Fluorescein phototoxicity in a premature infant.
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Biomedical subjects
Publications and source records attributed to B J Williams.
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Fever is a remarkably sensitive indicator of infectious disease. The thermometer in clinical use today is basically that developed over a century ago, measuring heat conducted from skin or mucous membranes to an adjacent probe. In dealing with immunosuppressed granulocytopenic patients, the need was realized for an instrument by which temperature might be determined without a probe contact. Infrared pyrometers have been used in industry to record the temperature of mechanical objects at a distance. We tested the feasibility of using such an instrument to detect fever in humans. In a controlled and blinded fashion, infrared measurements from the eyes, axillae, and areas below the ear lobes (E spot) of 140 febrile and afebrile patients were compared with rectal temperatures recorded by a standard thermometer. The eye and E spot provided the most accurate readings. Infrared measurements of the right eye identified 57 (95%) of 60 febrile and 72 (90%) of 80 afebrile patients correctly. Overall, 92% of all patients were correctly categorized by use of the infrared thermometer at this site. We conclude that this approach is feasible and, with further technical developments, may be applicable for routine clinical use.
We investigated the effect of sleep on blood pressure control in seven lambs aged 10-14 days. Each lamb had previously been anesthetized and instrumented for measurements of electrocorticogram, electron-oculogram, nuchal and diaphragm electromyograms, pulmonary blood flow (electromagnetic flow transducer), and aortic and pulmonic blood pressure. The lambs were allowed to recover from surgery at least 3 days before they were studied. Measurements were made at the highest and lowest mean aortic pressure during quiet wakefulness, quiet sleep, and active sleep. The lowest values of mean aortic pressure progressively decreased as the animals went from quiet wakefulness to quiet sleep to active sleep. Mean aortic pressure was most variable during active sleep. During active sleep, transient hypertensive episodes were superimposed upon a tonic hypotensive phase. During the transient hypertensive episodes in active sleep, changes in mean aortic pressure were primarily caused by an increase in systemic vascular resistance rather than by changes in cardiac output. Heart rate was always lower during active sleep than during quiet wakefulness or quiet sleep. These results provide evidence that sleep state has a marked influence on blood pressure control in lambs.
Chickens were orally inoculated with Salmonella typhimurium and fed rations medicated with either 200 g/ton neomycin sulfate, 200 g/ton oxytetracycline, or a combination of 200 g/ton neomycin sulfate plus 200 g/ton oxytetracycline for 16 days. The incidence of salmonellosis was lower in chickens fed the combined antibiotics, and the numbers of viable S. typhimurium in feces were significantly fewer than in chickens receiving only one antibiotic. Chickens fed the combination also gained significantly more weight on less feed than those fed only one antibiotic.
In this paper, we have presented a general covariance structure model for quantitative genetic research that incorporates measurement theory, components of variance, and regression theory for specification of structural relations among variance components. Each portion of the general model addresses specific issues important in delineating the genetic etiology of continuous traits. Through specification of a measurement model, genetic and environmental influences can be estimated independently of measurement error. Genetic and environmental sources of variance are defined from familial sampling designs through the components of variance model. Structural relationships among several traits at the genetic or environmental level can be specified through the regression model. The significance of parameters specified in each part of the model can be tested through model comparisons using a likelihood ratio chi-square test. We utilized the general model to test genetic covariance as a source of observed covariation of obesity and glucose tolerance in the Pima Indians. We initially applied the modeling approach using full-sib, half-sib sampling among the Pima with a second application including offspring as well as parental scores. Our initial applications of the methodology suggest that the covariance structure model can be a useful tool in genetic epidemiological research. Through model comparisons, our findings suggest that the association of glucose tolerance and obesity in the Pima is not due to a common set of genes but rather due to non-familial environmental influences. In conclusion, one task important for future research, as we see it, is the application of covariance structure models to other familial sampling designs and the evaluation of the usefulness of this approach through further applications to data.
The regional distribution of xenopsin-like immunoreactivity (XPLI) and of neurotensin-like immunoreactivity (NTLI) was studied by radioimmunoassay in tissues of Xenopus laevis and rat. In Xenopus laevis, XPLI showed a wide distribution throughout central and peripheral tissues with the highest concentration in the skin; NTLI was found in both central and peripheral tissues with the exception of the skin. Gel chromatography on Sephadex G-25 was used in order to characterize the immunoreactive material; both XPLI and NTLI eluted in a single peak at the position of synthetic xenopsin and neurotensin. No XPLI could be detected in central and peripheral tissues from mouse, rat, guinea-pig, rabbit or cat. In contrast, NTLI was found in a variety of peripheral tissues of the rat and it coeluted with synthetic neurotensin on reverse phase high-performance liquid chromatography. It is probably present in preganglionic parasympathetic nerve fibres.
The characteristics of [3H]neurotensin binding were studied using membranes prepared from the rat brain. Binding of [3H]neurotensin was found to be specific, saturable and reversible. Under the conditions of the assay non-specific binding represented less than 20% of the total binding at a radioligand concentration of 2 nM. The specific [3H]neurotensin binding increased linearly with protein concentration and was dependent on the pH and the temperature of the incubation medium. At 25 degrees C equilibrium was reached rapidly and the association kinetics appeared to be monophasic. The dissociation was not monophasic and it could be resolved into two distinct components. Scatchard analysis of the saturation data indicated a single population of binding sites with a density of 432 fmol/mg protein and an equilibrium dissociation constant of 2.85 nM. A Hill transformation of the competitive inhibition of specific [3H]neurotensin binding by increasing concentrations of unlabelled peptide yielded a slope not significantly different from unity. Neurotensin 1-13 and various neurotensin analogues were tested for their ability to compete with [3H]neurotensin for its binding site. Neurotensin 1-13, neurotensin 8-13 and the amphibian skin peptide xenopsin were equipotent and strongly inhibited the specific binding of [3H]neurotensin. Neurotensin 9-13 and the chicken intestinal peptide Lys8,Asn9-neurotensin 8-13 were weakly active, whereas neurotensin 10-13 and the amino-terminal fragments neurotensin 1-6, neurotensin 1-8 and neurotensin 1-11 were inactive. Physiological concentrations of sodium chloride inhibited specific [3H]neurotensin binding, whereas divalent cations and guanyl nucleotides did not produce a significant change in either the equilibrium dissociation constant or the total number of binding sites. There was no apparent correlation between the content of neurotensin-like immunoreactivity in the rat brain and the density of [3H]neurotensin binding sites in the various brain regions. The highest density of binding sites was found in the hypothalamus and the frontal cortex, intermediate levels in striatum, thalamus, midbrain, hippocampus and olfactory bulb, and low levels in cerebellum and pons-medulla oblongata. In general, there was less variation between different brain regions in the number of [3H]neurotensin binding sites than in the content of neurotensin-like immunoreactivity. The characteristics of this binding assay are consistent with [3H]neurotensin binding to a physiological receptor.
The descending and the intrinsic components of the serotoninergic (5HT) innervation of the Atlantic stingray spinal cord were described by comparing the distributions of neuronal elements exhibiting 5HT-like immunoreactivity (peroxidase-antiperoxidase method) in sections caudal and rostral to spinal transections. The cells of origin of the descending 5HT system were located with a double labeling method for both retrogradely transported horseradish peroxidase (HRP) and 5HT staining. The descending system provides virtually the entire 5HT innervation of the dorsal horn, the intermediate zone, and the dorsal and lateral portions of the ventral horn. Fibers of the descending 5HT system course in the lateral funiculus, the dorsal portion of the ventral funiculus, and in the submeningeal zones of the dorsal and lateral aspects of the spinal cord. This projection primarily originates from the 5HT cell groups of the caudal rhombencephalon (groups II and III; Ritchie et al., '83), with a minor contribution from group IV in the rostral rhombencephalon. The organization of the descending 5HT system in stingrays is remarkably similar to that of mammals. The intrinsic spinal 5HT system consists of cells distributed in the ventromedial spinal cord that have processes extending longitudinally in a ventral submeningeal fiber network. Fibers were traced from the submeningeal system to the ventral horn, where varicose processes were restricted largely to the neuropil ventral to the somata of the fin motoneurons. The existence of a well-defined intrinsic 5HT system in stingrays supports the hypothesis that such a system exists in the spinal cords of a variety of vertebrates.
The Neurological Disorders Workshop was a continuing education experience for school nurses in central Vermont. It examined neurologically-related clinical problems commonly encountered by school nurses such as neurological screening, mental retardation, seizure disorders, motor system disorders, attention and behavior disorders, diagnostic screening tools, and referral sources. The six-day workshop (five consecutive days plus a follow up four months later) used didactic presentations, demonstrations, and practicum experiences. After the workshop, written evaluations were conducted.
In spinally transected stingrays, electrical stimulation of a site just ventral to the dorsal root entry zone or a site in the intermediate portions of the lateral funiculus produced rhythmic swimming like movements of the contralateral pectoral fin. Electromyographic (EMG) records collected during cord-stimulated rhythms had the same pattern of activity and sometimes the same intersegmental coordination as those collected during spontaneous swimming of the same animal. In paralyzed, high-spinal stingrays, the only stimulation sites that produced rhythmic activity (fictive swimming) in the pectoral fin motor nerves were in the intermediate portion of the lateral funiculus. The evoked rhythm occurred in the motor nerves that were contralateral to the stimulated side of the spinal cord. The effects of subtotal lesions of the rostral spinal cord on spontaneous swimming behavior were assessed by analysis of EMG records taken before and after the lesions were made. Severe deficits in swimming occurred after bilateral ablation of intermediate portions of the lateral funiculi. In agreement with previous results, the stimulation experiments indicate that the stingray spinal cord contains an inherent capacity to generate properly coordinated rhythmic swimming. The current experiments also suggest that the descending pathways(s) that normally functions to initiate swimming projects through the intermediate aspects of the lateral funiculi.
Intracellular recordings were made from antidromically identified pectoral fin motoneurons in unanesthetized, decerebrate stingrays (Dasyatis sabina). These recordings had the three all-or-none components seen in other vertebrate motoneuron recordings. About 25% of the impalements had resting membrane potentials that were greater than -80 mV, which is larger than those of motoneurons from other vertebrate species. A novel depolarizing afterpotential (DAP) is associated with the isolated action potential occurring at the first node of Ranvier of the axon (M-spike). Occlusion experiments exclude recurrent events as the source of this potential. A capacitive source for the DAP is postulated. Using morphological and passive electrical data on motoneurons from previous studies, calculations of the passive decay of the nodal spike indicate that the membrane resistance of the initial segment is low and nearly equal to that of nodal membrane. The soma-dendritic (SD) spike is followed by a prominent, humped delayed depolarization (DD). The DD is temporally associated with the onset of the action potential produced by the initial segment (IS spike). Sources of the long-lasting period of repolarization recorded with the IS spike, which may underlie the DD, are postulated. The afterhyperpolarization (AHP) of stingray motoneurons tends to be shorter and smaller in amplitude than that of other vertebrate motoneurons. A negligible conductance change was often found during the period following an SD spike. No significant correlation was found between AHP duration and axonal conduction velocity. The input conductance of stingray motoneurons ranged between 1.5 X 10(-7) and 13.3 X 10(-7) S. The relationship between input conductance and axonal conduction velocity was determined from 42 motoneurons. These data were fitted by a power function with an exponent of 1.7, indicating that, in terms of membrane conductance properties, large stingray motoneurons are simply scaled-up versions of the small motoneurons.
We used chronically instrumented, unanesthetized lambs to study the circulatory response to tolazoline and prostacyclin. During normoxia, tolazoline given in ten incremental doses from .01 to 6 mg/kg increased heart rate beginning at 1.1 mg/kg, cardiac output, and PVR/SVR. Systemic vascular resistance (SVR) fell, and pulmonary vascular resistance (PVR) did not change. Tolazoline given during hypoxemia, when basal PVR and heart rate were increased, caused SVR to fall at both 3.3 and 6.6 mg/kg doses, while PVR fell only at 6.6 mg/kg. During hypoxemia, even .01 mg/kg of tolazoline caused tachycardia, but cardiac output rose insignificantly, due to high variability. Prostacyclin given during normoxia caused SVR to fall without change in PVR. A significantly greater fall in SVR occurred when 6.6 micrograms/kg of PGI2 was the first dose given than when the same dose was given later in an incremental titration. Thus, neither drug is a selective pulmonary vasodilator in unanesthetized lambs. Dosing protocol may be important in determining the overall circulatory response to a given drug dose.
We investigated the effect of behavioural state on the cardiovascular response to an acute venous haemorrhage in 7 lambs aged 13 to 19 days. Each lamb had previously been anaesthetized and instrumented for measurements of electrocorticogram, electro-oculogram, nuchal and diaphragm electromyograms, pulmonary blood flow (electromagnetic flow transducer), aortic and right atrial blood pressures. The lambs were allowed to recover from surgery at least three days before they were studied. Measurements were made during a 1-minute control period and during a 1-minute experimental period that followed a 10 ml/kg body weight haemorrhage during quiet wakefulness, quiet sleep and active sleep; the haemorrhage took approximately 30s. Haemorrhage produced similar decreases in right atrial pressure and pulmonary blood flow during the three behavioural states. However, mean aortic pressure decreased more following haemorrhage during active sleep than during quiet sleep or quiet wakefulness. These results provide evidence that reflex control of the peripheral circulation is altered during active sleep compared to quiet sleep and quiet wakefulness in lambs.
We investigated the effect of sleep on the cardiovascular response to alveolar hypoxia in seven lambs aged 17 to 21 days. Each lamb had previously been anesthetized and instrumented for measurements of electrocorticogram, electro-oculogram, nuchal and diaphragm electromyograms, pulmonary blood flow (electromagnetic flow transducer), aortic and pulmonic blood pressures. The lambs were allowed to recover from surgery at least three days before they were studied. Measurements were made during a 1-min control period and during an experimental period of alveolar hypoxia (FIO2 0.10) during quiet wakefulness, quiet sleep and active sleep. Alveolar hypoxia produced similar increases in cardiac output, heart rate, mean aortic and pulmonic blood pressures and a similar decrease in systemic vascular resistance during the three behavioral states. These data provide evidence that sleep does not affect the integrated cardiovascular response to arterial chemoreceptor stimulation in lambs.
Sixty-six Staphylococcus intermedius isolates from canine clinical specimens were tested for susceptibility to various antimicrobial agents by the Bauer-Kirby disk diffusion method and a commercial microdilution system. All isolates were susceptible to cephalothin, cloxacillin, gentamicin, methicillin, and vancomycin. Resistance to ampicillin, penicillin G, and tetracycline was frequent. There was an overall 87% agreement of results from the disk diffusion and microdilution methods for 10 antimicrobial agents. There was greater than or equal to 94% agreement between the 2 methods for 7 antimicrobics; discrepancies were minor.
We evaluated the cardiopulmonary interaction of tolazoline and low-, medium-, and high-dose dopamine infusion (2.7, 27, and 270 micrograms/kg/min) in 11 normal, chronically instrumented, unsedated neonatal lambs. Concomitant tolazoline and dopamine infusions caused tachycardia at all dopamine doses and blocked alpha-adrenergic-mediated increases in systemic resistance and left atrial pressure caused by medium and high doses of dopamine. Moderate doses of dopamine alone increased cardiac output. During simultaneous tolazoline infusion, dopamine increased cardiac output at both moderate and high doses. The effect of dopamine on pulmonary artery pressure was not modified by tolazoline; pulmonary pressure increased similarly with dopamine alone and with dopamine plus tolazoline. Calculated pulmonary vascular resistance rose with dopamine alone, but not with infusion of tolazoline and dopamine, because pulmonary blood flow rose in proportion to pulmonary artery pressure.
Some 3-[(alkylthio)methyl]quinoxaline 1-oxide derivatives (1) have been synthesized and screened for antibacterial activity. 2-Acetyl-3-[(methylsulfonyl)methyl]quinoxaline 1-oxide (7a) was found to possess good in vitro activity against some pathogens important to veterinary medicine including Treponema hyodysenteriae, a causative agent in swine dysentery. In an in vivo experiment, this compound (7a) completely protected pigs against a swine dysentery challenge over a 21-day period.
Three modified replications (N = 32, 46, and 32) investigated verbal and nonverbal interactions during role playing of family conflict by family groups of father, mother, and one child. Half the fathers had essential hypertension and half were normotensive. Nonverbal but not verbal behavior differed between families with hypertensive vs. normotensive fathers. Hypertensive fathers and their normotensive wives and children looked at each other less (gaze aversion), both while listening and speaking, than did the members of normotensive families. The difference in duration of gaze aversion occurred more prominently during emotionally negative verbalizations. The results suggest a pattern of conflict avoidance in families with a hypertensive father.