilocarpine seizures (380 mg/kg i.p.). Diphenylhydantoin (up to 100 nmol) remained inactive, while ethosuximide (ED 50 38 nmol; range 22–65.5 nmol) reduced the threshold for pilocarpine seizures, converting subconvulsant doses of pilocarpine (200 mg/kg i.p.) into convulsant ones. The profiles of action of antiepileptic drugs on pilocarpine seizures were similar following intranigral and systemic administration. These observations suggest that the substantia nigra may mediate some actions of antiepileptic drugs.

Abecarnil (isopropyl 6-benzyloxy-4-methoxymethyl-beta-carboline-3-carboxylate) is a novel ligand for central benzodiazepine (BZ) receptors, possessing anxiolytic and anticonvulsant properties, but with considerably reduced muscle relaxant effects in comparison to diazepam (DZP). In vitro, abecarnil inhibited the binding of the BZ [3H]lormetazepam to rat cerebral cortex membranes with an IC50 value of 0.82 nM in comparison to 56 nM for DZP. The ability of abecarnil to displace [3H]lormetazepam was enhanced 1.24-fold in the presence of 30 microM gamma-aminobutyric acid; the corresponding value for DZP was 2.8-fold. DZP and abecarnil were equally effective in enhancing the binding of t-[35S]butylbicyclophosphorothionate to rat cortical membranes. In vivo, abecarnil exhibited a 3- to 6-fold higher affinity to forebrain BZ receptors than DZP. Abecarnil was from 2 to 10 times more potent than DZP in most rodent tests of anxiolytic activity, and in reducing locomotor activity in mice and rats thoroughly habituated to the test chamber. However, in rats newly exposed to a novel cage, abecarnil was less potent than DZP in reducing locomotor activity. In tests of motor coordination, abecarnil, in contrast to DZP, showed no or only weak activity, and in potentiating the effects of ethanol and hexobarbital on motor performance abecarnil was 4 to 25 times less potent than DZP. Abecarnil antagonized the effects of BZs in the chimney and loss of righting reflex tests, but not in the rotarod test.(ABSTRACT TRUNCATED AT 250 WORDS)

The discriminative stimulus induced by a subconvulsive dose of pentylenetetrazole (PTZ) in rats is suggested to be anxiogenic in nature; therefore, antagonism of the discriminative stimulus indicates anxiolytic and not anticonvulsant activity. Repeated administration of subconvulsive doses of PTZ eventually leads to seizures, a process known as kindling. The effects of several anxiolytic and anticonvulsant drugs in antagonizing the discriminative stimulus in rats were compared with the effects of the same substances in preventing seizures in rats treated acutely with a high dose of PTZ or in rats exhibiting kindled seizures following repeated low-dose PTZ treatment. Irrespective of status as an anxiolytic or an anticonvulsant substance, only compounds that antagonized PTZ-kindled seizures antagonized the PTZ discriminative stimulus. These results illustrate the difficulty in separating the anxiolytic from the anticonvulsant properties of a substance in this model.

Drug addicts abusing heroin substitutes contaminated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and perhaps those who work with this substance, may develop symptoms similar to those seen in Parkinson's disease [7, 12, 13]. We describe the results of a study in which rats were given daily injections of MPTP for two weeks. A progressive suppression of activity was seen, but the subjects rapidly recovered when treatment ceased. The animals were then injected with d -amphetamine or apomorphine; the former drug enhanced activity, to levels seen in control (non-MPTP treated) subjects. Apomorphine had no effect, either on control or MPTP-treated subjects. The effects of acute (0, 2.5, 5.0 and 10.0 mg per rat) administration of MPTP were also studied. The two lower doses significantly decreased activity, but the highest dose did not. Histological examination showed that 2 weeks' treatment with MPTP did not produce neuronal degeneration in the pars compacta of the substantia nigra (SN). In these animals, there were no changes in levels of dopamine, 5-hydroxytryptamine, or their metabolites in either the SN or the caudate nucleus. MPTP had no effect on the levels of neurotensin, somatostatin and substance P in several brain areas. It is concluded that MPTP has reliable effects on locomotor activity in rats without producing measurable histological or neurochemical changes in the nigrostriatal dopaminergic system.

The presence of toluidine blue-staining vesicles and leaky membranes in the Philly mouse lens as early as 10 days after birth led us to investigate the phospholipid metabolism of these lenses. On a dry weight, or per lens, basis, the Philly mouse lens had a slightly higher than normal concentration of phosphatidyl choline (PC), phosphatidyl ethanolamine (PE), sphingomyelin (S) and cholesterol (C) at 10 days. The levels of PC and PE dropped between 10 and 30 days in the Philly mouse, while in the control lenses the amounts of both phospholipids, on a per lens basis, was increasing. 32P incorporation indicated an increased rate of turnover in the Philly lenses. Cholesterol and sphingomyelin concentrations closely paralleled the dry weight per lens curves in the Philly and control, Swiss-Webster, lenses. Sphingomyelin specific activity dropped rapidly in the first 10 day period, possibly reflecting the lowered PC pool available for S biosynthesis. These results suggest a lower utilization of biosynthesized lipids for membrane assembly in the Philly lens. The observed higher turnover of metabolically-active phospholipid supports the presence of increased degradative activity which may, in turn, result in leaky membranes and, thus, contribute to cataract development.

In einer bekannten Reaktion von o-Carboran (I) mit I2 und AlCl3 in CCl4 erhalt man die Titelverbindung (II) in 28% Ausb. neben einer Reihe anderer halogenierter Carborane wie 9-Chloro-o-carboran (13%), 9,12-Dichloro-ocarboran (11%), 9-Chloro-12-iodo-o-carboran (28%) und 9,12-Diiodo-o-carboran (20%).

Review of employment and chemical production records at a Missouri chemical plant and of questionnaires with self-reported occupational exposure to 2,3,7,8-tetrachloro-dibenzo-p-dioxin (2,3,7,8-TCDD) for 16 Missouri workers has explained the wide diversity of 2,3,7,8-TCDD levels previously reported in the workers' adipose tissue (3.5-750 ppt on whole-weight basis). We show that the highest exposures reported to date in the United States occurred in a group of nine production workers who made products contaminated with 2,3,7,8-TCDD. The nine workers had adipose tissue levels with a mean of 246 ppt and a range of 42 to 750 ppt. Seven persons who worked at the same chemical company, but not in the 2,3,7,8-TCDD-contaminated process, had a mean of 8.7 ppt and a range of 3.5 to 25.8 ppt. We also report serum levels of 2,3,7,8-TCDD in these individuals. The adipose tissue from a subset of four production workers with elevated levels of 2,3,7,8-TCDD and seven Missouri residents with normal 2,3,7,8-TCDD levels was also analyzed for other isomers of the PCDDs and PCDFs. The mean adipose tissue level of 2,3,7,8-TCDD in the subset of production workers was 45 times higher than the mean level in the unexposed Missouri residents, but similar levels of the other PCDDs and PCDFs were found in both groups.

The effects of d-amphetamine, morphine, and naloxone on visual discrimination were investigated using a two-choice discrete-trial procedure in which rats were trained to discriminate the position of a lightflash. Morphine (0.3-5.6 mg/kg) but not amphetamine (0.1-1.0 mg/kg) caused a significant dose-dependent disruption in discriminative performance. Both amphetamine and morphine increased response latencies. Naloxone (1.0 mg/kg) prevented the disruption of any aspect of performance by up to 100 mg/kg morphine. Performance after naloxone/amphetamine co-administration was not significantly different from that observed after amphetamine alone. Naloxone alone (0.3-10 mg/kg) had no effect on discrimination, spatial bias or response latencies. These results suggest that morphine and amphetamine affect different components of discrimination performance.

To determine the risk of severe secondary illness in household contacts of patients with Haemophilus influenzae meningitis, telephone interviews were conducted with contacts of patients with reported cases. Four probable or proved secondary cases of severe disease were identified for a secondary attack rate of 0.4%. The secondary attack rate for household contacts of patients 2 years of age and younger was 4.9%. Until safe, effective prophylactic measures become available, physicians should explain to parents that any person who becomes ill in the month after a household case of H influenzae meningitis should be brought to the attention of a physician for appropriate evaluation and treatment.