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Biomedical subjects

C Gillies

Publications and source records attributed to C Gillies.

At least 19 recordsLinked to original sources
PubMed2005

Tailored interventions to overcome identified barriers to change: effects on professional practice and health care outcomes.

BACKGROUND: Strategies to implement change in health professional performance have variable impact. A potential explanation is that the barriers to implementation are different in different settings and at different times. Change may be more likely if the strategies were specifically chosen to address the identified barriers. OBJECTIVES: To assess the effectiveness of strategies tailored to address specific, identified barriers to change in professional performance. SEARCH STRATEGY: We searched the Cochrane Effective Practice and Organisation of Care Group (EPOC) specialised register and pending files until end of December 2002. English language articles only were included. SELECTION CRITERIA: Randomised controlled trials (RCTs) that reported objectively measured professional practice or health care outcomes in which at least one group received an intervention designed (or tailored) to address prospectively identified barriers to change. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data and assessed quality. We also contacted study authors to obtain any missing information. Quantitative and qualitative analyses were undertaken. MAIN RESULTS: We included 15 studies. For Comparison 1 (an intervention tailored to address identified barriers to change compared to no intervention or an intervention(s) not tailored to the barriers), there was no consistency in the results and the effect sizes varied both across and within studies.A meta-regression of a subset of the included studies, using a classical approach estimated a combined OR of 2.18 (95% CI: 1.09, 4.34), p = 0.026 in favour of tailored interventions. However, when a Bayesian approach was taken, meta-regression gave a combined OR of 2.27 (95% Credible Interval: 0.92, 4.75), which was not statistically significant. AUTHORS' CONCLUSIONS: Interventions tailored to prospectively identify barriers may improve care and patient outcomes. However, from the studies included in this review, we were unable to determine whether the barriers were valid, which were the most important barriers, whether all barriers were identified and if they had been addressed by the intervention chosen. Based on the evidence presented in this review, the effectiveness of tailored interventions remains uncertain and more rigorous trials (including process evaluations) are needed. Further research needs to address explicitly the questions of identifying and addressing barriers.

Humans↗
PubMed2002

Interventions in the management of serum lipids for preventing stroke recurrence.

BACKGROUND: A close association between serum lipid levels and the incidence of coronary heart disease (CHD) has been well proven in middle aged and older persons, up to the age of 70-75 years. Individual studies have shown interventions to reduce total and low density lipoprotein (LDL) cholesterol levels, especially with 3-hydroxy-3-methylglutaryl coenzyme a (HMG-CoA) reductase inhibitors (statins), to be of benefit in reducing CHD and stroke events in those with a history of coronary heart disease. However, the relation of serum cholesterol and cholesterol sub-fractions with cerebrovascular disease is less clear. It is unclear whether lipid levels in the post-stroke period are a predictor of recurrence and whether treatment to alter levels can prevent recurrence of either stroke or cardiovascular events. OBJECTIVES: To investigate the effect of altering serum lipids in the prevention of cardiovascular disease and stroke recurrence in subjects with a history of stroke. SEARCH STRATEGY: The Cochrane Group Trials Register was searched up to 8 May 2001 along with MEDLINE (from 1966), EMBASE (from 1980) and the Cochrane Controlled Trials Register. All pharmaceutical firms known to produce a lipid lowering agent were also contacted and asked to provide information on publications or unpublished work relevant to this review. SELECTION CRITERIA: This review included unconfounded randomised trials of subjects aged 18 years and over with a history of stroke or Transient Ischaemic Attack (TIA). DATA COLLECTION AND ANALYSIS: The data were extracted independently by the three reviewers. MetaView 4.1 was used for all statistical analyses. MAIN RESULTS: Five studies involving 1700 patients were included in the review. The active intervention in two of the studies was Clofibrate, Pravastatin in another two and Conjugated Oestrogen in the fifth. Fixed effects analysis showed no evidence of a difference in stroke recurrence between the treatment and placebo groups for those with a previous history of stroke or TIA (odds ratio 0.96, 95% confidence interval 0.71 to 1.30). In addition there was also no evidence, based on two studies, that intervention reduced the odds of all cause mortality (odds ratio 0.87, 95% confidence interval 0.55 to 1.39) nor, from one study, that there was any effect on subsequent vascular events (odds ratio 1.27, 95% confidence interval 0.84 to 1.89). REVIEWER'S CONCLUSIONS: These trials do not provide evidence for a benefit, or harm, from interventions to alter serum lipid levels in patients with a history solely of cerebrovascular disease. Their use, therefore, cannot yet be recommended routinely in this patient group, but ischaemic stroke patients with a history of myocardial infarction should receive statin therapy along the lines of the previous recommendations for those patients with a history of myocardial ischaemia. There are currently three ongoing trials which will recruit approximately 30,000 patients, including those with a history of stroke, and the results of these trials may have a significant effect on these conclusions.

Cardiovascular Diseases↗
PubMed2002

Continuous cardiac baroreceptor measurement during tilt in healthy elderly subjects.

INTRODUCTION: Abnormalities of cardiac baroreceptor sensitivity (BRS) may contribute towards the high prevalence of orthostatic hypotension and falls in the elderly. Most mathematical analyses used to determine BRS in the time or frequency domains assume a stationary physiological state and cannot be performed under dynamic change and therefore are not valid during tilt. We describe a new method of estimating BRS during tilt. METHODS: Twenty-five healthy elderly volunteers with a mean age of 69 +/- 3 years underwent head-up tilt to 70 degrees, within 5 s, 3 times on 2 separate visits. Blood pressure (BP) and heart rate were recorded continuously using a Finapres beat-to-beat BP monitor and surface ECG. A continuous estimate of BRS was obtained by combining beat-to-beat linear regression with Legendre polynomial interpolation. RESULTS: The values for supine BRS prior to tilt on the two visits, calculated using the new regression method (10.4 +/- 8.2 ms/mmHg and 12.5 +/- 9.7 ms/mmHg) were similar to those using fast Fourier analysis (10.7 +/- 6.7 ms/mmHg and 12.4 +/- 7.1 ms/mmHg). A rapid fall in BP and pulse interval along with cardiac BRS values occurred with tilt within the first 20 s of onset on both visits and remained reduced up to 90 s post tilt (p < 0.01). CONCLUSIONS: The values for cardiac BRS obtained using continuous time domain analysis agree well with those calculated using spectral methods and can be used to assess the dynamic changes in BRS to rapid perturbations in BP such as that occur with tilt.

Aged↗
PubMed1999

Sympathectomy decreases and adrenergic stimulation increases the release of tissue plasminogen activator (t-PA) from blood vessels: functional evidence for a neurologic regulation of plasmin production within vessel walls and other tissue matrices.

Our recent morphologic studies indicated that peripheral nervous system (PNS) adrenergic neurons synthesize, transport, and store the serene protease, tissue plasminogen activator (t-PA) in axon terminals, many of which innervate vessel walls. Sympathoadrenal stimulation induces a surge of t-PA from vessel walls into the blood. The vascular endothelium, which constitutively secretes t-PA into blood also has long been widely assumed to be the principal source of this stress-induced release, but has not been verified as such. A neurologically regulated release from adrenergic stores could thus augment the known constitutive endothelial release. To functionally test this possibility, we quantitated the effects of guanethidine-induced systemic sympathectomy on the basal and stimulated release of t-PA from isolated vessel explants in superfused organ cultures. Moment-to-moment changes in the release rate were plotted from serial assays of the t-PA free activity. The effects of endothelial and adventitial nerve plexus ablations were also tested. Sympathectomy induced 30-50% reductions in t-PA release from both arterial and microvascular explants. An acute release induced by alpha-1 adrenergic receptor stimulations was also strongly suppressed, as were basal levels of the circulating enzyme in vivo. Adventitial and endothelial ablations from normal large vessel explants produced greater reductions than small vessel endothelial ablations. Ganglion electrical stimulation also induced an acute microvascular release in vivo. These and past morphologic findings indicate a physiological infusion of t-PA into the vessel walls, blood, and other innervated matrices by sympathetic neurons.

Animals↗
PubMed1998

Functional and morphologic evidence of the presence of tissue-plasminogen activator in vascular nerves: implications for a neurologic control of vessel wall fibrinolysis and rigidity.

Tissue plasminogen activator (t-PA) is expressed by hypothalamic and peripheral sympathetic neurons. The sympathetic axons that permeate artery walls have not been investigated as possible sources of intramural t-PA. The plasmin produced by such a system would locally activate both fibrinolysis and matrix metalloproteinases that regulate arterial collagen turnover. To assess this neural t-PA production, we investigated the capacity of rat cervical sympathetic ganglion neurons to synthesize and release t-PA, and the expression of the enzyme in carotid artery and the iris-choroid microvascular tissues that receive the ganglion axon distribution. Functional studies confirmed that (i) the ganglion neuron cell bodies synthesize t-PA mRNA, (ii) cultured ganglion carotid artery and iris-choroid microvascular explants predominantly release t-PA rather than urokinase, (iii) microvascular tissues release approximately 20 times more t-PA per milligram than carotid explants (which accords with the higher innervation density of small vessels), and (iv) removal of the endothelium did not cause major reductions in the t-PA release from carotid and microvascular explants. Immunolocalization studies then confirmed a strong expression of the enzyme within the ganglion axons, the carotid adventitia that receives these axons, and the predominantly sympathetic axon terminals in the iris-choroid microvasculature. These data indicate the existence of a previously undescribed system for the delivery of neural t-PA to vessel walls. The intramural production of plasmin induced by this system represents a novel principle for the regulation of arterial matrix flexibility, especially in the media of densely innervated small arteries and resistance arterioles involved in the pathogenesis of stroke, hypertension, and vascular aging. Thus, the data suggest an important new interface between neuroscience and vascular biology that merits further exploration.

Aging↗
PubMed1997

Morphologic evidence for a preferential storage of tissue plasminogen activator (t-PA) in perivascular axons of the rat uvea.

The uveal layer is thought to hold the largest stores of tissue plasminogen activator (t-PA) within the eye. However, the uveal cell types that contain and could release t-PA to contiguous tissues and fluids have not been clearly identified. In the present study the general distribution pattern of t-PA antigen in fresh rat iris and choroid tissue was determined by immunofluorescence in preliminary light microscopic (LM) cryosections. Transmission electron microscopic (TEM) immunogold localization was then used to detect specific cellular and subcellular sites of t-PA antigen. The primary antibody was rabbit anti-mouse t-PA IgG. The immunofluorescence in preliminary LM cryosections of both tissues was most intense over discrete linear and cross-sectioned structures that resembled the contours of axon bundles. This impression was strengthened when silver impregnation highlighted similar structures in separate sections of the same tissue samples. TEM immunogold labeling of thin sections then confirmed that the t-PA antigen was confined to the axoplasm of both myelinated and unmyelinated perivascular nerve fibers in both the iris and choroid. Gold particles were not observed over axonal membranes, myelin sheaths, Schwann cells, retinal pigment epithelium or vascular endothelial cells. Ultrathin TEM cryosections of the iris showed a localization of some particles over structures that resembled tubules and vesicles within the axoplasm, but not over mitochondria. The axonal location of t-PA was shown by the co-localization of t-PA with an antibody against rat neurofilaments. The typical axon morphology that enclosed the t-PA particle markers in all TEM sections also indicated an axonal location. Separate TEM sections were processed with conventional fixatives and stains to highlight the typical uveal axon morphology, which also confirmed the identity of perivascular axons as the sites of t-PA localization. Affinity of the primary antibody for rat t-PA was shown by an inhibition ELISA against rat uveal tissue extracts and by the inhibition of t-PA activity in aqueous humor. An amidolytic assay was used to quantify t-PA activity. Possible explanations for the preferential immunolocalization of t-PA antigen to the axoplasm of uveal nerve terminals and the need for additional functional studies to confirm a putative neural t-PA synthesis are discussed.

Animals↗
PubMed1995

Extravascular secretion of t-PA by the intact superfused choroid.

PURPOSE: Demonstrate the continuous extravascular secretion of enzymatically active t-PA by the intact choroid. METHODS: Enucleated rat eyes were dissected under microscopic control to prepare eyecups for superfusion in a small organ culture system. Individual preparations provided access to intact retinal, retinal pigment epithelial, or choroidal surfaces in situ. Cups were superfused with oxygenated Kreb's buffer (100 microliters/minute) at 37 degrees C and pH 7.4 while suspended in a microincubator. Released t-PA activity was measured by an amidolytic assay in 1-minute overflow samples and in cup media after flow interruptions. RESULTS: Minimal basal secretion was detected in the overflow with the retina in place. Interruption of flow (10 minutes) produced a static accumulation of 0.10 +/- 0.01 IU/ml. With the retinal pigment epithelium in place after retinal removal, t-PA release was moderately accelerated. Removal of the retinal pigment epithelium to expose the Bruch's-choroidal surface produced the greatest acceleration. The 10-minute static level was 0.48 +/- 0.13 IU/ml. Release from the scleral shell after choroid removal was negligible. An acute burst release of t-PA activity (1.3 +/- 0.18 IU/ml) followed the infusion of bradykinin (5 to 20 microM) into choroidal cups. CONCLUSION: Choroid appears to be the dominant source of a continuously secreted t-PA in superfused rat eyecup organ cultures. This enzymatically active t-PA is able to pass through an apparently intact Bruch's membrane but is largely impeded by an intact retinal pigment epithelium. It is also possible that retinal pigment epithelium contains inhibitors that could reduce the released t-PA activity. The authors propose that this secretory function of the uveal tissue, which has thus far not been recognized, may be a principal mechanism for the regulation of intraocular fluid circulation and matrix remodeling by plasmin in vivo.

Animals↗
PubMed1994

Enhancement of the recovery of rat hearts after prolonged cold storage by cyclocreatine phosphate.

The present study determined whether the administration of cyclocreatine phosphate (CCrP) prior to ischemia can enhance the recovery of rat hearts hypothermically preserved for a prolonged period. Rats (n = 6 per group) were injected intravenously with 1 ml saline or CCrP (500 mg/kg). After 2 hr, hearts were excised and arrested by an infusion of University of Wisconsin solution. Saline hearts were then incubated in 40 ml UW, while CCrP hearts were incubated in 40 ml UW containing 100 mg CCrP; a mixture that is now referred to as Hartford Hospital (HH) solution. After 6 hr of storage at 4 degrees C, hearts were reperfused in the Langendorff mode for 15 min and then in the working heart mode for 30 min. Results indicated that the recovery of cardiac function--measured as aortic flow, coronary flow, cardiac output, stroke volume, and stroke work--was significantly better in CCrP group (50-55% baseline) compared with that of saline hearts (20-25%). Although no difference in enzyme leakage (i.e., creatine kinase) or lactate was detected between the two groups, the increase in heart weight after the initial 6-hr storage was significantly higher in saline hearts compared with that of CCrP hearts. Results of this study support the conclusion that CCrP treatment provides improved functional recovery after prolonged hypothermic preservation.

Animals↗
PubMed1994

Evidence of cardiac inflammation after open heart operations.

In this study, 6 anesthetized dogs underwent global cardiac arrest for 1 hour, followed by reperfusion on bypass for 45 minutes. The hearts were then weaned off cardiopulmonary bypass and monitored for an additional 2 hours. Using modified Boyden chambers, high levels of neutrophil chemotactic activity were detected (using a checkerboard analysis) in the coronary sinus effluents obtained during cardiac arrest. The activity tended to decline during reperfusion. Assay of myeloperoxidase (a marker for neutrophils) revealed an accumulation of large numbers of neutrophils in the right (14 +/- 1.1 x 10(4) cells/g wet weight) and left (16 +/- 1 x 10(4) cells/g wet weight) ventricles after 2 hours of reperfusion. Light microscopy evaluation confirmed the presence of neutrophils, not only in the ventricles, but also in a greater number in the right and left atria. Electron microscopy study of these hearts revealed the presence of mild reversible changes, indicating good preservation of the hearts during arrest. Results of this study provide evidence for an acute inflammatory reaction that takes place after cardiac operations and suggest a role for myocardial tissues in the initiation of such a response through their release of neutrophil chemotactic factors.

Animals↗
PubMed1992

Urinary neutrophil chemotactic factors in interstitial cystitis patients and a rabbit model of bladder inflammation.

The present study investigates a possible source of inflammatory mediators involved in the pathogenesis of bladder inflammation characteristics of interstitial cystitis disease. Our tested hypothesis is that in response to injury, tissues of the urinary bladder participate in the initiation of bladder inflammation by releasing inflammatory mediators such as neutrophil chemotactic factors. Bladders of anesthetized rabbits (n = 7) were instilled with an acidic solution (pH 4.5) for 15 minutes, then washed with saline and instilled with sterile phosphate buffered saline (PBS) (pH 7.2) for an additional 45 minutes prior to sacrificing the rabbits. Control rabbits (n = 7) were instilled with sterile PBS (pH 7.2) for 15 minutes, then 45 minutes. The levels of neutrophil chemotactic factors were measured using modified Boyden chambers and rabbit peritoneal neutrophils as indicator cells. Results indicated the release of high levels of neutrophil chemotactic factors (via a checkerboard analysis) from acid-treated bladders after 15 minutes (70 +/- 4% of standard) and 45 minutes (80 +/- 7%). Electron microscopy analysis of these acid-treated bladders revealed the infiltration of a large number of neutrophils, which correlates with the recovery of neutrophil chemotactic factors. Control rabbits, on the other hand, showed low levels of chemotactic activity (less than 10 percent) and exhibited normal bladder morphology with absence of neutrophils. The glycosaminoglycan (GAG) layer was intact in both acid-treated and control bladders. High levels of neutrophil chemotactic factors were also detected in urine samples from eleven patients with interstitial cystitis (113 +/- 25%) (not due to interleukin-1 or leukotriene B4) which were not detected in urine samples from healthy volunteers (n = 9) or from thirteen control patients with bladder diseases other than interstitial cystitis. These preliminary studies indicate the capability of injured bladder tissues to release neutrophil chemotactic factors which contribute to the initiation of bladder inflammation. The presence of neutrophil chemotactic factors in urine samples of interstitial cystitis patients suggests a possible role of these mediators in the pathogenesis of the disease.

Animals↗
PubMed1991

Technical and therapeutic aspects of dynamic stereotactic radiosurgery.

A treatment procedure that results in a uniform dose in a single fraction over the entire treatment volume while minimizing the dose to other tissues has been developed to treat intracranial lesions such as arteriovenous malformations (AVMs). This technique is called dynamic stereotactic radiosurgery. Its main characteristic is simultaneous and continuous gantry and couch motion during the treatment procedure. It employs an isocentrically mounted linear accelerator as the source of radiation. Target localization is determined by digital subtraction angiography and CT. From results obtained in other centres, this technique has shown that an AVM less than 2.5 cm in diameter has an 85% chance of being completely obliterated within two years after a single treatment of stereotactic radiosurgery. This technique is suitable for those patients with inoperable, surgically inaccessible lesions, or whose current medical profile shows them to be high-risk candidates for surgical intervention.

Angiography, Digital Subtraction↗
PubMed1989

Abnormalities of pathways of fibrin turnover in lung lavage of rats with oleic acid and bleomycin-induced lung injury support alveolar fibrin deposition.

Alveolar fibrin deposition commonly accompanies acute lung injury, but the nature of the local abnormalities of coagulation and fibrinolysis that support pathologic fibrin deposition are not well understood. The trended abnormalities of procoagulant and fibrinolytic activities occurring in lung lavage fluids of Fischer 344 rats after lung injury induced by intravenous oleic acid (OA) or intratracheal bleomycin were studied. After injury by either agent, bronchoalveolar lavage (BAL) contained increased procoagulant activity and decreased fibrinolytic activity. Lavage procoagulant activity was mainly due to an activator of Factor X attributable to the extrinsic coagulation pathway, and fibrinolytic activity was almost completely plasminogen dependent. Major mechanisms of inhibition of fibrinolytic activity involved both the inhibition of the plasminogen activator (PA) and plasmin. These abnormalities were temporally associated with prominent alveolar fibrin deposition in both models. In OA-treated animals, lavage fibrinolytic activity was absent or profoundly decreased, and antiplasmin and procoagulant activities were increased within 4 hours after the induction of acute lung injury. By 24 hours after OA, lavage PA inhibitor (PAI) activity was elevated with sustained antiplasmin activity. By 3 days after OA, these abnormalities had resolved in association with almost complete resolution of alveolar fibrin deposits. Within 3 days after bleomycin-induced lung injury, lavage procoagulant activity was increased and fibrinolytic activity was depressed due to increased antiplasmin and PAI activities. These conditions persisted for 2 weeks, during which time alveolar fibrin deposition was associated with the development of pulmonary fibrosis. These data indicate that a disruption of the normal balance between procoagulant and fibrinolytic activities occurs in alveolar lining fluids of rats with alveolitis induced by either OA or bleomycin, and that concurrent abnormalities of pathways of fibrin turnover that occur in alveolar lining fluids promote the alveolar fibrin deposition associated with these lung injuries.

Animals↗
PubMed1988

Effects of sodium hypochlorite (Dakin's solution) on cells of the wound module.

This study investigates the effects of sodium hypochlorite, or Dakin's solution (DS), on the function and viability of cells of the wound module (neutrophils, fibroblasts, and endothelial cells). For functional studies, the influence of DS on the in vitro migration of neutrophils was evaluated. Our data indicate that DS (2.5 x 10(-2)% to 2.5 x 10(-4)%) results in greater than 90% inhibition of the migration of both stimulated and nonstimulated neutrophils. Electron microscopy and trypan blue evaluation of neutrophils exposed to DS at these concentrations revealed normal structural features, which indicates that the observed reduction in neutrophil migration is not a result of cell death. In contrast to neutrophils, cultured fibroblasts and endothelial cells exposed to DS (2.5 x 10(-2)% or 2.5 x 10(-3)%) for 30 minutes show marked cell injury characterized by convoluted nuclei, cytoplasmic vacuolization, dilated endoplasmic reticulum, and swollen mitochondria on electron microscopy. These data suggest that DS, even at very dilute concentrations, is toxic to cells of the wound module. We therefore recommend abandonment of the use of DS in open wounds.

Animals↗
PubMed1988

Glomerular spherical electron dense deposits in a patient undergoing long-term regional heparinization.

Spherical electron dense deposits in the glomerular capillary basement membranes and the mesangial matrix were observed in a patient undergoing long-term regional heparinization during treatment with continuous arteriovenous hemofiltration (CAVH). CAVH is a fairly new approach to renal replacement therapy and requires continuous infusion of heparin into the prefilter blood line. In order to limit systemic anticoagulation, protamine may be infused into the postfilter blood line. In the patient described, during 26 days of continuous treatment, 318,620 units of heparin and 5,204 mg of protamine had been infused. Ultrastructural studies of the kidneys obtained at autopsy revealed a striking resemblance between the electron dense deposits seen in this patient and the protamine-heparin complexes described in animal models. Heavy metals, including calcium, phosphorus, and aluminum were excluded by electron probe x-ray microanalysis.

Adult↗
PubMed1987

Bronchoalveolar lavage procoagulant activity in bleomycin-induced lung injury in marmosets. Characterization and relationship to fibrin deposition and fibrosis.

Although pulmonary fibrin deposition and coagulation abnormalities have been observed in acute lung injury in humans, their role in the pathogenesis of pulmonary disorders is unclear. In order to gain further insights into the role of the coagulation in lung injury, we examined the relationship between procoagulant activity in bronchoalveolar lavage (BAL) fluids and the evolution of bleomycin-induced lung injury in marmosets. The BAL procoagulant activity was increased at 1, 2, and 4 wk after bleomycin challenge compared with that in control subjects, and it was capable of shortening the recalcification times of plasmas deficient in factor VII and factor VIII but not in factor X. This profile suggested the presence in BAL of an activator of factor X. Activation of purified human factor X by BAL was demonstrated by measuring the amidolytic activity of the generated factor Xa on its N-benzoyl-L-isoleucyl L-glutamyl-glycyl-L-argenine-p-nitroanilide substrate. Factor X activating activity was increased in BAL at 2 wk after bleomycin challenge. Cleavage of 125I-labeled human factor X by BAL from bleomycin-challenged marmosets yielded a 55,500 Mr product that comigrated with factor Xa, the appearance of which correlated strongly with amidolytic evidence of factor Xa activity. Electron microscopy of the lungs of animals from all groups revealed pulmonary fibrin deposition at 2 wk after bleomycin challenge, at the time of increased BAL procoagulant and factor X activating activity. The BAL procoagulant activity was completely sedimentable by ultracentrifugation and was inhibited by concanavalin A and phospholipase C. Activation of purified factor X by BAL was inhibited by monospecific polyclonal goat and rabbit antibodies to human factor VII as well as antibody to bovine tissue factor, demonstrating that factor X activating activity in BAL was attributable to tissue factor associated with material similar to factors VII or VIIa. We conclude that procoagulant activity in BAL increases after bleomycin challenge in marmosets and is attributable to activation of factor X by tissue factor associated with factors VII or VIIa-like material. Increased BAL procoagulant activity is temporally associated with pulmonary fibrin deposition and pulmonary fibrosis during bleomycin-induced pulmonary injury in the marmoset.

Animals↗
PubMed1985

The implications of anorexia nervosa in a ballet school.

Features important in the diagnosis of anorexia nervosa were common in a sample of 100 ballet students. Defining a "case" of anorexia nervosa proved difficult. Follow-up one year later showed that seven girls who were designated "possible cases" had continued to dance and were considerably improved in their physical status without medical intervention.

Adolescent↗