Publications by authors named "SJ Allen"

The adsorption of a basic dye from aqueous solutions onto peat has been examined. Intraparticle diffusion in the peat pore structure is proposed as a mass transfer mechanism. The results indicate a diffusion process in occurring by a macropore and micropore controlled process.

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Effects of naloxone on acquisition of autoshaped behavior were investigated. Rats deprived to 85% of free-feeding weights were trained to touch a retractable lever; delivery of a food pellet occurred on every trial following lever retraction. The lever was retracted immediately if a touch occurred within 15 s, or automatically after 15 s.

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Choline acetyltransferase (ChAT) and nerve growth factor (NGF) receptors have previously been shown to be expressed in magnocellular forebrain neurones in the rat. We have now examined their colocalization in these neurones. Using monoclonal antibodies raised against ChAT and NGF receptors we demonstrate here a high degree of colocalization.

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We have studied the transcription of the argininosuccinate synthetase gene in cultured RPMI 2650 cells under conditions where the enzyme is subject to metabolite regulation and in canavanine-resistant variants (Canr1 cells) which overproduce the enzyme greater than 200-fold. When grown continuously in medium with citrulline substituted for arginine, the argininosuccinate synthetase activity of RPMI 2650 cells increases 5- to 10-fold. In these cells, expression of a transfected minigene containing the 5'-flanking region of the argininosuccinate synthetase gene was increased 20-fold by short term starvation for arginine and 10-fold by short term starvation for leucine.

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The effect of superior vena caval pressure (SVCP) elevation on the formation of pleural effusions (PE) was studied in sheep. Through a right thoracotomy, a Silastic cuff was placed around the superior vena cava. Catheters for monitoring SVCP and pulmonary artery pressure (PAP) were also placed.

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The risk of nosocomial pneumonia and atelectasis is high among critically ill immobilized patients. We hypothesized that continuous turning on the kinetic treatment table would reduce their incidence. Sixty-five critically ill patients, immobilized because of head injury or traction, were prospectively randomized for treatment in a conventional bed (n = 38) or the kinetic treatment table (n = 27).

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Maxillary sinusitis as a complication of nasotracheal intubation has long been recognized as difficult to diagnose and equally difficult to treat. To better define this problem from a diagnostic and therapeutic standpoint, we studied patients admitted to the surgical intensive care unit at the University of Texas Health Science Center at Houston-Hermann Hospital over a six-month period. During this time, we identified 19 cases of maxillary sinusitis.

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In Alzheimer's disease there is a reported loss of large cells in the cholinergic nucleus basalis of Meynert. It has been suggested, however, that there may be neurons in the nucleus basalis in Alzheimer's disease which are atrophied and therefore difficult to distinguish from neuroglia by size. This has important therapeutic implications and we have attempted to clarify the situation using a neuron-specific antiserum directed against neuron-specific enolase (NSE).

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Using a monoclonal antibody (192-IgG) directed against the rat beta-nerve growth factor (beta-NGF) receptor the distribution of beta-NGF receptors in the forebrain of the rat has been determined. beta-NGF receptor-containing cells were located in presumed cholinergic cells of the medial septal nucleus, vertical and horizontal limbs of the diagonal band of Broca and the nucleus basalis of Meynert.

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The adsorption of basic dyes onto peat from single component and multi-component solution is reported. The adsorption is presented in the form of the equilibrium isotherms. The Freundlich, Langmuir and Redlich-Peterson isotherm equations are fitted to the results and the isotherm constants obtained.

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Escherichia coli endotoxin causes increased capillary membrane permeability and increased pulmonary arterial pressure (PAP) in sheep. If the pulmonary hypertension extends to the level of the microvasculature, then the increased microvascular pressure may contribute to the pulmonary edema caused by endotoxin. We tested the hypothesis that reducing the pulmonary hypertension would reduce the amount of edema caused by endotoxin.

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Our model of the pulmonary interstitial-lymphatic system is based on the assumption that the lung interstitial space can be divided into two compartments. The first compartment (C1) contains the terminal lymph vessels. Increases in the fluid pressure within this compartment, along with increased pressure generated by lymph vessel pumping, cause the lymph flow rate to increase.

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We measured the flow rate (QLV) from cannulated lung lymph vessels in anesthetized dogs. Low-resistance lymph cannulas were used and the vessels were cannulated at the lung hilus. When we increased left atrial pressure to 42.

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Respiratory muscle fatigue is considered a common cause of weaning failure but its detection is hampered by the lack of a satisfactory diagnostic test. Abdominal paradox has been proposed as a valuable clinical index of fatigue and thus its presence may lead to curtailment of weaning trials. However, sensitivity and specificity of this sign as a predictor of weaning outcome is unknown.

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In many sheep Escherichia coli endotoxin results in pulmonary hypertension, increased microvascular permeability, pulmonary edema, and increased central venous pressure. Since lung lymph drains into the systemic veins, increases in venous pressure may impair lymph flow sufficiently to enhance the accumulation of extravascular fluid. We tested the hypothesis that, following endotoxin, elevating the venous pressure would increase extravascular fluid.

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The preparation for collecting lung lymph from sheep caudal mediastinal lymph node (CMN) efferent vessels is widely used to study the effects of endotoxin on lung microvascular permeability. However, there are nonpulmonary lymph vessels that drain into the CMN along with the afferent lymph vessels from the lung. Thus CMN lymph is a mixture of lymph from the lung and diaphragm lymph vessels as well as from other nonpulmonary lymph vessels.

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We previously reported that the very act of cannulating a lung lymph vessel could alter the unique flow characteristics that existed within the lymphatic before cannulation. We postulated that this phenomenon could hold true for lymphatics draining any organ within the body. Since it is frequently important to know the relationship between the transmicrovascular fluid flux and true lymph flow rate, it would be critical that a cannulated lymphatic vessel have the same flow characteristics as those uncannulated vessels draining the same organ.

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We prospectively examined the pattern of breathing in patients being weaned from mechanical ventilation: one group (n = 10) underwent a successful weaning trial and were extubated, whereas another group (n = 7) developed respiratory failure and required the reinstitution of mechanical ventilation. During the period of ventilator support, minute ventilation (VI), tidal volume (VT), and respiratory frequency (f) were similar in the 2 groups. After discontinuation of the ventilator, VI remained similar in the 2 groups, but VT was lower and f was higher in the patients who failed the trial compared with those who were successful, 194 +/- 23 and 398 +/- 56 ml (p less than 0.

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The caudal mediastinal lymph node (CMN) has several efferent lymph vessels in most sheep. When investigators cannulate one of the CMN efferent vessels in order to collect lung lymph, it is possible that lymph may be shunted between the cannulated vessel and other vessels which drain from the CMN into the systemic veins. If shunting does occur then an increase in venous pressure could cause lymph to be shunted to the cannulated lymph vessel.

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Pulmonary lymph drains into the thoracic duct and then into the systemic venous circulation. Since systemic venous pressure (SVP) must be overcome before pulmonary lymph can flow, variations in SVP may affect lymph flow rate and therefore the rate of fluid accumulation within the lung. The importance of this issue is evident when one considers the variety of clinical interventions that increase SVP and promote pulmonary edema formation, such as volume infusion, positive-pressure ventilation, and various vasoactive drug therapies.

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