Presentation and reporting of results.
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Audiovisual Aids↗
Biomedical subjects
J Hobson
Publications and source records attributed to J Hobson.
Venous insufficiency at work.
Chronic venous disease of the lower limbs is one of the most common conditions affecting humankind. It has been postulated that certain workplace conditions may be risk factors for venous insufficiency and varicose veins in particular. This paper examines the evidence for a link between occupation and the prevalence of venous disease. It also reviews recent French research carried out to estimate the prevalence of chronic venous insufficiency in a working population; work and nonwork risk factor and the cost to industry from this condition are also examined.
France↗
Reported benefits and problems experienced with bone-anchored hearing aids.
Within this study we have examined the self-reported benefits and shortcomings experienced by patients fitted with bone-anchored hearing aids using an open-ended approach developed for hearing aid users. Reports were obtained from 39 patients who, between them, listed 165 benefits and 105 shortcomings. Benefits and shortcomings could be sub-divided into four main groups: practical, acoustical, psychological and medical, in that order of frequency. The most commonly reported benefits included hearing better and clearer, ease of use, inconspicuousness, and the fact that it made the individual more confident. The main shortcomings were difficulties with the telephone, wind noise and hearing speech in noise.
Acoustics↗
Organ blood flow following cardiac arrest in a swine low-flow cardiopulmonary bypass model.
STUDY OBJECTIVE: To determine organ blood flow changes, relative to baseline, following cardiac arrest and resuscitation in a closed-chest cardiac arrest swine model using cardiopulmonary bypass to achieve reproducible return of spontaneous circulation (ROSC). INTERVENTIONS: Following 10 min of ventricular fibrillation (VF), animals (n = 10) received low-flow cardiopulmonary bypass at 10 ml/kg/min from 10-15 min. At 15 min of VF, norepinephrine (0.12 mg/kg) was given and bypass flow increased to 50 ml/kg/min, followed by countershocks at 16 min. Following ROSC, cardiopulmonary bypass was immediately weaned off with norepinephrine support. Organ blood flows were determined during normal sinus rhythm, during reperfusion of VF and during the early post-ROSC period while off cardiopulmonary bypass support. Organ blood flows during the early ROSC period were compared with organ blood flow at baseline and during VF. RESULTS: During early reperfusion of VF prior to any drug therapy, myocardial, cerebral and abdominal organ blood flows were all low. All animals achieved ROSC at 16.9 +/- 0.7 min and were weaned from bypass in < 5 min following ROSC. During the early post-ROSC period, blood flow to the myocardial, cerebral and adrenal vascular beds was significantly elevated relative to baseline. Simultaneously, blood flow to the kidneys, liver, spleen and lungs was reduced relative to baseline. CONCLUSIONS: This low-flow bypass model produces reproducible high resuscitation rates and ROSC times. Early post-resuscitation organ blood flow is characterized by a selective hyperemia involving the cerebral, myocardial and adrenal vascular beds, in contrast to hypoperfusion of the pulmonary and mesenteric vascular beds.
Animals↗
The effect of intravenous magnesium administration on aortic, right atrial and coronary perfusion pressures during CPR in swine.
OBJECTIVE: To determine the effect of magnesium administration on aortic, right atrial and coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR). DESIGN: Twelve swine weighing 23.2 +/- 3.1 kg were instrumented for CPP, aortic systolic (AOSP) and aortic diastolic (AODP) pressures. INTERVENTION: Ventricular fibrillation was induced and after 20 min of CPR the animals were allocated to receive epinephrine 0.2 mg/kg, or epinephrine 0.2 mg/kg plus magnesium 0.14 g/kg. Epinephrine was repeated every 5 min. Arterial blood gases were determined during normal sinus rhythm and prior to drug administration. RESULTS: Pressures were recorded and averaged over four consecutive 5-min intervals following initial drug administration. AOSP, AODP and CPP were compared using an analysis of covariance. AOSP was statistically lower in the group receiving magnesium. There was a trend toward lower AODP and CPP in the group receiving magnesium as well. These statistical differences and trends were absent after adjusting for pressures during normal sinus rhythm and serum bicarbonate prior to drug administration. CONCLUSIONS: In this model of prolonged cardiac arrest, the administration of magnesium with epinephrine appeared to have a negative effect on aortic pressures during CPR. Further study is needed to determine the confounding effect of serum bicarbonate on the response to epinephrine and magnesium during CPR.
Animals↗
Changes in myocardial blood flow rates during hyperdynamic sepsis with induced changes in arterial perfusing pressures and metabolic need.
OBJECTIVE: To determine whether hyperdynamic sepsis is associated with dysregulation in the control of myocardial blood flow rates unrelated to hypotension or the use of anesthetic agents. DESIGN: Prospective, nonrandomized, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Fifteen mature male sheep (34 to 61 kg). INTERVENTIONS: Data were recorded in study subjects before and after the induction of sepsis following cecal ligation and perforation. Data were then recorded during: a) an infusion of prostaglandin E1 (PGE1), which decreased mean arterial perfusing pressure; and b) an infusion of zymosan-activated plasma, which increased mean pulmonary arterial pressures. MEASUREMENTS AND MAIN RESULTS: Myocardial blood flow rates were measured by the radiolabeled microsphere technique and cardiac index was measured by the thermodilution technique. Cardiac index (change delta) postcecal ligation and perforation minus baseline (+2.3 +/- 1.0 L/min/m2; p < .01) was increased in the septic study. Blood flow rate to the left ventricle was simultaneously increased, and was not further affected when the PGE1 infusion decreased the mean arterial perfusing pressures (-19 +/- 4%). During the infusion of zymosan-activated plasma, mean pulmonary arterial pressures increased (50 +/- 30%) and right ventricular blood flow was increased (zymosan minus postcecal ligation and perforation study: delta 17.8 +/- 50 mL/100 g/min; p < .01). CONCLUSIONS: In this model of hyperdynamic sepsis, increases in blood flow to both the left and right ventricles were positively coupled to changes in respective ventricular work. From the interventional PGE1 and zymosan-activated plasma infusion studies, we found no evidence to support previous suggestions that the regulation of myocardial blood flow rates according to changes in perfusing pressure and/or metabolic oxygen need is significantly altered during hyperdynamic sepsis.
Alprostadil↗
Effects of cigarette smoke on epithelial uptake of non-asbestos mineral particles in tracheal organ culture.
Cigarette smoke is believed to increase the pulmonary retention of many different types of mineral dusts, but the mechanisms of this process are unclear. We have previously shown, using a tracheal organ culture system, that exposure to cigarette smoke directly increases the uptake of asbestos fibers by tracheal epithelial cells, and that this process is mediated by active oxygen species. To determine whether the same effects are seen with other types of mineral dust, we exposed rat tracheal explants to cigarette smoke or air (control) and then to a variety of dusts generally considered "inert" or of low pathogenicity. Explants were maintained in organ culture to allow dust uptake, and segments fixed and prepared for light microscopy at various times up to 1 wk; particle uptake was determined morphometrically. We observed that cigarette smoke significantly increased the epithelial uptake of nonfibrous titanium dioxide and talc, and of fibrous silicon carbide, but not of fibrous or nonfibrous iron oxide, nonfibrous silicon carbide, or fibrous wollastonite. Scavengers of active oxygen species (catalase) or agents that prevent the formation of active oxygen species (deferoxamine) blocked the effects of smoke in enhancing titanium dioxide uptake but did not block the effects of smoke on talc uptake. These observations indicate that cigarette smoke may potentiate the effects of many types of dust, including relatively inert dusts, by directly increasing the numbers of particles entering the tracheobronchial epithelium and eventually reaching the interstitium. However, smoke does not directly enhance the uptake of every dust.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres.
Long asbestos fibres are generally considered to have greater disease-producing potential than short asbestos fibres. However, recent reports have suggested that short fibre asbestos appears to be as effective an inducer of macrophage growth factors and toxic oxygen species as long fibre asbestos, but that short fibres are readily removed from lung and do not gain access to tissues. Because smoke is believed to impair the clearance of asbestos fibres from lung, we examined the clearance of a short (geometric mean length 1.3 microns) amosite preparation administered by intratracheal instillation to guinea-pigs. Half the animals in each group were exposed to the smoke of 10 cigarettes daily. Animals were sacrificed 1 day, 1 week, or 1 month later, the macrophages recovered by lavage, and fibre concentrations and sizes determined by analytical electron microscopy in macrophages and lung tissue. A 30-fold increase was seen in total numbers of fibres retained in macrophages in smokers compared to non-smokers by 1 month, and there was an eightfold increase in retention of short fibres in the lung tissue by 1 month. By contrast, a long fibre amosite preparation (geometric mean length 8.9 microns) showed approximately the same increase in fibre retention in macrophages, but only a twofold increase in tissue retention. We conclude that (1) cigarette smoke markedly impairs the clearance of short amosite fibres from the lung with enhanced retention of fibres in both macrophages and tissue; (2) the effects of smoke on short fibre tissue retention appear to be greater than those on long fibre retention; (3) with the long fibre preparation, smoke causes increased tissue retention of relatively shorter fibres; (4) for both fibre size experiments, the increase in total fibres in macrophages in smoke-exposed animals reflects an increase in the total number of fibre-containing macrophages, rather than an increase in the number of fibres phagocytized per macrophage; (5) enhanced short fibre retention markedly increases total fibre surface area, a parameter which has been suggested as a measure of fibre toxicity, to the point where short fibres might under some circumstances have roughly the same potential toxicity as long fibres. These observations suggest that short asbestos fibres could play an important role in the pathogenesis of some types of asbestos-related disease in cigarette smokers.
Animals↗
Interpractice collaboration for functional assessment in the elderly.
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Activities of Daily Living↗
Effect of PGE1 on altered distribution of regional blood flows in hyperdynamic sepsis.
Since the sepsis syndrome is associated with depressed vascular reactivity, it may be incorrect to assume that pharmacologically mediated changes in cardiac output will be proportionately distributed at the regional level of the circulation. We examined the effect of hyperdynamic sepsis and the concurrent administration of the vasodilatory prostaglandin (PGE1) on the regional distribution of blood flows (Q) in unanesthetized sheep rendered septic by cecal ligation and perforation. Systemic Q progressively increased throughout a 48-h study period after cecal ligation and perforation. Simultaneously, organ Q, measured by the radioactive microsphere technique, was depressed to the pancreas, but increased to the heart, gallbladder, brain, and colon; the increased Q to both heart and gallbladder was greater than the simultaneous increase in systemic Q in this septic study. With the infusion of PGE1 (1 microgram/kg/min), mean arterial perfusing pressures fell, while the cardiac index increased further over that recorded during the 48-h septic study. Despite this depression in arterial pressures, the only significant effect of PGE1 on the interorgan distribution of Q was in the renal circulation, where it was demonstrated that kidney Q fell. We conclude that (1) hyperdynamic and normotensive sepsis exerted nonhomogeneous effects on the distribution of organ Q, and (2) an increased systemic Q during PGE1 infusion was proportionately distributed to all organs, except the kidneys, where Q paradoxically fell. The latter finding suggests that the regulation of kidney Q may be depressed across the normal range of arterial perfusing pressures in the sepsis syndrome. Further investigation is essential to understand the effect of clinical interventions on the control of tissue O2 flux at both the regional and microregional levels of the circulation.
Alprostadil↗
Histochemical evidence for generation of active oxygen species on the apical surface of cigarette-smoke-exposed tracheal explants.
Cigarette smoke is known to contain many types of free radicals, and solutions of smoke tar have been shown to liberate hydrogen peroxide as well as superoxide radical. To further investigate the relationship of smoke exposure and generation of active oxygen species, the authors exposed rat tracheal explants to varying amounts of smoke for 10 minutes in a humidified chamber. After smoke exposure was completed, tracheal segments were incubated in a modification of the ultrastructural cerium chloride technique that was devised by Briggs et al. to demonstrate hydrogen peroxide production. Smoke dose-dependent deposition of cerium-containing reaction product was found on the cilia and the apical membranes; with low-dose smoke, the reaction product appeared as individual dots along the apical surface, but with greater amounts of smoke, heavy linear deposits of reaction product were found along the apical membranes. Smoke produced focal dose-related cell damage with blebbing of the apical membranes, loss of cilia, and focal cell necrosis. Catalase prevented both the positive histochemical reaction and the cell damage; if the catalase was first boiled, its protective effect was destroyed. Similarly, after smoke exposure was completed, tracheal segments were covered with a solution of nitroblue tetrazolium to demonstrate production of superoxide anion. A positive reaction was observed by light microscopy on the surface of tracheas that was exposed to smoke but not that exposed to air; the reaction could be prevented by addition of superoxide dismutase. The authors conclude that exposure of tracheal explants to cigarette smoke in vitro is associated with histochemical evidence of continuing production of both hydrogen peroxide and superoxide anion at the apical cell membrane.
Animals↗
Active oxygen species mediate asbestos fiber uptake by tracheal epithelial cells.
To examine the mechanism whereby asbestos fibers penetrate tracheal epithelial cells, we exposed rat tracheal explants to amosite asbestos alone, or with varying concentrations of substances that scavenge active oxygen species (catalase and superoxide dismutase) or prevent formation of active oxygen species (deferoxamine). All three agents decreased asbestos fiber uptake in a dose-response fashion, but no agent provided complete protection against fiber penetration. We conclude that uptake of amosite asbestos fibers is mediated in part by active oxygen species (most likely OH.), but that other mechanisms of fiber uptake must also exist.
Animals↗
Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells.
We have previously shown that exposure of excised rat tracheal segments to cigarette smoke followed by exposure to a solution of amosite asbestos increases uptake of asbestos fibers compared to exposure to air followed by asbestos. To learn more about the mechanism of smoke-enhanced fiber uptake, we evaluated the effects of amount of smoke and time delay between smoke exposure and asbestos exposure on fiber penetration into the epithelium. To determine whether amount of smoke exposure affected this process, we exposed tracheal segments to 1, 3, or 6 puffs of smoke and subsequently to 5 mg/ml amosite asbestos for 1 h. The segments were then maintained in organ culture for up to 7 d. Asbestos uptake was evaluated by counting fibers in the epithelium by light microscopy. Exposure to increasing numbers of puffs of smoke produced a dose-related increase in fiber uptake at 1 d, 3 d, and 7 d after exposure. To determine whether asbestos exposure needed to occur immediately after smoke exposure for enhanced uptake of fibers to occur, we exposed tracheal segments to 6 puffs of smoke and then delayed exposure to asbestos for 0 (immediate exposure), 3, 18, or 48 h. Tracheas were again maintained in organ culture for up to 7 d after asbestos exposure. Delayed exposure to asbestos after 6 puffs of smoke produced an increase in fiber uptake, even with an interval as long as 48 h between smoke and asbestos exposure; however, the absolute magnitude of fiber uptake was less than that seen with immediate postsmoke asbestos exposure. If catalase was added to the asbestos solution, the smoke-enhanced uptake was abolished, no matter what the time delay.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Functional and morphologic comparison of silica- and elastase-induced airflow obstruction.
We have previously shown that intratracheally instilled silica (quartz) produces both morphologic evidence of emphysema and small-airway changes, and functional evidence of airflow obstruction. To further define the nature of the airflow-associated lesions induced by silica, we compared silica-exposed rats to rats given intratracheal elastase, a standard model of emphysema. Both silica and elastase produced increases in RV and FRC along with upward shifts in the pressure-volume curves. Flows were decreased in both groups, but the changes were more severe in the silica-treated animals. Morphologically, the two treatments produced about the same degree of airspace enlargement, present in both alveoli and alveolar ducts, as well as decreased alveolar and alveolar duct surface area/unit lung volume. Elastic fiber length per unit volume was also decreased in both groups. However, small-airway walls were markedly thickened in the silica-treated compared to the elastase-treated group. We conclude that, in the parenchyma, both these agents produce morphologically similar airspace dilatation, and both induce destruction of elastic fibers. These lesions appear to correlate with abnormalities in the pressure-volume curve. Flow reductions seem to be primarily correlated with changes in small-airway wall structure.
Animals↗
Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants.
It was previously shown that rat tracheal explants first exposed to cigarette smoke and then to amosite asbestos take up more asbestos fibers than explants exposed to air and asbestos. To examine the mechanism of this process, the same experimental design was followed but test groups were added in which the asbestos was mixed with catalase or superoxide dismutase, scavengers of active oxygen species, or deferoxamine, an iron chelator that prevents formation of hydroxyl radical. All three agents protected against the cigarette smoke effect. Heat inactivated catalase or superoxide dismutase was not protective. These observations indicate that active oxygen species, probably derived from the cigarette smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia.
Animals↗
Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants.
Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.
Animals↗
Comparison of inflammatory cells in bronchoalveolar fluid with those in the lumen and tissue peripheral airways and alveolar airspace.
This study compares the inflammatory cell types in the alveolar airspace, peripheral airways, and bronchoalveolar lavage fluid of 65 human lung specimens removed surgically. The data show that the cellular population in the airway tissue is composed of approximately 2-4% neutrophils, and 96-98% mononuclear inflammatory cells. This contrasts with the airway lumen, which contains approximately 5-14% neutrophils, while the alveolar airspace contains 3%, and the lavage fluid contains 4% neutrophils. There is a significant correlation between the percentage of PMN in the walls of the membranous and respiratory bronchioles, as well as between the walls and lumens of respiratory and membranous bronchioles. We conclude that: 1. The lumen of the membranous bronchioles contains a greater percentage of PMN than the lumen of the respiratory bronchiole or of the alveoli. 2. Neutrophils are present in the alveolar airspace. 3. The percentages of PMN present in the lumen of the respiratory bronchiole, alveoli, and lavage fluid are similar. 4. The correlation between percentage of PMN in airway wall and lumen suggests a cellular equilibrium between the 2 sites. 5. In this groups of lungs, there is an apparent stereotypic inflammatory response in that the percentages of PMN in the different anatomical sites are relatively similar from case to case. Various workers have suggested that analysis of the cell types present in bronchopulmonary lavage can be used as a therapeutic index, or as a diagnostic test. Our data suggest that lavage does indeed sample the lower airways and alveolar spaces, and that such usage may well be justified.
Animals↗