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Biomedical subjects

R Patterson

Publications and source records attributed to R Patterson.

At least 127 records · Page 7Linked to original sources
PubMed1988

Sensitivity and reliability of force tracking and joint-movement tracking scores in healthy subjects.

The purpose of this study was to examine the sensitivity and reliability of two tracking tests designed to measure control of handgrip force and finger movement. In one test, the subject exerts careful control of handgrip force on a dynamometer, which is interfaced with a computer, and attempts to guide a cursor as accurately as possible along a stationary target track displayed on the computer screen. In the second test, the subject attempts to trace a different target track by precise flexion-extension movement of the metacarpophalangeal joint of the index finger to which an electrogoniometer is attached. For both tests, the computer quantifies the subject's performance with an accuracy index. Fourteen healthy subjects participated in the force tracking test (FTT), which involved three pretest tracking trials, a 20-minute inactivity period, and three posttest trials. Thirteen different healthy subjects participated in the joint-movement tracking test (JMTT) using the same testing format. One-tailed, paired t tests of the pretest-posttest tracking scores showed significant (p less than .01) improvement in tracking accuracy for both the FTT and the JMTT. Additionally, intraclass correlation coefficients for both the pretest and the posttest trials showed acceptable reliability in the FTT and the JMTT. We concluded, for healthy subjects, that 1) these tracking tests are sensitive to small changes in force control and joint-movement control, and 2) the tracking scores are reliable. We believe that these tests could be very useful in documenting objectively the effects of treatment applied to the hand.

Adult↗
PubMed1988

Evidence for in vitro regulation of IgE receptors on the human basophil membrane by their removal and reexpression: effects of Ca2+, Mg2+, some metabolic inhibitors and fetal calf serum.

Human basophils free of receptor-bound IgE and suspended in RPMI-1640 + 0.2% EDTA or in a buffered salt solution lacking Ca2+ and Mg2+ bound optimal quantities of 125I IgE. In media containing Ca2+ and Mg2+ such as RPMI-1640 alone or a buffered physiologic salt solution binding was reduced significantly in the first 60 min and remained essentially unchanged in the next 120 min. Scatchard analysis showed the reduction to be due both to loss of number and affinity of receptors. The presence of both 2-deoxy-d-glucose and 2,4-dinitrophenol usually prevented the reduction of binding in RPMI-1640. Suspension of cells in RPMI-1640 supplemented with fetal calf serum (FCS) demonstrated reduction in binding at 60 min characteristic of divalent-cation-containing media but this was followed by a rise in binding to approximately control levels in the next 120 min. This pattern of binding occurred in about 70% of the experiments. In most of the remaining experiments there was no difference from control binding in that there was no early decrease and no late rise in binding. This variability was not leukocyte-donor-dependent. When cells were preloaded with 125I IgE and incubated in RPMI-1640 dissociation of IgE was more rapid than in media free of Ca2+ and Mg2+. The results suggest that membrane-bound IgE receptors on basophils may be shed by an energy and Ca2+ and Mg2+ requiring process and reexpressed dependent on a factor or factors present in FCS.

2,4-Dinitrophenol↗
PubMed1988

Irritant symptoms and immunologic responses to multiple chemicals: importance of clinical and immunologic correlations.

An evaluation of workers in a plant was conducted because of multiple complaints of ocular, nasal, skin and chest symptoms. Antibody activity against 4 different chemicals was identified: an aliphatic diisocyanate, 4-vinylcyclohexene dioxide, trimellitic anhydride (TMA) and an unknown chemical present in a plasticizing ester known as n-octyl-n-decyl-trimellitate. The source of TMA which resulted in immunization in the plant is unknown. The presence or absence of antibodies did not correlate with the presence or absence of symptoms and it was concluded that no occupational allergic disease was present in these workers. Antibody studies alone do not make a diagnosis of occupational allergic disease and clinical correlation is required. Immunoassays may be useful in identifying exposures to immunizing chemicals in the workplace for potential clinical correlation or for exposure monitoring in the workplace.

Air Pollutants, Occupational↗
PubMed1988

Effect of a leukotriene D4 (LTD4) antagonist on LTD4 and ascaris antigen-induced airway responses in rhesus monkeys.

An acute airway response to aerosolized leukotriene D4 (LTD4) qualitatively simulates an IgE-mediated ascaris antigen-induced airway response. The LTD4 airway response is completely inhibited by the LTD4 antagonist, ICI 198615, in normal monkeys. This LTD4 antagonist was then evaluated to determine whether it could inhibit the IgE-mediated ascaris antigen response using the threshold antigen dose-response system or the single antigen dose-response system. In 6 ascaris airway-reactive monkeys, the LTD4 antagonist demonstrated partial inhibition in 2 animals by either the threshold dose system in 1 animal or the single dose system in another animal. In the remaining animals there was no inhibition of the antigen-induced response by the LTD4 antagonist.

Animals↗
PubMed1988

A serial immunologic and histopathologic study of lung injury induced by trimellitic anhydride.

Trimellitic anhydride (TMA) can induce immunologic lung disease in exposed workers. We have developed a rat model of TMA lung injury characterized by lung hemorrhage and an immune response to trimellityl (TM) haptenized lung proteins. The model is similar to the pulmonary disease-anemia syndrome (PDA) seen in workers exposed to TMA fumes. Sprague-Dawley rats, 15 per exposure period, inhaled micronized TMA powder, 100 micrograms/m3, 6 h/day, for 2,6, or 10 days and were sacrificed. At each time period, total, IgG, IgA, and IgM antibody to TM-rat serum albumin (TM-RSA) were measured by radiolabeled antigen binding and enzyme-linked immunosorbent assay (ELISA) in serum and bronchoalveolar lavage fluid (BAL). Hemorrhagic lung foci, weight, and displacement volume were determined, and lungs were examined by light and electron microscopy. There was no lung injury or antibody response at 2 days. There was minimal lung injury at 6 days with low levels of antibody in BAL and serum. At 10 days, there was a marked increase in hemorrhagic foci and in BAL and serum antibody levels. BAL antibody levels at 6 and 10 days had higher correlations with measures of lung injury than corresponding serum levels. There was minimal ultrastructural change at 6 days. By Day 10, there was marked intraalveolar hemorrhage, alveolar septal inflammatory nodules, abundant alveolar macrophages, and evidence of endothelial and epithelial cell injury. These results indicate that the immune response to inhaled TMA occurs parallel with the development of lung lesions, and antibody levels in BAL and serum are highly correlated with lung injury.

Animals↗
PubMed1988

Mechanism of platelet activating factor-induced bronchoconstriction in humans.

The inhalation of platelet activating factor (PAF) produces bronchoconstriction in normal and asthmatic subjects. To identify the mechanism by which PAF-induced bronchoconstriction occurs in humans, bronchoprovocation testing was performed in 7 subjects (3 normal, 4 with mild asthma) after pretreatment with phosphate-buffered saline (PBS), atropine, chlorpheniramine, or indomethacin. We determined the nebulizer concentration of PAF which reduced specific airway conductance (SGaw) 35% (PC35 SGaw) and the slope of the PAF dose-response curve. Atropine produced baseline bronchodilatation (SGaw increased 50%), while chlorpheniramine and indomethacin had no effect on baseline pulmonary function. Atropine increased airway responsiveness to PAF: the PC35 SGaw decreased 40% (p less than 0.05) and the slope of the PAF dose-response curve increased 86% (p less than 0.05). In contrast, chlorpheniramine inhibited the airway response to PAF: the PC35 SGaw increased 87% (p less than 0.05), while the slope of the PAF dose-response curve decreased an insignificant 37%. Indomethacin did not affect either measurement. Chlorpheniramine also prevented the PAF-induced facial flushing and feeling of warmth; atropine and indomethacin did not. These results suggest that PAF-induced bronchoconstriction in humans is mediated at least in part by histamine release, not by cholinergic or cyclooxygenase-dependent mechanisms. Other indirect effects, such as the release of sulfidopeptide leukotrienes, or a direct effect on airway smooth muscle may also contribute to PAF-induced bronchoconstriction. Why atropine heightened the airway response to PAF is unclear.

Adolescent↗
PubMed1988

Localized neuroblastoma treated by surgery: a Pediatric Oncology Group Study.

A prospective study was designed to evaluate the outcome of patients with localized resectable neuroblastoma without regional lymph node involvement when no therapy beyond surgical resection was administered. One hundred one patients observed for 3 to 60 months had a 2-year disease-free survival of 89% (SE = 5%). Of the nine patients experiencing relapse, only three have died. There were no apparent distinguishing characteristics of the nine failures. Due to the favorable prognosis of the subset of neuroblastoma patients, prognostic factor analysis had very limited power and lacked clinical importance. Complete gross removal of the localized tumors is adequate therapy to ensure the survival of the majority of these patients.

Child↗
PubMed1988

Induction of antigen-specific bronchial reactivity to trimellityl-human serum albumin by passive transfer of serum from humans to rhesus monkeys.

A rhesus monkey model was developed to demonstrate the pathogenetic role of IgE to chemical hapten-protein conjugates in causing human occupational asthma from reactive chemicals. Serum from a worker with trimellitic anhydride (TMA) asthma that contained high titers of IgE, IgG, IgM, and IgA to trimellityl-human serum albumin (TM-HSA) was aerosolized into the lungs of two monkeys to afford passive airway sensitization. After the monkeys were challenged with aerosolized TM-HSA, pulmonary functions demonstrated acute airway responses similar to that of Ascaris antigen-induced, IgE-mediated bronchospasm in Ascaris-sensitive monkeys. The monkeys had no airway reactivity when challenged with TM-HSA 1 week after the first positive TM-HSA response elicited with passive sensitization. Passive cutaneous reactivity to TM-HSA was also elicited by the donor serum, but heat-treated donor serum failed to confer cutaneous or bronchial reactivity. These results indicate that airway reactivity in this passive-transfer monkey model of TMA asthma is an antigen-specific response mediated by heat-labile serum factors, presumably IgE to TM-HSA, and does not occur by irritant mechanisms. This experimental model could become a valuable system for evaluating the role of IgE to hapten-protein conjugates in the immunopathogenesis of asthma caused by other reactive chemicals capable of acting as haptens. We postulate that immunologic and clinical features should be consistent with asthma caused by such reactive chemicals and mediated by such mechanisms.

Animals↗
PubMed1988

Desensitization of human basophils with suboptimal concentrations of agonist. Evidence for reversible and irreversible desensitization.

Leucocytes from allergic donors were preincubated with suboptimal concentrations of ragweed or anti-IgE and then challenged with increasing concentrations of the homologous or heterologous agonist. The initial incubation resulted in desensitization, as judged by a reduced reactivity relative to controls preincubated without agonist but challenged similarly. Both homologous and heterologous desensitization were observed and were dose dependent. Evidence was obtained for both a reversible and irreversible component of desensitization, which was also agonist-concentration related. Reversibility occurred to a similar degree either by incubation of suboptimally desensitized cells with optimal concentrations of agonist or by removal of IgE and resensitization. This could implicate IgE-agonist aggregation on the basophil surface as a mechanism of desensitization. Histamine release from desensitized cells was highly correlated with degranulation, suggesting that individual cells were desensitized in an all-or-none manner.

Antibodies, Anti-Idiotypic↗
PubMed1988

Prenatal lead exposure and its potential significance for developmental disabilities: a preliminary study of umbilical cord blood lead levels.

It has been reported that between 1976-1980 the mean blood lead level in American preschool children was 16 micrograms/dl. The Centers for Disease Control (CDC) recently set a blood level of 25 micrograms/dl as the highest acceptable level for children. However, current research findings have provided evidence that detrimental effects on development can occur when lead levels are below this acceptable value. In particular, recent work has shown a relationship between early (prenatal) exposure to lead and delayed cognitive development. Because the developing fetus is particularly vulnerable to insult, it is of critical importance to obtain information about the developmental effects of prenatal exposure to lead and about those factors that may influence this exposure. This report presents initial findings of an ongoing investigation pertaining to issues surrounding early lead exposure. To date umbilical cord blood samples have been measured in 802 infants born at Children's Hospital of Buffalo between November 1987 and April 1988. These infants' residence span approximately 50 townships with most residing in Buffalo proper. Approximately 60 percent of the infants had measurable cord blood lead levels in the range of 4 to 20 micrograms/dl.

Cognition Disorders↗
PubMed1988

Limiting concentrations of human basophil-bound IgE antibody required for histamine release.

Human blood basophils were treated to remove resident IgE, and passively sensitized with mixtures of ragweed antigen E-specific and non-specific IgE under receptor-saturating conditions. At a ratio of about 0.005 (0.5%) specific IgE or higher, maximal histamine release was observed, but below this a progressive decrease occurred. With leucocytes of four donors, minimal ratios producing mediator release above background varied from 0.001 to 0.00034, which was roughly inversely related to the number of IgE receptors per basophil. This indicated that for these donors' cells a similar number of specific IgE molecules was required for histamine release, and calculation showed the numbers to be 30-55, despite a five-fold difference in total numbers of IgE receptors between different donor basophils. Therefore, it could be estimated that the minimal number of bridges required for basophil activation was to the order of 10-15, depending on whether divalent or trivalent bridges were involved. Since percentage histamine release and percentage degranulated cells were highly correlated after suboptimal sensitization, individual cells or subsets of basophils were apparently differentially responsive. This is consistent with other evidence of functional heterogeneity and that histamine release by individual cells is an all or none process.

Allergens↗
PubMed1987

Trimellitic anhydride exposure in a 55-gallon drum manufacturing plant: clinical, immunologic, and industrial hygiene evaluation.

Nine workers at a 55-gallon drum manufacturing plant had history of exposure to a paint powder that contained trimellitic anhydride (TMA). Environmental monitoring revealed airborne levels of TMA to be over 100 times the OSHA permissible exposure limit of 0.04 mg/m3. The exposed workers were evaluated in a cross-sectional study by questionnaire, physical examination, screening pulmonary function tests, serial peak expiratory flow rates (PEFR), and serum antibody levels. Four workers had symptoms consistent with TMA-induced irritant effects. Three had symptoms and IgG levels consistent with TMA late respiratory systemic syndrome (LRSS). Two of these three had PEFR changes that showed significant drops (greater than 20%) 12-18 hours after the end of a work shift. The material safety data sheet for the paint powder failed to list TMA as an ingredient. Despite the well-described toxic effects of TMA, the present study documents that TMA-related illness may continue to be a problem in situations where workers and management are not properly notified of the potential hazards. The measurement of PEFR may be useful in identifying TMA-exposed workers with LRSS.

Adult↗
PubMed1987

What causes stereoscopic tilt from spatial frequency disparity.

A controversy still exists concerning whether the tilt created with interocular spatial frequency disparity arises from a computation of spatial frequency differences or from cumulative positional disparity. In a first experiment, we examined the influence of positional disparity on tilt created with frequency disparity, reasoning that if tilt were computed from spatial frequency differences, the perceived angle should remain unaltered since adding a positional disparity does not change the harmonic content of the stimulus. The results indicated that positional disparity weakened perceived tilt. In a second experiment, we tested the idea that tilt results from the calculation of increasing positional disparity across the display, arguing if local matches of features in the two eyes are made in computing tilt, then the solution to binocular correspondence may be less ambiguous if the same number of cycles was displayed for both spatial frequencies. Perceived tilt increased when the number of cycles was equal, although the angle of tilt still decreased with positional disparity. In Experiment 3, we further reduced potential sources of ambiguity for the binocular matching process by employing D10s (the tenth derivative of a Gaussian) instead of grating patterns. Positional disparity exerted essentially no influence on the perceived angle of tilt of the D10s. Taken together, the results of these experiments suggest that tilt from frequency disparity can be explained solely on the basis of positional disparity.

Depth Perception↗
PubMed1987

Mechanism of leukotriene D4-induced bronchoconstriction in normal subject.

Leukotriene (LT) D4 is a potent constrictor of human airways and a putative mediator of asthma. However, its mechanism of action in man has not been established. In the present study we sought to determine the role of upper airway reflexes, cholinergic pathways, and cyclooxygenase products of arachidonic acid metabolism in mediating LTD4-induced bronchoconstriction in man. Six normal subjects underwent bronchoprovocation testing with LTD4 after pretreatment with either aerosolized phosphate-buffered saline, aerosolized atropine (1.5 mg), aerosolized lidocaine (80 to 160 mg), or oral indomethacin (50 mg three times daily for 10 doses). Specific airway conductance (SGaw), the flow rate at 30% of vital capacity from a partial forced expiratory maneuver (V30P), and the FEV1 were measured at each concentration of LTD4. We calculated the provocative concentration of LTD4 required to produce a 35% fall in SGaw (PC35SGaw) or a 30% fall in V30P (PC30V30P) and the slope of the LTD4 dose-response curve. Atropine increased baseline SGaw 49% (p less than 0.01) and V30P 43% (p less than 0.005). Atropine also increased the PC35SGaw and PC30V30P and increased the slope of the LTD4 dose-response curve. However, neither of these opposing effects was significant. Lidocaine had no effect on either baseline function or the airway response to LTD4. Indomethacin produced small decreases in baseline V30P (12%) and FEV1 (3%) (p less than 0.05 for both), but it too had no effect on the airway response to LTD4. These results indicate that the bronchoconstriction produced by aerosolized LTD4 in normal subjects is not mediated by cyclooxygenase products of arachidonic acid metabolism or irritant receptors in the upper airways. Although cholinergic pathways may play some role, the data suggest that bronchoconstriction results, at least in part, from a direct effect of LTD4 on airway smooth muscle.

Adult↗
PubMed1987

Six-year clinical and immunologic follow-up of workers exposed to trimellitic anhydride.

We report a 6-year study from 1979 through 1985 of workers exposed to trimellitic anhydride (TMA) in three groups of volunteers. Twenty-nine percent of workers (5/17) originally studied had immunologically induced respiratory disease. Subsequent to this evaluation, increased environmental control of TMA exposure was instituted. Since that time, there have been decreasing clinical symptoms and decreasing levels of antibody against TMA conjugated to human serum albumin. These long-term studies originally used radioimmunoassays, but enzyme-linked immunoassays against TMA-conjugated proteins are now demonstrated to be equally appropriate and are more cost-effective. With appropriate clinical and immunologic studies, immunologic airway reactions to TMA may be identified and then prevented by environmental control to decrease inhalation exposure to TMA. This is likely applicable to certain other chemical antigens that immunize by inhalation.

Air Pollutants, Occupational↗