Pierre Drion

University of Liège, Luik, Walloon, Belgium

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Publications (35)110.14 Total impact

  • International journal of cardiology 06/2015; 197:72-75. DOI:10.1016/j.ijcard.2015.06.035 · 6.18 Impact Factor
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    ABSTRACT: Les propriétés « réparatrices » des plaquettes, par la libération locale de facteurs de croissance, sont employées dans divers domaines médicaux. Cet article passe en revue les études fondamentales et cliniques relatives au plasma riche en plaquettes (PRP) appliqué aux lésions tendineuses.
    Journal de Réadaptation Médicale Pratique et Formation en Médecine Physique et de Réadaptation 04/2015; DOI:10.1016/j.jrm.2015.03.004
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    ABSTRACT: BACKGROUND: A limitation of current antiplatelet therapies is their inability to separate thrombotic events from bleeding occurrences. A better understanding of the molecular mechanisms leading to platelet activation is important for the development of improved therapies. Recently, protein tyrosine phosphatases have emerged as critical regulators of platelet function. METHODS AND RESULTS: This is the first report implicating the dual-specificity phosphatase 3 (DUSP3) in platelet signaling and thrombosis. This phosphatase is highly expressed in human and mouse platelets. Platelets from DUSP3-deficient mice displayed a selective impairment of aggregation and granule secretion mediated by the collagen receptor glycoprotein VI and the C-type lectin-like receptor 2. DUSP3-deficient mice were more resistant to collagen- and epinephrine-induced thromboembolism compared with wild-type mice and showed severely impaired thrombus formation on ferric chloride-induced carotid artery injury. Intriguingly, bleeding times were not altered in DUSP3-deficient mice. At the molecular level, DUSP3 deficiency impaired Syk tyrosine phosphorylation, subsequently reducing phosphorylation of phospholipase Cγ2 and calcium fluxes. To investigate DUSP3 function in human platelets, a novel small-molecule inhibitor of DUSP3 was developed. This compound specifically inhibited collagen- and C-type lectin-like receptor 2-induced human platelet aggregation, thereby phenocopying the effect of DUSP3 deficiency in murine cells. CONCLUSIONS: DUSP3 plays a selective and essential role in collagen- and C-type lectin-like receptor 2-mediated platelet activation and thrombus formation in vivo. Inhibition of DUSP3 may prove therapeutic for arterial thrombosis. This is the first time a protein tyrosine phosphatase, implicated in platelet signaling, has been targeted with a small-molecule drug.
    Circulation 02/2015; 131(7):656-68. DOI:10.1161/CIRCULATIONAHA.114.010186 · 14.95 Impact Factor
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    ABSTRACT: Multiple myeloma (MM) is a malignant plasma cell disorder with poor long-term survival and high recurrence rates. Despite evidence of graft-versus-myeloma (GvM) effects, the use of allogeneic hematopoietic stem cell transplantation (allo-SCT) remains controversial in MM. In the current study, we investigated the anti-myeloma effects of allo-SCT from B10.D2 mice into MHC-matched myeloma-bearing Balb/cJ mice, with concomitant development of chronic graft-versus-host disease (GvHD). Balb/cJ mice were injected intravenously with luciferase-transfected MOPC315.BM cells, and received an allogeneic (B10.D2 donor) or autologous (Balb/cJ donor) transplant 30 days later. We observed a GvM effect in 94% of the allogeneic transplanted mice, as the luciferase signal completely disappeared after transplantation, whereas all the autologous transplanted mice showed myeloma progression. Lower serum paraprotein levels and lower myeloma infiltration in bone marrow and spleen in the allogeneic setting confirmed the observed GvM effect. In addition, the treated mice also displayed chronic GvHD symptoms. In vivo and in vitro data suggested the involvement of effector memory CD4 and CD8 T cells associated with the GvM response. The essential role of CD8 T cells was demonstrated in vivo where CD8 T-cell depletion of the graft resulted in reduced GvM effects. Finally, TCR Vβ spectratyping analysis identified Vβ families within CD4 and CD8 T cells, which were associated with both GvM effects and GvHD, whereas other Vβ families within CD4 T cells were associated exclusively with either GvM or GvHD responses. We successfully established an immunocompetent murine model of graft-versus-myeloma. This is the first murine GvM model using immunocompetent mice that develop MM which closely resembles human MM disease and that are treated after disease establishment with an allo-SCT. Importantly, using TCR Vβ spectratyping, we also demonstrated the presence of GvM unique responses potentially associated with the curative capacity of this immunotherapeutic approach.
    PLoS ONE 11/2014; 9(11):e113764. DOI:10.1371/journal.pone.0113764 · 3.53 Impact Factor
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    ABSTRACT: Abdominal aortic aneurysm (AAA) is a complex multifactorial disease with genetic and environmental components. AAA is more common in males, whereas women have a greater risk of rupture and more frequently have concomitant thoracic aortic aneurysms. Moreover, women are diagnosed with AAA about 10 years later and seem to be protected by female sex hormones. In this MEDLINE-based review of literature we examined human and animal, in vivo and in vitro studies, to further deepen our understanding of the sexual dimorphism of AAA. We focus on the role of sex hormones during the formation and growth of AAA. Endogenous estrogens and exogenous 17β-estradiol were found to exert favorable actions protecting from AAA in animal models, whereas exogenous hormone replacement therapy in humans had inconclusive results. Androgens, known to have detrimental effects in the vasculature, in sufficient levels maintain the integrity of the aortic wall through their anabolic actions and act differentially in males and females, whereas lower levels of testosterone have been associated with AAA in humans. In conclusion, sex differences remain an important area of AAA research, but further studies especially in humans are needed. Furthermore, differential molecular mechanisms of sex hormones constitute a potential therapeutic target for AAA.
    Annals of Vascular Surgery 08/2014; 28(8). DOI:10.1016/j.avsg.2014.07.008 · 1.03 Impact Factor
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    ABSTRACT: BackgroundDUSP3 phosphatase, also known as V accinia-H1 Related (VHR) phosphatase, encoded by DUSP3/Dusp3 gene, is a relatively small member of the dual-specificity protein phosphatases. In vitro studies showed that DUSP3 is a negative regulator of ERK and JNK pathways in several cell lines. On the other hand, DUSP3 is implicated in human cancer. It has been alternatively described as having tumor suppressive and oncogenic properties. Thus, the available data suggest that DUSP3 plays complex and contradictory roles in tumorigenesis that could be cell type-dependent. Since most of these studies were performed using recombinant proteins or in cell-transfection based assays, the physiological function of DUSP3 has remained elusive.ResultsUsing immunohistochemistry on human cervical sections, we observed a strong expression of DUSP3 in endothelial cells (EC) suggesting a contribution for this phosphatase to EC functions. DUSP3 downregulation, using RNA interference, in human EC reduced significantly in vitro tube formation on Matrigel and spheroid angiogenic sprouting. However, this defect was not associated with an altered phosphorylation of the documented in vitro DUSP3 substrates, ERK1/2, JNK1/2 and EGFR but was associated with an increased PKC phosphorylation. To investigate the physiological function of DUSP3, we generated Dusp3-deficient mice by homologous recombination. The obtained DUSP3−/− mice were healthy, fertile, with no spontaneous phenotype and no vascular defect. However, DUSP3 deficiency prevented neo-vascularization of transplanted b-FGF containing Matrigel and LLC xenograft tumors as evidenced by hemoglobin (Hb) and FITC-dextran quantifications. Furthermore, we found that DUSP3 is required for b-FGF-induced microvessel outgrowth in the aortic ring assay.ConclusionsAll together, our data identify DUSP3 as a new important player in angiogenesis.
    Molecular Cancer 05/2014; 13(1):108. DOI:10.1186/1476-4598-13-108 · 5.40 Impact Factor
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    ABSTRACT: Objective To assess the potential protective effects of three polyphenols oleuropein, rutin and curcumin, on joint ageing and osteoarthritis development. Design Sixty 4-week-old Dunkin-Hartley guinea pigs were randomized into four groups and received daily during 31 weeks either standard guinea pig diet (control group) or a standard guinea pig diet enriched with oleuropein (0.025 %), rutin (0.5%) or rutin/curcumin (0.5%/0.25%) association. Biomarkers of osteoarthritis (Coll2-1, Coll2-1NO2, Fib3-1, Fib3-2, ARGS), as well as inflammation (PGE2) were quantified in the serum. Histological assessments of knee cartilage and synovial membrane were performed at week 4 (5 young reference guinea pigs) and week 35. Results At week 35, guinea pigs in the control group spontaneously developed significant cartilage lesions with mild synovial inflammation. The histological scores of cartilage lesions and synovitis were well correlated with the increased level of serum biomarkers. Histologically, all treatments significantly reduced the cartilage degradation score (p<0.01), but only oleuropein significantly decreased the synovial histological score (p<0.05) and serum PGE2 levels (p<0.01) compared to the control group. Coll2-1 was decreased by rutin and the combination of rutin/curcumin, Fib3-1 and Fib3-2 were only decreased by the rutin/curcumin mixture, while Coll2-1NO2 was significantly decreased by all treatments (p<0.05). Conclusion Oleuropein and rutin +/- curcumin significantly slowed down the progression of spontaneous OA lesions in guinea pigs. While no additive effect was seen in the curcumin+rutin group, the differential effects of oleuropein and rutin on inflammatory and cartilage catabolic markers suggest an interesting combination for future studies in OA protection.
    Osteoarthritis and Cartilage 04/2014; 23(1). DOI:10.1016/j.joca.2014.08.016 · 4.66 Impact Factor
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    ABSTRACT: Even if eccentric exercises appear favourable in primary prevention of tendons lesions and, especially, in secondary prevention after tendinopathy, the biomechanical changes to the tissue are not yet clear. We aimed to better define the biomechanical changes that affect healthy tendon after eccentric and concentric training. Randomised controlled trial. Animal study. 18 Sprague-Dawley rats of 2 months. The 6 rats in the control group (U) were not subjected to physical exercise. The 12 remaining rats (6 in each group) ran on a treadmill set at a +15° incline for concentric training (C) or a -15° incline for eccentric training (E), at a speed of 17 m/min for 1 h, three times per week for 5 weeks. The tricipital, patellar and Achilles tendons were subsequently removed to perform a traction test until rupture, and a histological analysis was performed. There was a significant improvement in the rupture force of the patellar and tricipital tendons between the U and E groups. The tricipital tendons in the control group presented a significantly smaller cross-section than the E- and C-trained groups, but none between E and C groups. No significant difference was observed for the mechanical stress at rupture per surface unit between the three groups for all three tendons. However, a tendency towards improvement these values was observed between the trained and the U groups for the patellar tendon. Histological studies demonstrated the tendency of the development of a greater number of blood vessels and a larger quantity of collagen in the eccentric group. The mechanical properties of tendons in rats improve after specific training, especially following eccentric training. Our results partly explained how mechanical loading, especially in eccentric mode, could improve the tendon structure and perhaps prevent to tendon pathologies.
    British Journal of Sports Medicine 04/2014; 48(7):617. DOI:10.1136/bjsports-2014-093494.155 · 5.03 Impact Factor
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    ABSTRACT: Tendon lesions are among the most frequent musculoskeletal pathologies. Vascular endothelial growth factor (VEGF) is known to regulate angiogenesis. VEGF-111, a biologically active and proteolysis-resistant splice variant of this family, was recently identified. This study aimed at evaluating whether VEGF-111 could have a therapeutic interest in tendon pathologies. Surgical section of one Achilles tendon of rats was performed before a local injection of either saline or VEGF-111. After 5, 15 and 30 days, the Achilles tendons of 10 rats of both groups were sampled and submitted to a biomechanical tensile test. The force necessary to induce tendon rupture was greater for tendons of the VEGF-111 group (p<0.05) while the section areas of the tendons were similar. The mechanical stress was similar at 5 and 15 days in the both groups but was improved for the VEGF-111 group at day 30 (p <0.001). No difference was observed in the mRNA expression of collagen III, tenomodulin and MMP-9. In conclusion, we observed that a local injection of VEGF-111 improves the early phases of the healing process of rat tendons after a surgical section. Further confirmatory experimentations are needed to consolidate our results.
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    ABSTRACT: Platelets contain growth factors released during their degranulation following activation. These growth factors promote tissue remodeling, wound healing and angiogenesis. Currently, the clinical effect of Platelet-Rich Plasma (PRP) is still discussed, or even controversial. Our researches have assessed the effectiveness of PRP on the healing of animal tendons and human beings suffering from chronic jumper's knee.
    Revue médicale de Liège 01/2014; 69 Spec No:72-7.
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    ABSTRACT: The positive effect of leukocyte- and platelet-rich fibrin (L-PRF) on osteogenesis has been widely described in vitro. However, clinical and preclinical studies are very little and controversial in demonstrating a significant beneficial effect of L-PRF in bone regeneration. The goal of the present study was to compare the potential effect of L-PRF in a standardized model. A total of 72 hemispheres were implanted on the calvaria of 18 rabbits and filled with three different space fillers: L-PRF, bovine hydroxyapatite (BHA), BHA + L-PRF, and an empty hemisphere was used as control. Six rabbits were sacrificed at three distinct time points: 1 week, 5 weeks, and 12 weeks. Histological and histomorphometrical analyses were carried out. At the early phase of bone regeneration (1 week), from a descriptive analysis, a higher proportion of connective tissue colonized the regeneration chamber in the two groups containing BHA particles. Nevertheless, no statistical differences were found within the four groups in terms of bone quantity and quality at each timepoint (p = .3623). According to the present study, L-PRF does not seem to provide any additional effect on the kinetics, quality, and quantity of bone in the present model of guided bone regeneration.
    Clinical Implant Dentistry and Related Research 09/2013; 17. DOI:10.1111/cid.12146 · 2.80 Impact Factor
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    ABSTRACT: ABSTRACT Background: No systemic preventive therapy has been successful in inhibiting the development of postoperative peritoneal adhesions (PPAs). Objective: The aim of this study was to evaluate the potential effects of 5 day administration of parecoxib, on PPA prevention and on suture or wound healing in rats. Methods: In a model of PPAs induced by peritoneal electrical burn, 30 rats were randomized into 3 groups according to parecoxib administration route (control; intraperitoneal (IP); intramuscular (IM)). Plasma and peritoneal levels of PAI-1 and tPA were measured at T0, after 90 min of surgery (T90), and on postoperative day 10 (D10). In a cecum resection model, 20 rats were randomized into two groups (control and IP parecoxib), and abdominal wound healing and suture leakage were assessed at D10. In both models, PPAs were evaluated quantitatively and qualitatively on D10. Results: Administration of parecoxib significantly decreased the quantity (p < .05) and the severity (p < .01) of PPAs in both models. In addition, parecoxib administration did not cause healing defects or infectious complications in the two models. In the peritoneal burn model, IP or IM parecoxib administration inhibited the increase of postoperative plasma and peritoneum PAI-1 levels, an increase that was observed in the control group (p < .01). No anastomosis leakage could be demonstrated in both groups in the cecum resection model. Conclusion: This study showed that, in these rat models, parecoxib might reduce PPA formation. Confirmation of the safety of parecoxib on intestinal anastomoses is required and should be investigated in further animal models.
    Journal of Investigative Surgery 08/2013; DOI:10.3109/08941939.2013.810316 · 1.19 Impact Factor
  • Veterinary Anaesthesia and Analgesia 07/2013; 40(6). DOI:10.1111/vaa.12071 · 1.78 Impact Factor
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    ABSTRACT: BACKGROUND: We investigated the ability of clinical-grade enriched human regulatory T cells (Treg) to attenuate experimental xenogeneic graft-versus-host disease (GVHD) induced by peripheral blood mononuclear cells (PBMNCs; autologous to Treg) infusion in NSG mice, as well as verified their inability to induce xenogeneic GVHD when infused alone. STUDY DESIGN AND METHODS: Human Treg were isolated from peripheral blood apheresis products with a cell separation system (CliniMACS, Miltenyi Biotec GmbH) using a two-step procedure (simultaneous CD8 and CD19 depletion followed by CD25-positive selection) in six independent experiments with six different healthy volunteer donors. Sublethally (2.5 Gy) irradiated NSG mice were given 2 × 10(6) cytapheresis (PBMNC) product cells intravenously (IV) without (PBMNC group) or with 1 × 10(6) Treg (PBMNC + Treg group), while other NSG mice received 2 × 10(6) enriched Treg alone (also in IV; Treg group). RESULTS: The first five procedures were successful at obtaining a relatively pure Treg population (defined as >50%), while the sixth procedure, due to a technical problem, was not (Treg purity, 42%). Treg cotransfusion significantly delayed death from xenogeneic GVHD in the first five experiments, (p < 0.0001) but not in the sixth experiment. Importantly, none of the mice given enriched Treg alone (Treg group) experienced clinical signs of GVHD, while, interestingly, the CD4+ cells found in these mice 26 days after transplantation were mainly conventional T cells (median CD25+FoxP3+ cells among human CD4+ total cells were only 2.1, 3.1, and 12.2% in spleen, marrow, and blood, respectively). CONCLUSIONS: Infusion of clinical-grade enriched Treg delayed the occurrence of xenogeneic GVHD without inducing toxicity in this murine model.
    Transfusion 06/2013; 54(2). DOI:10.1111/trf.12279 · 3.57 Impact Factor
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    ABSTRACT: Transmission is a matter of life or death for pathogen lineages and can therefore be considered as the main motor of their evolution. Gammaherpesviruses are archetypal pathogenic persistent viruses which have evolved to be transmitted in presence of specific immune response. Identifying their mode of transmission and their mechanisms of immune evasion is therefore essential to develop prophylactic and therapeutic strategies against these infections. As the known human gammaherpesviruses, Epstein-Barr virus and Kaposi's Sarcoma-associated Herpesvirus are host-specific and lack a convenient in vivo infection model; related animal gammaherpesviruses, such as murine gammaherpesvirus-68 (MHV-68), are commonly used as general models of gammaherpesvirus infections in vivo. To date, it has however never been possible to monitor viral excretion or virus transmission of MHV-68 in laboratory mice population. In this study, we have used MHV-68 associated with global luciferase imaging to investigate potential excretion sites of this virus in laboratory mice. This allowed us to identify a genital excretion site of MHV-68 following intranasal infection and latency establishment in female mice. This excretion occurred at the external border of the vagina and was dependent on the presence of estrogens. However, MHV-68 vaginal excretion was not associated with vertical transmission to the litter or with horizontal transmission to female mice. In contrast, we observed efficient virus transmission to naïve males after sexual contact. In vivo imaging allowed us to show that MHV-68 firstly replicated in penis epithelium and corpus cavernosum before spreading to draining lymph nodes and spleen. All together, those results revealed the first experimental transmission model for MHV-68 in laboratory mice. In the future, this model could help us to better understand the biology of gammaherpesviruses and could also allow the development of strategies that could prevent the spread of these viruses in natural populations.
    PLoS Pathogens 04/2013; 9(4):e1003292. DOI:10.1371/journal.ppat.1003292 · 8.06 Impact Factor
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    ABSTRACT: The treatment of choice for tendinopathies is eccentric reeducation. Although the clinical results appear favorable, the biomechanical changes to the tissue are not yet clear. Even if the mechanotransduction theory is commonly accepted, the physiology of tendons is not clearly understood. We aimed to better define the biomechanical and histological changes that affect healthy tendon after eccentric and concentric training. This study compared the effects of two methods of training (eccentric [E] training and concentric [C] training) with untrained (U) rats. The animals were trained over a period of 5 weeks. The tricipital, patellar, and Achilles tendons were removed, measured and a tensile test until failure was performed. A histological analysis (hematoxylin and eosin and Masson's trichrome stains) was also realized. There was a significant increase in the rupture force of the patellar and tricipital tendons between the U and E groups. The tricipital tendons in the control group presented a significantly smaller cross-sectional area than the E- and C-trained groups, but none was constated between E and C groups. No significant difference was observed for the mechanical stress between the three groups for all three tendons. Histological studies demonstrated the development of a greater number of blood vessels and a larger quantity of collagen in the E group. The mechanical properties of tendons in rats improve after specific training, especially following eccentric training. Our results partly explained how mechanical loading, especially in eccentric mode, could improve the healing of tendon. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.
    Journal of Orthopaedic Research 01/2013; 31(1). DOI:10.1002/jor.22202 · 2.97 Impact Factor
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    ABSTRACT: Platelet-rich plasma (PRP) contains growth factors involved in the tissular healing process. The aim of the study was to determine if an injection of PRP could improve the healing of sectioned Achilles tendons of rats. After surgery, rats received an injection of PRP (n = 60) or a physiological solution (n = 60) in situ. After 5, 15, and 30 days, 20 rats of both groups were euthanized and 15 collected tendons were submitted to a biomechanical test using cryo-jaws before performing transcriptomic analyses. Histological and biochemical analyses were performed on the five remaining tendons in each group. Tendons in the PRP group were more resistant to rupture at 15 and 30 days. The mechanical stress was significantly increased in tendons of the PRP group at day 30. Histological analysis showed a precocious deposition of fibrillar collagen at day 5 confirmed by a biochemical measurement. The expression of tenomodulin was significantly higher at day 5. The messenger RNA levels of type III collagen, matrix metalloproteinases 2, 3, and 9, were similar in the two groups at all time points, whereas type I collagen was significantly increased at day 30 in the PRP group. In conclusion, an injection of PRP in sectioned rat Achilles tendon influences the early phase of tendon healing and results in an ultimately stronger mechanical resistance.
    Wound Repair and Regeneration 08/2012; 20(5):748-56. DOI:10.1111/j.1524-475X.2012.00826.x · 2.77 Impact Factor
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    ABSTRACT: Abstract Background: Adhesion formation is common after abdominal surgery. The incidence and severity of adhesion formation following open or laparoscopic surgery remain controversial. The role of CO(2) pneumoperitoneum is also widely discussed. This study aimed to compare adhesion formation following peritoneal injury by electrocoagulation performed through open or laparoscopic procedures in a rat model. Materials and Methods: Sixty male rats were randomized to undergo a 1.5-cm peritoneal injury with unipolar cautery under general anesthesia: open surgery (Group A, n=20), laparoscopic surgery with CO(2) pneumoperitoneum (Group B, n=20), and laparoscopic surgery with air pneumoperitoneum (Group C, n=20). Duration of the procedures was fixed at 90 minutes in all groups, and pneumoperitoneum pressure was kept at 10 mm Hg. Ten days later, the animals underwent a secondary laparotomy to score peritoneal adhesions using qualitative and quantitative parameters. Results: Forty-five rats developed at least one adhesion: 95% in Group A, 83% in Group B, and 55% in Group C (P<.01; Group C versus Group A, P<.01). According to number, thickness, tenacity, vascularization, extent, type, and grading according to the Zühkle classification, no significant difference was observed between Groups A and B. The distribution of adhesions after open surgery was significantly different than after laparoscopic surgery (P<.001). It is interesting that Group C rats developed significantly fewer adhesions at the traumatized site, and their adhesions had less severe qualitative scores compared with those after open surgery (P<.01). Conclusions: In this animal model, CO(2) laparoscopic surgery did not decrease the formation of postoperative adhesion, compared with open surgery. The difference with the animals operated on with air pneumoperitoneum emphasizes the role of CO(2) in peritoneal injury leading to adhesion formation.
    Journal of Laparoendoscopic & Advanced Surgical Techniques 06/2012; 22(7):651-7. DOI:10.1089/lap.2012.0102 · 1.19 Impact Factor
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    ABSTRACT: BACKGROUND: There is a need for better animal models of fulminant liver failure (FHF). Eguchi et al described an interesting surgical model of FHF in the rat. This model includes 68% partial hepatectomy, ischemia of 24% of the liver mass, and 8% of remnant liver left intact. In the original description by Eguchi et al, rats were administered subcutaneous glucose. However, the authors found that normothermic FHF rats with subcutaneous glucose died from deep hypoglycemia. In this report, we describe a modification of that model, and show that administration of intravenous glucose allows better survival and development of intracranial hypertension. METHODS: We operated on FHF rats using the procedure described by Eguchi et al, kept them normothermic, and maintained normoglycemia by continuous intravenous glucose injection (glucose 10%, 1 mL/h). At 24 h, we monitored liver blood tests (n = 5), intracranial pressure (n = 5), clinical encephalopathy, and survival (n = 10), and compared them with sham and 68% hepatectomy rats. RESULTS: The FHF rats developed acute cytolysis, cholestasis, and liver failure, as demonstrated by the liver blood tests. They experienced progressive encephalopathy and intracranial hypertension leading to death. Mean survival was 45.9 h. Of 10 FHF rats from the survival evaluation cohort, one survived 7 d. Laparotomy showed necrosis of lateral liver lobes and enlargement of omental lobes with a normal hepatic aspect, suggesting liver recovery. CONCLUSIONS: This surgical rat model mimics the features of human FHF and seems interesting for further research into the pathophysiology and therapeutic management of the disease.
    Journal of Surgical Research 06/2012; 181(1). DOI:10.1016/j.jss.2012.05.080 · 2.12 Impact Factor

Publication Stats

158 Citations
110.14 Total Impact Points

Institutions

  • 2005–2015
    • University of Liège
      • • Laboratory of Connective Tissues Biology
      • • Department of Pathology
      • • Department of Infectious and Parasite Diseases
      • • Faculty of Medicine
      • • Hemodynamics Research Laboratory (HemoLiege)
      Luik, Walloon, Belgium