Effect of odor treatment systems on bioaerosol microbial concentration and diversity from wastewater treatment plants.

Biofiltration, activated carbon and chemical scrubbing are technologies used for odor control in wastewater treatment plants. These systems may also influence the airborne microbial load in treated air. The study objectives were to 1) evaluate the capacity of three odor control system technologies to reduce the airborne concentration of total bacteria, Legionella, L. pneumophila, non-tuberculous mycobacteria (NTM) and Cladosporium in winter and summer seasons and 2) to describe the microbial ecology of the biofiltration system and evaluate its impact on treated air microbial diversity. A reduction of the total bacterial concentration up to 25 times was observed after odor treatment. Quantification by qPCR revealed the presence of Legionella spp. in all air samples ranging between 26 and 1140 GC/m3, while L. pneumophila was not detected except for three samples below the limit of quantification. A significant increase of up to 25-fold of Legionella spp. was noticed at the outlet of two of the three treatment systems. NTM were ubiquitously detected before air treatment (up to 2500 GC/m3) and were significantly reduced by all 3 systems (up to 13-fold). Cladosporium was measured at low concentrations for each system (< 190 GC/m3), with 68 % of the air samples below the limit of detection. Biodiversity results revealed that biofiltration system is an active process that adapts to air pollutants over time. Legionella spp. were detected in significant abundance in the air once treated in winter (up to 27 %). Nevertheless, the abundance of protozoan hosts is low and does not explain the multiplication of Legionella spp. The season remains the most influential factor shaping biodiversity. In summer only, air biofiltration caused a significant enrichment of the biodiversity. Although odor control technologies are not designed for bacterial mitigation, findings from this study suggest their potential to reduce the abundance of some genera harboring pathogenic species.

Photobiomodulation with a combination of two wavelengths in the treatment of oral mucositis in children: The PEDIALASE feasibility study.

Photobiomodulation is recommended in adults for the prevention of mucositis induced by cervicofacial irradiation or pre-transplant chemotherapy. The results of pediatric studies are promising but this support treatment is still underused. The objective was to conduct a feasibility study in the pediatric hematology-oncology unit at X Children's Hospital. Extra- and intraoral scans were performed a minimum of three times every 2 days for grade 2 or higher mucositis in children (median age, 8.6 years) using the Oncolase laser (Biophoton, Saint Alban, France), with a combination of two wavelengths (635 and 815nm). The effect of the laser on mucositis grade, pain, the child's tolerance, and the time dedicated to this care were also evaluated. The success of the procedure was 77% in 1 year, with the inclusion of 84% of the patients (n=22) and 146 laser treatment sessions (median of four per episode of mucositis). We observed excellent tolerance and pain relief with a gain of two points on the VAS and the HEDEN mucositis scale. This study shows that photobiomodulation that incorporates two application modes (intra- and extraoral) through the combination of two wavelengths is feasible when integrated into the care of a pediatric hematology-oncology department and is perfectly tolerated, even by young children. Along with oral hygiene and analgesic management, it alleviates pain associated with oral mucositis.

T1- or T2-weighted magnetic resonance imaging: what is the best choice to evaluate atrophy of the hippocampus?

BACKGROUND AND PURPOSE: Magnetic resonance imaging is part of the diagnostic criteria for Alzheimer's disease (AD) through the evaluation of hippocampal atrophy. The objective of this study was to evaluate which sequence of T1-weighted (T1WI) and T2-weighted (T2WI) imaging allowed the best visual evaluation of hippocampal atrophy. METHODS: Visual qualitative ratings of the hippocampus of 100 patients with mild cognitive impairment (MCI) and 50 patients with AD were made independently by four operators according to the medial temporal lobe atrophy score based either on T1WI or T2WI. These two evaluations were compared in terms of interobserver reproducibility, concordance with a quantitative volumetric measure, discrimination power between AD and MCI groups, and correlation with several neuropsychological tests. RESULTS: The medial temporal lobe atrophy score evaluated on either T1WI or T2WI exhibited similar interobserver variability and accordance with quantitative volumetric evaluation. However, the visual evaluation on T2WI seemed to provide better discrimination power between AD and MCI groups for both left (T1WI, P = 0.0001; T2WI, P = 7.072 × 10-5 ) and right (T1WI, P = 0.008; T2WI, P = 0.001) hippocampus, and a higher overall correlation with neuropsychological tests. CONCLUSIONS: The present study suggests that T2WI provides a more adequate visual rating of hippocampal atrophy.

Perceptions of a good death: A qualitative study in intensive care units in England and Israel.

OBJECTIVES: To explore factors perceived to contribute to 'a good death' and the quality of end of life care in two countries with differing legal and cultural contexts. DESIGN AND METHODS: Multi-centre study consisting of focus group and individual interviews with intensive care nurses. Data were analysed using qualitative thematic analysis; emotional content was analysed using specialist linguistic software. SETTINGS/PARTICIPANTS: Fifty five Registered Nurses in intensive care units in Israel (n=4) and England (n=3), purposively sampled across age, ICU experience and seniority. FINDINGS: Four themes and eleven sub-themes were identified that were similar in both countries. Participants identified themes of: (i) timing of communication, (ii) accommodating individual behaviours, (iii) appropriate care environment and (iv) achieving closure, which they perceive prevent, and contribute to, a good death and good quality of end of life care. Emotional content showed significant amount of 'sadness talk' and 'discrepancy talk', using words such as 'could and 'should' when participants were talking about the actions of clinicians. CONCLUSIONS: The qualities of a good death were more similar than different across cultures and legal systems. Themes identified by participants may provide a framework for guiding end of life discussions in the intensive care unit.

Measuring workload with electrodermal activity during common braking actions.

How to assess mental load remains a recurrent question. We aimed to explore whether slight differences in real-world driving task demands could be discriminated by electrodermal response (EDR). A sample of 33 participants was observed under five conditions: controlled braking from 50 to 30 km/h, 80 to 50 km/h, 50 to 0 km/h, 80 to 0 km/h, and a single unexpected emergency braking event from 80 to 0 km/h. The likelihood of EDR and, whenever present, its duration were both correlated with workload as represented by the deceleration demand. A higher base travel speed and the unexpected demand of the emergency braking situation impacted EDR, thus attesting higher workload level. EDR explains why stopping the vehicle from 50 km/h and slowing down from 80 to 50 km/h was of similar strain. The results further demonstrate that EDR measures can be successfully employed to discriminate multiple levels of workload. PRACTITIONER SUMMARY: Common braking elicited different loads as revealed by electrodermal response (EDR) with sensitivity to deceleration of - 0.2 g. Even the slightest braking elicited a strain measurable with EDR. Accordingly, EDR may objectively assess the resulting strain during driving, with enhanced reliability if associated with other variables, e.g. cardiac activity.

Notch-induced mammary tumorigenesis does not involve the lobule-limited epithelial progenitor.

The mouse mammary epithelial cell hierarchy contains both multipotent stem cell as well as lineage-limited duct and lobular progenitor cell functions. The latter-also termed parity-identified mammary epithelial cells (PI-MECs)-are marked by beta-galactosidase (ß Gal) expression following pregnancy and involution in whey acidic protein promoter (WAP)-Cre/Rosa26-flox-stop-flox-lacZ (WC/R26) mice, and are the targets of tumorigenic transformation in mouse mammary tumor virus-erbB2 transgenic mice. In this study, we demonstrate that an epithelial population distinct from PI-MECs is transformed during WAP-Int3 tumorigenesis. As expected, WAP-Int3/WC/R26 triple-transgenic mice failed to undergo secretory alveolar development, failed to lactate and developed mammary tumors. Following pregnancy and involution, ß Gal+ mammary epithelial cells were found in the normal mammary tissue, but the resulting mammary tumors were all ß Gal-. WAP-Int3/WC/R26 mammary glands contained ample estrogen receptor alpha (ERα)+ MECs, but only rare (<1%) progesterone receptor (PR)+ and RANKL+ cells. In addition, dissociated MECs from WAP-Int3/WC/R26 glands failed to regenerate a mammary tree upon transplantation into a cleared fat-pad of a nu/nu recipient mouse. However, when mixed with normal MECs, PI-MECs from WAP-Int3/WC/R26 mice contributed progeny to the resulting functional outgrowth. The WAP-Int3/WC/R26-derived PI-MECs displayed all of the properties of fully functional lobular progenitors including giving rise to ERα+, PR+, smooth muscle actin+ and RANKL+ epithelial progeny. These results demonstrate that WAP-Int3 has no oncogenic effect upon PI-MECs and that the expansion of functional lobular progenitors is required for secretory alveolar development and lactation. Furthermore, lobular progenitor function is ultimately controlled by signals within its microenvironment.

The normal mammary microenvironment suppresses the tumorigenic phenotype of mouse mammary tumor virus-neu-transformed mammary tumor cells.

The microenvironment of the mammary gland has been shown to exert a deterministic control over cells from different normal organs during murine mammary gland regeneration in transplantation studies. When mouse mammary tumor virus (MMTV)-neu-induced tumor cells were mixed with normal mammary epithelial cells (MECs) in a dilution series and inoculated into epithelium-free mammary fat pads, they were redirected to non-carcinogenic cell fates by interaction with untransformed MECs during regenerative growth. In the presence of non-transformed MECs (50:1), tumor cells interacted with MECs to generate functional chimeric outgrowths. When injected alone, tumor cells invariably produced tumors. Here, the normal microenvironment redirects MMTV-neu-transformed tumorigenic cells to participate in the regeneration of a normal, functional mammary gland. In addition, the redirected tumor cells show the capacity to differentiate into normal mammary cell types, including luminal, myoepithelial and secretory. The results indicate that signals emanating from a normal mammary microenvironment, comprised of stromal, epithelial and host-mediated signals, combine to suppress the cancer phenotype during glandular regeneration. Clarification of these signals offers improved therapeutic possibilities for the control of mammary cancer growth.

Stability in shifting sands: contemporary leadership roles in critical care.

BACKGROUND: Contemporary nursing leadership roles in critical care are a reflection of the changing environment in which critical care is provided. KEY ISSUES: In the UK, critical care nursing faces challenges in the form of: reduced number and seniority of medical staff cover for acute wards; mandated responsibility for management of patients outside of critical care units, without corresponding responsibility for managing staff; increased public and political awareness of deficits in critical care; increased use of Assistant Practitioners; and emphasis on longer-term outcomes from intensive care. EVALUATION: New leadership roles have met these challenges head on with two main foci: patient management across the acute/critical care interface and hospital wide policies and practice. CONCLUSIONS: The leadership roles examined in this paper highlight three underpinning goals: improved quality and safety of patient care; improved communication between professionals; and empowerment of junior nurses and doctors. IMPLICATIONS FOR NURSING MANAGEMENT: There has been considerable investment in strategic leadership roles for critical care nursing; evidence is developing of the return on this investment for patient and service outcomes. Consideration must now be given to the preparation, mentorship and development of leadership roles for the next generation of nurse leaders.

[Circulating endothelial microparticles: a new marker of vascular injury]. / Microparticules endothéliales circulantes: un nouveau marqueur du dysfonctionnement vasculaire.

Cell activation or apoptosis leads to plasma membrane blebbing and microparticles (MPs) release. MPs are submicron membrane vesicles expressing a panel of oxidized phospholipids and proteins specific of the cells they originate from. Exposure of negatively charged phospholipids and tissue factor confers a procoagulant potential to MPs. Increases in plasma MPs levels, particularly those of endothelial origin, reflects cellular injury and appears now as a surrogate marker of vascular dysfunction. MPs are also biologically active and stimulate pro-inflammatory responses in target cells. Thus, MPs can promote a prothrombogenic and pro-inflammatory vicious circle leading to vascular dysfunction. A better understanding of MPs composition, as well as their effects and the mechanisms leading to their clearance will likely open new therapeutic approaches in the treatment and the prognosis of cardiovascular diseases.

Microparticles and type 2 diabetes.

Cell activation or apoptosis leads to plasma membrane blebbing and microparticles (MPs) release in the extracellular space. MPs are submicron membrane vesicles, which harbour a panel of oxidized phospholipids and proteins specific to the cells they derived from. MPs are found in the circulating blood of healthy volunteers. MPs levels are increased in many diseases, including cardiovascular diseases with high thrombotic risk. Exposure of negatively charged phospholipids and tissue factor confers a procoagulant potential to MPs. Elevation of plasma MPs levels, particularly those of endothelial origin, reflects cellular injury and appears now as a surrogate marker of vascular dysfunction. Recent studies demonstrate an elevation of circulating levels of MPs in diabetes. MPs could also be involved in the development of vascular complications in diabetes for they stimulate pro-inflammatory responses in target cells and promote thrombosis, endothelial dysfunction and angiogenesis. Thus, these studies provide new insight in the pathogenesis and treatment of vascular complications of diabetes.

Role of microparticles in atherothrombosis.

Cell activation or apoptosis leads to plasma membrane blebbing and microparticle (MP) release in the extracellular space. MPs are submicron membrane vesicles which express a panel of phospholipids and proteins specific of the cells they are derived from. Exposure of negatively charged phospholipids and tissue factor confers a procoagulant potential to MPs. MPs accumulate in the lipid core of the atherosclertotic plaque and is a major determinant of its thrombogenecity. Elevation of plasma MPs levels, particularly those of endothelial origin, reflects cellular injury and is considered now as a surrogate marker of vascular dysfunction. Thus, MPs can be seen as triggers of a vicious circle for they promote prothrombogenic and pro-inflammatory responses as well as cellular dysfunction within the vascular compartment. A better knowledge of MP composition and biological effects as well as the mechanisms leading to their clearance will probably open new therapeutic approaches in the treatment of atherothrombosis.

Surface electromyography as a tool to assess the responses of car passengers to lateral accelerations. Part II: Objective comparison of vehicles.

The purpose of this study was to objectively assess the response of car passengers to lateral accelerations. Surface EMG signals were collected bilaterally from the cervical erector spinae (CES), latissimus dorsi (LD), erector spinae (ES), external oblique (EO), and vastus lateralis (VL) muscles of 10 subjects. Lateral acceleration was also recorded. Three chassis-seat configurations AA, BA and BB were tested, with the first letter denoting the chassis and the second the seat. SEMG signals were often contaminated by noise, and were, therefore, denoised using the methods explained in part I. Reciprocal phasic activity was observed for all muscles except for the EO, and the reaction of passengers to lateral accelerations was interpreted as a bust torsion. The RMS of EMG segments was used as an indication of muscle activity. Muscle activation of VL and ES were significantly affected by the configuration tested (p<0.05), with greater activation levels observed for the chassis A than for the chassis B. Such a finding implies that greater roll requires greater muscle activity, thus resulting in less comfortable vehicles. Therefore, SEMG can be used to provide an objective measure of discomfort in passengers subjected to lateral accelerations in a car seat.

Normal pregnancy in a woman with nesidioblastosis treated with somatostatin analog octreotide.

OBJECTIVE: We report the case of a 36-yr-old woman with nesidioblastosis treated throughout pregnancy with high doses of octreotide. We studied the course of blood glucose, foetal growth and development. METHODS: Blood samples were obtained every month throughout pregnancy and taken at birth from the umbilical cord. Sonography was performed repeatedly to monitor foetal growth. RESULTS: The daily dose of octreotide was adapted to blood glucose levels: a dose of 1000 microg was infused during the first part of pregnancy, then it was decreased step by step during the last trimester of gestation. An elective cesarean section was performed at 32 weeks of gestation. High octreotide concentrations were obtained during the first part of gestation (range 2888-5021 pg/ml). During the third trimester of pregnancy blood glucose increased despite high insulin levels attesting physiological insulin-resistance. Plasma levels of placental GH and IGF-1 levels were similar to those observed in a normal pregnancy. Despite the presence of octreotide in the umbilical cord, TSH, free T4, PRL and pituitary GH concentrations were normal at birth. The female newborn (weight 3520 g, length 52 cm) had no malformation, and presented with normal postnatal development. CONCLUSION: Our study demonstrates that: 1) octreotide treatment can be effective in controlling endogenous hyperinsulinism during pregnancy; 2) octreotide does not affect physiological changes during pregnancy such as insulin-resistance or placental GH level; 3) exposure of the foetus to octreotide throughout pregnancy does not induce any malformation and does not affect foetal development.

Circulating microparticles from patients with myocardial infarction cause endothelial dysfunction.

BACKGROUND: Shed membrane microparticles circulate in the peripheral blood of nonischemic (NI) patients and patients with myocardial infarction (MI). We investigated whether or not these microparticles would affect endothelium-dependent responses. METHODS AND RESULTS: Rat aortic rings with endothelium were exposed for 24 hours to circulating microparticles isolated from 7 patients with NI syndromes and 19 patients with acute MI. Endothelium-dependent relaxations to acetylcholine were not affected by high concentrations of microparticles from NI patients (P=0.80). However, significant impairment was observed in preparations exposed to microparticles from patients with MI at low and high concentrations, corresponding to 0.7-fold and 2-fold circulating plasma levels (P=0.05 and 0.001, respectively). Impairment was not affected by diclofenac (P=0.47), nor by the cell-permeable superoxide dismutase mimetic Mn(III)tetra(4-benzoic acid) porphyrin chloride (P=0.33), but it was abolished by endothelium removal or by N(omega)monomethyl-L-arginine. Relaxations to the calcium ionophore ionomycin were decreased in rings exposed to microparticles from MI patients (P=0.05 and 0.009 for low and high concentrations, respectively), but microparticles from NI patients had no effect (P=0.81). Finally, high concentrations of microparticles from MI patients affected neither endothelium-independent relaxation to sodium nitroprusside (P=0.59) nor expression of the endothelial nitric oxide synthase (P=0.43). CONCLUSIONS: Circulating microparticles from patients with MI selectively impair the endothelial nitric oxide transduction pathway and, therefore, could contribute to the general vasomotor dysfunction observed after MI, even in angiographically normal arteries.

In vitro cationic lipid-mediated gene delivery with fluorinated glycerophosphoethanolamine helper lipids.

There is a need for the development of nonviral gene transfer systems with improved and original properties. "Fluorinated" lipoplexes are such candidates, as supported by the remarkably higher in vitro and in vivo transfection potency found for such fluorinated lipoplexes as compared with conventional ones or even with PEI-based polyplexes (Boussif, O., Gaucheron, J., Boulanger, C., Santaella, C., Kolbe, H. V. J., Vierling, P. (2001) Enhanced in vitro and in vivo cationic lipid-mediated gene delivery with a fluorinated glycerophosphoethanolamine helper lipid. J. Gene Med. 3, 109-114). Here, we describe the synthesis of fluorinated glycerophosphoethanolamines (F-PEs), close analogues of dioleoylphosphatidylethanolamine (DOPE), and report on their lipid helper properties vs that of DOPE, as in vitro gene transfer components of fluorinated lipoplexes based on pcTG90, DOGS (Transfectam), or DOTAP. To evaluate the contribution of the F-PEs to in vitro lipoplex-mediated gene transfer, we examined the effect of including the F-PEs in lipoplexes formulated with these cationic lipids (CL) for various CL:DOPE:F-PE molar ratios [1:(1 - x):x with x = 0, 0.5 and 1; 1:(2 - y):y with y = 0, 1, 1.5, and 2], and various N/P ratios (from 10 to 0.8, N = number of CL amines, P = number of DNA phosphates). Irrespective of the F-PE chemical structure, of the colipid F-PE:DOPE composition, and of the N/P ratio, comparable transfection levels to those of their respective control DOPE lipoplexes were most frequently obtained when using one of the F-PEs as colipid of DOGS, pcTG90, or DOTAP in place of part of or of all DOPE. However, a large proportion of DOGS-based lipoplexes were found to display a higher transfection efficiency when formulated with the F-PEs rather than with DOPE alone while the opposite tendency was evidenced for the DOTAP-based lipoplexes. The present work indicates that "fluorinated" lipoplexes formulated with fluorinated helper lipids and conventional cationic lipids are very attractive candidates for gene delivery. It confirms further that lipophobicity and restricted miscibility of the lipoplex lipids with the endogenous lipids does not preclude efficient gene transfer and expression. Their transfection potency is rather attributable to their unique lipophobic and hydrophobic character (resulting from the formulation of DNA with fluorinated lipids), thus preventing to some extent DNA from interactions with lipophilic and hydrophilic biocompounds, and from degradation.

Proangiogenic effect of angiotensin-converting enzyme inhibition is mediated by the bradykinin B(2) receptor pathway.

Recent studies have suggested a proangiogenic effect of angiotensin-converting enzyme (ACE) inhibition. We hypothesized that such a proangiogenic effect of ACE inhibition may be mediated, in part, by bradykinin (BK) B(2)-receptor pathway. This study therefore examined the neovascularization induced by ACE inhibitor treatment in B(2) receptor-deficient mice (B(2)(-/-)) in a model of surgically induced hindlimb ischemia. After artery femoral occlusion, wild-type and B(2)(-/-) mice were treated with or without ACE inhibitor (perindopril, 3 mg/kg/d) for 28 days. Angiogenesis was then quantitated by microangiography, capillary density measurement, and laser Doppler perfusion imaging. The protein levels of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) were determined by Western blot. In wild-type animals, vessel density and capillary number in the ischemic leg were raised by 1.8- and 1.4-fold, respectively, in mice treated with ACE inhibitor when compared with the nontreated animals (P<0.01). This corresponded to an improved ischemic/nonischemic leg perfusion ratio by 1.5-fold in ACE inhibitor-treated animals when compared with the untreated ones (0.87+/-0.07 versus 0.59+/-0.05, respectively, P<0.01). Activation of the angiogenic process was also associated with a 1.7-fold increase in tissue eNOS protein level in mice treated with ACE inhibitor (P<0.05 versus control) but not with changes in VEGF protein level. Conversely, ACE inhibition did not affect vessel density, blood flow, and eNOS protein level in ischemic hindlimb of B(2)(-/-) mice. Therefore, proangiogenic effect of ACE inhibition is mediated by B(2)-receptor signaling and was associated with upregulation of eNOS content, independently of VEGF expression.

Increased contribution of L-arginine-nitric oxide pathway in aorta of mice lacking the gene for vimentin.

Experiments were designed to investigate endothelial function in the aorta of mice lacking the gene for the cytoskeleton protein vimentin (vim -/- ). Rings with and without endothelium from wild-type (vim +/+ ), heterozygous (vim +/- ), and homozygous (vim -/- ) mice were suspended in organ chambers to record of changes in isometric tension. During phenylephrine contraction, acetylcholine evoked comparable endothelium-dependent relaxations in the three groups. In the presence of Nomega-nitro-L-arginine, acetylcholine caused endothelium-dependent contractions, which were greater in vim -/- than in vim +/+ and vim +/- aortas. Indomethacin did not affect relaxation to acetylcholine in vim +/+ or in vim +/-, but it significantly increased the maximal response in vim -/- (67 +/- 7 vs. 102 +/- 4%). Response to acetylcholine in vim -/- aortas was not affected by cyclooxygenase type 2 inhibitor NS-398, the thromboxane receptor antagonist SQ-29,548, or superoxide dismutase. Relaxations to sodium nitroprusside were not different between vim +/+ and vim -/- mice and were not affected by cyclooxygenase inhibition. Cyclic guanosine monophosphate levels, which were increased to a comparable level by acetylcholine in vim +/+ and vim -/-, were augmented by indomethacin in vim -/- aortas but not in vim +/+ aortas. Expression of endothelial nitric oxide synthase was not different between vim +/+ and vim -/- preparations. These results suggest that despite comparable endothelium-dependent responses to acetylcholine, endothelial cells from vim -/- mice release a cyclooxygenase product that compensates the augmented contribution of nitric oxide.

[Mechanical and functional predictive factors for restenosis and arterial remodeling after experimental angioplasty]. / Facteurs prédictifs mécaniques et fonctionnels de la resténose et du remodelage artériel après angioplastie expérimentale.

Arterial remodelling plays an important part in post-angioplasty restenosis but the physiopathology of this process is not fully understood. Abundant collagen synthesis and endothelial dysfunction have been demonstrated after angioplasty, but their role in restenosis and remodelling has not been studied. The aim of this study was therefore to assess endothelial function and collagen with respect to the severity of restenosis and the type of arterial remodelling. Atherosclerosis was induced by an association of endothelial abrasion and a high cholesterol diet in the femoral arteries of 22 white New Zealand rabbits. Four weeks later, angioplasty was performed. The acetylcholine endothelium-dependant vasomotricity (expressed as % inhibition of contraction to phenylephrine), collagen and morphology were assessed 28 days after angioplasty. The change in acetylcholine endothelium-dependant vasomotricity was greater in severe restenosis (r = 0.61, p = 0.02). Endothelium-dependant relaxation was not significantly altered when remodelling was expansive and very abnormal when it was constrictive (35.5 +/- 13.0 vs 3.7 +/- 7.9%; p = 0.04). Restenosis was associated with an increase in collagen (r = 0.69, p = 0.004). The density of collagen was significantly higher in constrictive remodelling than in expansive remodelling (34.5 +/- 4.5 vs 18.2 +/- 4.7%; p = 0.03). Endothelial dysfunction and collagen accumulation are correlated with the severity of restenosis and with constrictive remodelling after angioplasty in an experimental model.