A modified bite wing X-ray technique for small children.
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Biomedical subjects
Publications and source records attributed to T Adams.
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Gabexate mesilate (GM), a proteolytic enzyme inhibitor, was given to 31 chronically instrumented sheep either as a pretreatment or treatment to determine its effects on the cardiopulmonary response to endotoxin (ET). Twelve sheep received GM prior to endotoxin (0.75 microgram/kg), 10 after ET and 9 received GM without ET. A typical biphasic response was noted; phase I showed increased lymph flow (QL), reduced lymph to plasma protein ratio (L/P) and increased pulmonary artery pressure (PAP). Phase II occurred two hours after ET; the lymph flow remained elevated and the L/P ratio rose slightly above control. Both phases demonstrated an elevation in total peripheral vascular resistance (TPR) and hematocrit but a reduction in cardiac output (CO). In phase II, QL was reduced 35% with pretreatment; the L/P ratio did not rise as much and the PAP was unchanged. There was also a 35% reduction in lymph flow; no change in the lymph to plasma protein ratio but there was an elevation in pulmonary microvascular pressure. Pretreatment with GM diminished the fall in CO and the rise in TPR seen with endotoxin. The values were unaffected by treatment alone.
Technical grade dinitrotoluene (TDNT) was shown to be a potent hepatocarcinogen in rats; however, ambiguous results were obtained from bioassays which evaluated 2,4-DNT, the principal isomer in the technical mixture. The present studies were designed to determine the relative hepatocyte foci promoting activity of TDNT and the primary isomers present in the technical mixture, 2,4- and 2,6-DNT. A rat hepatic initiation-promotion protocol was used in which male Fischer-344 rats were initiated with a single dose of diethylnitrosamine (DEN) (150 mg/kg, i.p.) and permitted to recover for 2 weeks. Following the recovery period, the animals were fed diets containing TDNT,2,4-DNT,2,6-DNT or phenobarbital (PB). The TDNT animals were killed after 3 or 6 weeks of feeding and the 2,4-DNT-,2,6-DNT-and PB-treated animals were killed after 6 or 12 weeks of feeding. Appropriate DEN and DNT controls were also killed at each time point. Sections from three liver lobes of each animal were stained for gamma-glutamyl transferase (GGT) and the number of GGT+ foci per cm3 (Nv) was calculated using stereological methods. TDNT feeding produced a dose-dependent increase in GGT+ foci (Nv) at 3 and 6 weeks relative to both DEN and TDNT controls. Administration of 2,4-DNT and PB produced time-dependent increases in GGT+ foci (Nv), while 2,6-DNT produced dose- and time-dependent increases. Unlike 2,4-DNT and PB, the high dose (14 mg/kg) of 2,6-dNT produced an increase in GGT+ foci in the control groups and in mean foci volume relative to the DEN control. These results establish that TDNT, 2,4-DNT and 2,6-DNT have hepatocyte foci promoting activity and that 2,6-DNT is approximately 10 times more potent than 2,4-DNT. In addition, TDNT administration neither alters hepatocyte replication following partial hepatectomy nor acts as a 'growth selection' agent in the Solt-Farber 'growth selection' model suggesting that differential effects on hepatocyte replication are not responsible for the promoting activity of TDNT. Based on previous initiation study results from our laboratory and the present data, 2,6-DNT appears to be a complete hepatocarcinogen while under the conditions of these studies 2,4-DNT is an apparent 'pure promoter'. These results provide an explanation for the conflicting DNT bioassay results.
A newly developed probe was used to measure in vivo axial forces in the rectum-anal canal of the anesthetized cat. Spontaneous contractions of the smooth muscle of the internal anal sphincter were recorded, as were neurally evoked contractions of striated muscle of the external anal sphincter. Bilateral electrical stimulation (1-10 V, 1-5 Hz, 0.05 ms duration) of motor axons in pudendal nerves elicited two responses. One was synchronous phasic contractions of skeletal muscle fibers of the external anal sphincter that were not abolished by atropine but were by gallamine trithiodide. They occurred at short latencies (1-2 ms) and were mediated through low-threshold (1-3 V, 0.05 ms duration) efferent axons in the pudendal nerves. Contraction times ranged from 45 to 60 ms, and contraction duration ranged from 100 to 160 ms. The second response was a progressive elevation in tone of the anal canal due to contractions either of the smooth muscle of the rectum and/or that of the internal anal sphincter. The elevation in smooth muscle tone concomitant with pudendal nerve stimulation may be due to reflex activation of cholinergic neural pathways, since the response was abolished by atropine.
An investigation was initiated to determine the dosage of streptokinase (given IV) that would consistently produce systemic fibrinolysis, as determined by laboratory evaluation, and to determine the relative safety of this drug in the cat. Results indicated that a loading dose of 90,000 IU of streptokinase (given by continuous infusion over 20 to 30 minutes) and a maintenance dosage (IV) of 45,000 IU of streptokinase/hr predictably produced systemic fibrinolysis in the cat. There were no detectable adverse affects seen on physical examination, necropsy, or histopathologic examination. Using the foregoing dosage regimen, investigation was begun to evaluate the use of streptokinase for treatment of feline thromboembolism. Aortic thrombosis was created experimentally in 15 cats. There was no clearly predictable improvement in nonspecific venous angiograms or thermal circulatory indices for the cats given streptokinase, compared with the values for the control cats. After a total of 180 minutes of treatment, the mean weight of remaining clot removed at necropsy from the aortic trifurcation was 7.3 mg in the streptokinase-treated cats, compared with 13.4 mg in the control cats.
5-Fluorouracil (5-FU) has been reported to cause punctal-canalicular fibrosis with resultant severe epiphora. It is reported that the epiphora will often resolve when treatment ceases or is decreased. However, this report describes a case of punctal-canalicular fibrosis so severe that bilateral conjunctivodacryocystorhinostomies were necessary. This has not been previously reported to the best of the authors' knowledge. It is recommended that ophthalmic consultation be obtained for patients in whom long-term 5-FU therapy is anticipated or who develop tearing while on therapy.
The kidney, with its heterogeneous regional perfusion in the two anatomically and functionally distinct vascular beds of the renal cortex and medulla, and with its non-uniform blood vessel geometries, presents a unique challenge for measuring intrarenal blood flow distribution. Determining whole organ perfusion, on the other hand, is comparatively simple for the kidney, but it provides relatively little information about the suspected dependency of renal excretory function on local perfusion rate. Among the variety of methods proposed for gauging regional renal blood flow, some depend on measuring one or more of the tissue's thermal properties. The most straightforward, but least reliable, involve measurements either of focal tissue temperature alone, or of regional tissue thermal gradients. Simply using heat as a diffusible indicator, however, is unreliable as a measure of blood flow, for many of the same reasons that using an inert gas in a dilution technique is unreliable. Recently developed thermal analytical methods, though, hold promise for measuring local tissue blood flow with accuracy and precision. Two of them are reviewed here. One depends on measurement of the effective thermal conductivity of a small mass of tissue by evaluating the steady state ratio between regional unidirectional heat flux across it and the associated temperature gradient in one vector along a segment of it through an imposed spheroidal heat field. The other depends on analyses of tissue temperature decay subsequent to a controlled pulse of heat delivered through a small inserted thermistor bead. Both techniques use bioheat transfer equations to deduce regional blood flow by differentiating between heat dissipation due to local thermal conductivity and that attributable to the effects of regional convection. Although both methods are unavoidably invasive, neither produces debilitating damage in the tissue volume in which perfusion is measured, nor increases local temperature or metabolism enough to affect blood flow itself. Both techniques quantify local blood flow in small volumes of tissue by detailed evaluation of the many properties of tissue and blood which affect heat transfer, and both allow for a virtually unlimited number of nearly continuous sequential measurements at short (nom. 1 min) time intervals.
We studied the effects of superoxide dismutase (SOD), an enzyme that converts superoxide into peroxide, on the cardiopulmonary response to endotoxin in sheep. Sheep (n = 18) were prepared for chronic measurement of cardiopulmonary variables, including lung lymph flow, by surgically implanting catheters under halothane anesthesia. Nine of the animals were studied before and after the administration of endotoxin (0.75 microgram/kg) with and without SOD. An additional nine animals received SOD without the lipopolysaccharide. Endotoxin produced an increase in lung lymph flow that was initially associated with a marked pulmonary arterial (PA) hypertension and reduced lymph-to-plasma protein ratio (L/P). The lymph flow remained elevated later in the response, but there was only a mild increase in PA pressure, and the L/P was normal. There was also a fall in blood neutrophils and in cardiac index. SOD increased this secondary elevation in lung lymph flow, and the corresponding L/P was greater than the preendotoxin value. The fall in neutrophil count, cardiac output, and the elevation in PA pressure seen with endotoxin were not affected by SOD. When administered in the absence of endotoxin, SOD produced no perceptible change in the cardiopulmonary and lymph values. We conclude that peroxide, hydroxyl ion, and/or other free radicals formed by the action of SOD must be responsible for a portion of the endotoxin response rather than superoxide itself.
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The effects of aspirin on well-standardized commercially produced platelet adhesiveness devices and template bleeding times were simultaneously studied in 19 normal volunteers. As expected, there was significant prolongation of the bleeding time after aspirin, but there was no change in platelet adhesion. Reason for the different effects of aspirin on the two tests are discussed. In addition, the normal range of platelet adhesion was further defined utilizing commercially prepared glass-bead columns.
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Epidermal thermal conductivity (k) was calculated for the cat footpad by measuringtransepidermal heat flux and temperature gradient (¿T) while changes in stratum corneum water content were produced by "internal hydration" (IH; eccrine sweat gland activity by nerve stimulation) or by "external hydration" (HH; exposure to air saturated with water vapor). In some experiments, cutaneous vasoconstriction accompanying IH was prevented by an alpha-adrenergic receptor blocking agent, phenoxybenzamine (POB), 3.52 mg/kg iv. For dry skin k=0.167 plus or minus 0.023 (SE) W.m (-1) degree C (-1). With and without POB, IH produced 49.5% and 17.2% increases in k, respectively; HH after IH did not increase k more. With POB, IH increased k more than did HH alone (49.5% and 15.5%, respectively) and at a higher rate (4.22 times 10 minus 3 and 0.63 times 10 minus 3 W.m minus 1.degree C minus 1. min minus 1, respectively.) As k increased, usually deltaT decreased. Increasing k and decreasing deltaT with skin hydration explain the phenominon that air temperature is felt to be lower the more humid a cold exposure, since the temperature of thermoreceptors at the dermoepidermal junction is closer to that of the skin surface when the corneum is hydrated than when it has a low water content.
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