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1. In Vitro Assessment of the Neuroprotective Effects of Pomegranate (Punica granatum L.) Polyphenols Against Tau Phosphorylation, Neuroinflammation, and Oxidative Stress.

Author

Alami, Mehdi, Boumezough, Kaoutar, Zerif, Echarki, Zoubdane, Nada, Khalil, Abdelouahed, Bunt, Ton, Laurent, Benoit, Witkowski, Jacek M., Ramassamy, Charles, Boulbaroud, Samira, Fulop, Tamas, and Berrougui, Hicham

Abstract

Background: Oxidative stress and chronic inflammation, at both the systemic and the central level, are critical early events in atherosclerosis and Alzheimer's disease (AD). Purpose: To investigate the oxidative stress-, inflammation-, and Tau-phosphorylation-lowering effects of pomegranate polyphenols (PPs) (punicalagin, ellagic acid, peel, and aril extracts). Methods: We used flow cytometry to quantify the protein expression of proinflammatory cytokines (IL-1β) and anti-inflammatory mediators (IL-10) in THP-1 macrophages, as well as M1/M2 cell-specific marker (CD86 and CD163) expression in human microglia HMC3 cells. The IL-10 protein expression was also quantified in U373-MG human astrocytes. The effect of PPs on human amyloid beta 1-42 (Aβ1-42)-induced oxidative stress was assessed in the microglia by measuring ROS generation and lipid peroxidation, using 2′,7′-dichlorofluorescein diacetate (DCFH-DA) and thiobarbituric acid reactive substance (TBARS) tests, respectively. Neuronal viability and cell apoptotic response to Aβ1-42 toxicity were assayed using the MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) assay and the annexin-V-FITC apoptosis detection kit, respectively. Finally, flow cytometry analysis was also performed to evaluate the ability of PPs to modulate Aβ1-42-induced Tau-181 phosphorylation (pTau-181). Results: Our data indicate that PPs are significantly (p < 0.05) effective in countering Aβ1-42-induced inflammation through increasing the anti-inflammatory cytokines (IL-10) in U373-MG astrocytes and THP1 macrophages and decreasing proinflammatory marker (IL-1β) expression in THP1 macrophages. The PPs were also significantly (p < 0.05) effective in inducing the phenotypic transition of THP-1 macrophages and microglial cells from M1 to M2 by decreasing CD86 and increasing CD163 surface receptor expression. Moreover, our treatments have a significant (p < 0.05) beneficial impact on oxidative stress, illustrated in the reduction in TBARS and ROS generation. Our treatments have significant (p < 0.05) cell viability improvement capacities and anti-apoptotic effects on human H4 neurons. Furthermore, our results suggest that Aβ1-42 significantly (p < 0.05) increases pTau-181. This effect is significantly (p < 0.05) attenuated by arils, peels, and punicalagin and drastically reduced by the ellagic acid treatment. Conclusion: Overall, our results attribute to PPs anti-inflammatory, antioxidant, anti-apoptotic, and anti-Tau-pathology potential. Future studies should aim to extend our knowledge of the potential role of PPs in Aβ1-42-induced neurodegeneration, particularly concerning its association with the tauopathy involved in AD. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Genotype correlates with the natural history of severe bile salt export pump deficiency

Author

van Wessel, Daan B.E., Thompson, Richard J., Gonzales, Emmanuel, Jankowska, Irena, Sokal, Etienne, Grammatikopoulos, Tassos, Kadaristiana, Agustina, Jacquemin, Emmanuel, Spraul, Anne, Lipiński, Patryk, Czubkowski, Piotr, Rock, Nathalie, Shagrani, Mohammad, Broering, Dieter, Algoufi, Talal, Mazhar, Nejat, Nicastro, Emanuele, Kelly, Deirdre A., Nebbia, Gabriella, Arnell, Henrik, Björn Fischler, Hulscher, Jan B.F., Serranti, Daniele, Arikan, Cigdem, Polat, Esra, Debray, Dominique, Lacaille, Florence, Goncalves, Cristina, Hierro, Loreto, Muñoz Bartolo, Gema, Mozer-Glassberg, Yael, Azaz, Amer, Brecelj, Jernej, Dezsőfi, Antal, Calvo, Pier Luigi, Grabhorn, Enke, Sturm, Ekkehard, van der Woerd, Wendy J., Kamath, Binita M., Wang, Jian-She, Li, Liting, Durmaz, Özlem, Onal, Zerrin, Bunt, Ton M.G., Hansen, Bettina E., and Verkade, Henkjan J.

Published
2020
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3. Targeting Impaired Antimicrobial Immunity in the Brain for the Treatment of Alzheimer’s Disease

Author

Fulop,Tamas, Tripathi,Shreyansh, Rodrigues,Serafim, Desroches,Mathieu, Bunt,Ton, Eiser,Arnold, Bernier,Francois, Beauregard,Pascale B, Barron,Annelise E, Khalil,Abdelouahed, Plotka,Adam, Hirokawa,Katsuiku, Larbi,Anis, Bocti,Christian, Laurent,Benoit, Frost,Eric H, and Witkowski,Jacek M

Subjects
Neuropsychiatric Disease and Treatment
Abstract

Tamas Fulop,1 Shreyansh Tripathi,2,3 Serafim Rodrigues,3,4 Mathieu Desroches,5,6 Ton Bunt,7 Arnold Eiser,8 Francois Bernier,9 Pascale B Beauregard,10 Annelise E Barron,11 Abdelouahed Khalil,1 Adam Plotka,12 Katsuiku Hirokawa,13 Anis Larbi,14 Christian Bocti,15 Benoit Laurent,16 Eric H Frost,17 Jacek M Witkowski12 1Research Center on Aging, Geriatric Division, Department of Medicine, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada; 2Cluster Innovation Centre, North Campus, University of Delhi, Delhi, 110007, India; 3Ikerbasque, The Basque Foundation for Science, Bilbao, Spain; 4Mathematical Computational and Experimental Neuroscience (MCEN), BCAM - The Basque Center for Applied Mathematics, Bilbao, Spain; 5MathNeuro Team, Inria Sophia Antipolis Méditerranée, Sophia Antipolis, France; 6Department of Mathematics, Université Côte d’Azur, Nice, France; 7Izumi Biosciences, Inc., Lexington, MA, USA; 8Leonard Davis Institute, University of Pennsylvania, Drexel University College of Medicine, Philadelphia, PA, USA; 9Morinaga Milk Industry Co., Ltd, Next Generation Science Institute, Kanagawa, Japan; 10Department of Biology, Faculty of Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada; 11Department of Bioengineering, Stanford School of Medicine, Stanford, CA, USA; 12Department of Pathophysiology, Medical University of Gdansk, Gdansk, Poland; 13Institute of Health and Life Science, Tokyo Med. Dent. University, Tokyo and Nito-Memory Nakanosogo Hospital, Department of Pathology, Tokyo, Japan; 14Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Immunos Building, Biopolis, Singapore, Singapore; 15Research Center on Aging, Department of Medicine, Division of Neurology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada; 16Research Center on Aging, Department of Biochemistry and Functional Genomics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada; 17Department of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, CanadaCorrespondence: Tamas FulopResearch Center on Aging, Faculty of Medicine and Health Sciences, Université de Sherbrooke, 3001, 12th Avenue North, Sherbrooke, Quebec, J1H 5N4, CanadaTel +1 819 780 2220Fax +1 819 829 7141Email tamas.fulop@usherbrooke.caSerafim RodriguesIkerbasque Prof. Dr., Ikerbasque, The Basque Foundation for Science Bilbao, Spain and BCAM - The Basque Center for Applied Mathematics, Mathematical, Computational and Experimental (MCEN) Research Group, Alameda de Mazarredo 14, Bilbao, Bizkaia, Basque-Country, 48009, SpainTel +34 946 567 842Email srodrigues@bcamath.orgAbstract: Alzheimer’s disease (AD) is the most common form of dementia and aging is the most common risk factor for developing the disease. The etiology of AD is not known but AD may be considered as a clinical syndrome with multiple causal pathways contributing to it. The amyloid cascade hypothesis, claiming that excess production or reduced clearance of amyloid-beta (Aβ) and its aggregation into amyloid plaques, was accepted for a long time as the main cause of AD. However, many studies showed that Aβ is a frequent consequence of many challenges/pathologic processes occurring in the brain for decades. A key factor, sustained by experimental data, is that low-grade infection leading to production and deposition of Aβ, which has antimicrobial activity, precedes the development of clinically apparent AD. This infection is chronic, low grade, largely clinically silent for decades because of a nearly efficient antimicrobial immune response in the brain. A chronic inflammatory state is induced that results in neurodegeneration. Interventions that appear to prevent, retard or mitigate the development of AD also appear to modify the disease. In this review, we conceptualize further that the changes in the brain antimicrobial immune response during aging and especially in AD sufferers serve as a foundation that could lead to improved treatment strategies for preventing or decreasing the progression of AD in a disease-modifying treatment.Keywords: Alzheimer’s disease, mild cognitive impairment, neuroinflammation, antimicrobial immunity, brain, treatment

Published
2021

7. Factors influencing noncompliance and contamination in a randomized trial of 'Western' (r1) versus 'Japanese' (r2) type surgery in gastric cancer

Author

Bunt, Ton M.G., Bonenkamp, Han J., Hermans, Jo, Velde, Cornelis J.H. van de, Arends, Jan-Willem, Fleuren, Gertjan, and Bruijn, Jan A.

Subjects
Stomach cancer, Excision (Surgery) -- Methods, Lymph nodes, Health
Abstract

Background. A randomized trial was undertaken comparing the Western R1 resection with limited N1-level lymphadenectomy and the Japanese R2 resection with extended lymphadenectomy, including the N2-level for curative resection of gastric cancer patients. After 389 patients were entered in the trial, protocol deviations were observed that reduced the intended distinction between the two types of lymphadenectomy: noncompliance, i.e., no substantiation of lymphadenectomy by nodal yields at indicated stations, and contamination, i.e., extension of lymphadenectomy outside the allocated level of nodal clearance. Methods. To identify factors underlying these protocol deviations, the authors analyzed the influence of six patient-, tumor, and treatment-related characteristics on the magnitude of deviations per patient, and on the incidence of deviations per lymph node station. Results. Protocol deviations were influenced by the following station-specific factors: (1) the number of nodes per station; (2) the clarity of anatomical station definition; (3) the location of stations; (4) local conventions on the type of gastrectomy; and (5) technical features to allow complete en bloc dissection. Furthermore, nonspecific factors such as inadequate retrieval of nodes, incomplete dissection, and careful selection of clinically overt metastases outside the allocated level of nodal clearance were randomly distributed over stations, and they, too, contributed to the deviations. Conclusions. Based on the findings, the authors took additional steps to preserve the distinction between limited and extended lymphadenectomy and to improve the accuracy of nodal staging. These factors should be considered when standardization of both surgicopathologic trials and clinical protocols for the treatment of gastric cancer is pursued. Cancer 1994; 73:1544-51. Key words: randomized controlled trial, stomach neoplasms, quality control, lymph node excision, neoplasm staging.

Published
1994

10. Expression and Cellular Distribution of P-Glycoprotein and Breast Cancer Resistance Protein in Amyotrophic Lateral Sclerosis Patients.

Author

van Vliet, Erwin A, Iyer, Anand M, Mesarosova, Lucia, Çolakoglu, Hilal, Anink, Jasper J, van Tellingen, Olaf, Maragakis, Nicholas J, Shefner, Jeremy, Bunt, Ton, and Aronica, Eleonora

Abstract

For amyotrophic lateral sclerosis (ALS), achieving and maintaining effective drug levels in the brain is challenging due to the activity of ATP-binding cassette (ABC) transporters which efflux drugs that affect drug exposure and response in the brain. We investigated the expression and cellular distribution of the ABC transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) using immunohistochemistry in spinal cord (SC), motor cortex, and cerebellum from a large cohort of genetically well characterized ALS patients (n = 25) and controls (n = 14). The ALS group included 17 sporadic (sALS) and 8 familial (fALS) patients. Strong P-gp expression was observed in endothelial cells in both control and ALS specimens. Immunohistochemical analysis showed higher P-gp expression in reactive astroglial cells in both gray (ventral horn) and white matter of the SC, as well as in the motor cortex of all ALS patients, as compared with controls. BCRP expression was higher in glia in the SC and in blood vessels and glia in the motor cortex of ALS patients, as compared with controls. P-gp and BCRP immunoreactivity did not differ between sALS and fALS cases. The upregulation of both ABC transporters in the brain may explain multidrug resistance in ALS patients and has implications for the use of both approved and experimental therapeutics.

Published
2020
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11. Letter

Author

Walson, Philip D., primary and Bunt, Ton, additional

Published
1999
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13. Facilitation of primary coronary angioplasty by early start of a glycoprotein 2b/3a inhibitor: results of the ongoing tirofiban in myocardial infarction evaluation (On-TIME) trial.

Author

van't Hof, Arnoud W.J, Ernst, Nicolette, de Boer, Menko-Jan, de Winter, Rob, Boersma, Eric, Bunt, Ton, Petronio, Sonia, Marcel Gosselink, A.T, Jap, Walter, Hollak, Frans, Hoorntje, Jan C.A, Suryapranata, Harry, Dambrink, Jan-Henk E, and Zijlstra, Felix

Abstract

Aim Although primary angioplasty is effective despite additional transportation delay, improved patency before PCI might be obtained by starting pharmacological pre-treatment before transportation. [ABSTRACT FROM PUBLISHER]

Published
2004
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14. Genotype correlates with the natural history of severe bile salt export pump deficiency

Author

van Wessel, Daan B E, Thompson, Richard J, Gonzales, Emmanuel, Jankowska, Irena, Sokal, Etienne, Grammatikopoulos, Tassos, Kadaristiana, Agustina, Jacquemin, Emmanuel, Spraul, Anne, Lipiński, Patryk, Czubkowski, Piotr, Rock, Nathalie, Shagrani, Mohammad, Broering, Dieter, Algoufi, Talal, Mazhar, Nejat, Nicastro, Emanuele, Kelly, Deirdre A, Nebbia, Gabriella, Arnell, Henrik, Fischler, Björn, Hulscher, Jan B F, Serranti, Daniele, Arikan, Cigdem, Polat, Esra, Debray, Dominique, Lacaille, Florence, Goncalves, Cristina, Hierro, Loreto, Muñoz Bartolo, Gema, Mozer-Glassberg, Yael, Azaz, Amer, Brecelj, Jernej, Dezsőfi, Antal, Calvo, Pier Luigi, Grabhorn, Enke, Sturm, Ekkehard, van der Woerd, Wendy J, Kamath, Binita M, Wang, Jian-She, Li, Liting, Durmaz, Özlem, Onal, Zerrin, Bunt, Ton M G, Hansen, Bettina E, Verkade, Henkjan J, NAtural course and Prognosis of PFIC and Effect of biliary Diversion (NAPPED) consortium, Center for Liver, Digestive and Metabolic Diseases (CLDM), Lifestyle Medicine (LM), UCL - SSS/IREC/PEDI - Pôle de Pédiatrie, and UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique

Subjects
0301 basic medicine, Male, LIVER, Surgical biliary diversion, CHILDREN, Gastroenterology, Severity of Illness Index, PFIC2, Liver disease, 0302 clinical medicine, Genotype, ABCB11, ATP Binding Cassette Transporter, Subfamily B, Member 11, OUTCOMES, ddc:618, Bile acid, Liver Neoplasms, Prognosis, Biliary Tract Surgical Procedures, BSEP, Child, Preschool, Cohort, SURGICAL-MANAGEMENT, 030211 gastroenterology & hepatology, Female, EXPRESSION, Adult, medicine.medical_specialty, Carcinoma, Hepatocellular, medicine.drug_class, Natural history, Cholestasis, Intrahepatic, Time, Bile Acids and Salts, 03 medical and health sciences, TYPE-2, FAMILIAL INTRAHEPATIC CHOLESTASIS, Cholestasis, Predictive Value of Tests, Internal medicine, medicine, ABCB11 MUTATIONS, Humans, Genetic Testing, EXTERNAL BILIARY DIVERSION, Severe BSEP deficiency, Retrospective Studies, Hepatology, business.industry, Retrospective cohort study, medicine.disease, Bile Salt Export Pump, Survival Analysis, 030104 developmental biology, Mutation, business
Abstract

Background & Aims: Mutations in ABCB11 can cause deficiency of the bile salt export pump (BSEP), leading to cholestasis and end-stage liver disease. Owing to the rarity of the disease, the associations between genotype and natural history, or outcomes following surgical biliary diversion (SBD), remain elusive. We aimed to determine these associations by assembling the largest genetically defined cohort of patients with severe BSEP deficiency to date. Methods: This multicentre, retrospective cohort study included 264 patients with homozygous or compound heterozygous pathological ABCB11 mutations. Patients were categorized according to genotypic severity (BSEP1, BSEP2, BSEP3). The predicted residual BSEP transport function decreased with each category. Results: Genotype severity was strongly associated with native liver survival (NLS, BSEP1 median 20.4 years; BSEP2, 7.0 years; BSEP3, 3.5 years; p

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15. Facilitation of primary coronary angioplasty by early start of a glycoprotein 2b/3a inhibitor: results of the ongoing tirofiban in myocardial infarction evaluation (On-TIME) trial.

Author

van 't Hof AW, Ernst N, de Boer MJ, de Winter R, Boersma E, Bunt T, Petronio S, Marcel Gosselink AT, Jap W, Hollak F, Hoorntje JC, Suryapranata H, Dambrink JH, and Zijlstra F

Subjects
Aged, Double-Blind Method, Female, Follow-Up Studies, Humans, Male, Middle Aged, Time Factors, Tirofiban, Transportation of Patients, Treatment Outcome, Angioplasty, Balloon, Coronary methods, Fibrinolytic Agents therapeutic use, Myocardial Infarction drug therapy, Platelet Aggregation Inhibitors therapeutic use, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors, Tyrosine analogs & derivatives, Tyrosine therapeutic use
Abstract

Aim: Although primary angioplasty is effective despite additional transportation delay, improved patency before PCI might be obtained by starting pharmacological pre-treatment before transportation., Methods and Results: From June 2001 to November 2002, 507 patients with acute myocardial infarction, who were transferred to a PCI centre, were randomised to early, pre-hospital initiation of Tirofiban (Early) or to initiation in the catheterisation laboratory (Late). The primary end-point was TIMI flow grade 3 of the infarct-related vessel (IRV) at initial angiography, as assessed by an independent core-lab. The effect of Tirofiban on each TIMI flow component, the presence of thrombus at initial angiography and pre-PCI myocardial blush grade were secondary end-points. A large proportion of patients (41%) was diagnosed and randomised in the ambulance, without intervention of a physician. In the Early group, Tirofiban was administered a median of 59 min (range 11-178 min) earlier than in the Late group. At initial angiography, TIMI 3 flow was present in 19% the Early group and in 15% in the Late group (P = 0.22). The combined incidence of TIMI 2 or 3 flow was present in 43% in the Early group and in 34% in the Late group, respectively (P = 0.04). Thrombus or a fresh occlusion was present in 60% and 73% in the Early and Late group, respectively (P = 0.002). A pre-PCI myocardial blush grades 2 or 3 was more often present in the Early group (30% vs. 22%, P = 0.04). However, no difference in TIMI 3 flow or myocardial blush grade was found between the groups, post-PCI. At one-year follow-up, the combined incidence of death or recurrent MI was not different between the groups (7.0% vs. 7.0%, P = 0.99)., Conclusion: Early initiation of Tirofiban did not improve initial TIMI 3 flow of the IRV significantly. Despite a better patency (TIMI 2 or 3 flow), a lower prevalence of thrombus or fresh occlusion and a better myocardial perfusion in the infarct-related region pre-PCI, no beneficial effect on post-PCI angiographic or clinical outcome was found, as compared to initiation of Tirofiban in the catheterisation laboratory.

Published
2004
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