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Biomedical subjects

C Bruggeman

Publications and source records attributed to C Bruggeman.

At least 19 recordsLinked to original sources
PubMed2005

Selenite reduction in Boom clay: Effect of FeS(2), clay minerals and dissolved organic matter.

Several experiments were set up to study Se speciation and solubility in the reducing Boom clay environment, starting from oxidized Se species which were added in oversaturation with respect to the thermodynamic solubility of reduced Se solid phases. Upon introduction of SeO3(2-) to FeS(2)-containing samples, adsorption of SeO3(2-) occurred at the FeS2 surface, and led to a reduction and precipitation of a Se0 solid phase with a solubility of 3x10(-9) M (after 60 days). In the presence of humic substances, an association of Se with these humic substances was observed and the 3x10(-9) M solubility limit was not reached in the same time delay. Upon introduction of SeO3(2-) to Boom clay suspensions (equilibration up to 9 months), the initial adsorption of SeO3(2-) on the solid phase was increased with respect to systems containing only FeS2, due to the presence of (illite) clay minerals. This competing adsorption process, and the presence of humic substances, again decreased the kinetics of reduction with respect to FeS2 samples. Also, an association of Se with Boom clay humic substances was observed, and amounted up to approximately 10(-7) M in some samples after 9 months equilibration.

Aluminum Silicates↗
PubMed2004

Evidence for the interaction of technetium colloids with humic substances by X-ray absorption spectroscopy.

Spectroscopic extended X-ray absorption fine structure (EXAFS) evidence was obtained on the chemical environment of 99Tc(IV) atoms formed upon introduction of TcO4- into four types of laboratory-scale synthetic and natural systems which mimic in situ natural reducing conditions in humic-rich geochemical environments: (a) magnetite/pyrite in synthetic groundwater in the absence of humic substances (HSs), (b) magnetite/pyrite in natural Gorleben groundwater in the presence of HSs, (c) Boom clay sediment mixed with synthetic groundwater, and (d) Gorleben sand mixed with natural Gorleben groundwater. The investigated systems obey to pH 8-9 conditions, and all measured samples show similar EXAFS spectra for Tc, which could be fitted by a hydrated TcO2 x xH2O phase. The results are interpreted as follows: upon introduction of high concentrations (millimolar to micromolar) of TcO4-to chemically reducing environments, small Tc(IV) oxidic polymers are formed, which either may aggregate into larger units (colloids) and finally precipitate or may interact in their polymeric form with (dissolved and immobile) humic substances. This latter type of interaction--Tc(IV) colloid sorption onto HSs--differs significantly from the generally accepted metal--humate complexation and therefore offers new views on the possible reaction pathways of metals and radionuclides in humic-rich environments.

Aluminum Silicates↗
PubMed2003

Quantification of the interaction of Tc with dissolved boom clay humic substances.

Technetium-99 (Tc), a fission product of uranium-238, is an important radionuclide because of its long half-life and its high yield in radioactive waste. To elucidate the Tc geochemical behavior in reducing environments relevant to geological disposal and in the presence of humic substances (HS), experiments were set up that resulted forthe first time in the determination of an interaction constant for Tc with dissolved humic substances. A number of lab-scale Boom Clay (a possible geological underground High-Level Radioactive Waste storage site in Mol, Belgium) batch experiments were set up, combining both different initial Tc(VII) concentrations and different solid/liquid ratios. On these batches several sequential extraction steps with HS-free synthetic Boom Clay water were performed. Equilibration times were fixed at 1 week for each extraction step. Tc(VII) was found to be readily reduced to Tc(IV) by the solid Boom Clay phase. This solid phase was able to sorb Tc(IV) to a very large extent (log Kd approximately 2.5-4.0), and two sorption sinks (one of which is humic substances) were detected. In solution, Tc(IV) was mainly associated with HS. Concentrations in solution were found up to the order of 2 x 10(-6) M. The results were quantitatively described as a competition for Tc(IV) between the solid phase and the dissolved HS (Schubert-like approach). It was concluded that a hydrophobic sorption of uncharged Tc(IV) species in solution would act as the dominating interaction mechanism with HS, with an interaction constant log K(HS) = 5.3 +/- 0.3.

Adsorption↗
PubMed2000

Induction of vascular adhesion protein-1 during liver allograft rejection and concomitant cytomegalovirus infection in rats.

Vascular adhesion protein-1 (VAP-1) is an adhesion molecule controlling lymphocyte recirculation through high endothelial venules of the lymph nodes. It has also been shown to be induced and to mediate lymphocyte adhesion at sites of inflammation. We studied the expression of VAP-1 and two other inducible adhesion molecules ICAM-1 and VCAM-1 in our experimental model of rat liver allograft rejection and, in addition, the effect of concomitant rat cytomegalovirus (RCMV) infection on this expression. Expression of VAP-1, ICAM-1, and VCAM-1 was studied in rat liver allografts with or without RCMV infection, isografts, and normal rat liver. Immunoperoxidase technique and monoclonal antibodies including a novel anti-VAP-1 reagent were used. VAP-1 expression was induced by acute rejection in sinusoids, hepatocytes, and also in bile ducts, when compared to the isografts or normal liver, where only blood vessels were consistently positive. Sinusoidal and hepatocyte expression of VAP-1 was prolonged by the presence of RCMV. ICAM-1 and VCAM-1 expression was also induced by acute rejection. However, RCMV increased sinusoidal VCAM-1 expression compared to uninfected grafts. The present experimental study shows that VAP-1 is up-regulated in acute rejection of liver allografts, and that this up-regulation is prolonged by RCMV infection.

Acute Disease↗
PubMed1999

Antiviral and immunomodulatory effects of desferrioxamine in cytomegalovirus-infected rat liver allografts with rejection.

BACKGROUND: Cytomegalovirus (CMV) infection is associated with acute and chronic allograft rejection. We have recently shown that rat CMV increases portal inflammation and bile duct destruction in a model of rat liver allograft rejection. Desferrioxamine (DFO), an iron chelator and antioxidant, has recently been demonstrated to have antiviral as well as immunomodulatory effects in vitro. We therefore investigated whether DFO inhibits (a) CMV infection and (b) graft destruction in our rat model. METHOD: One day after liver transplantation, PVG (RT1c) into BN(RT1n), the rats were infected with rat CMV (RCMV, Maastricht strain; 10(5) plaque-forming units i.p.). The effects of 100 mg/kg body weight and 200 mg/kg body weight DFO were examined. RESULTS: In the untreated group, the grafts were uniformly RCMV culture-positive. In the group receiving 200 mg/kg DFO, RCMV replication was effectively inhibited. Inflammatory response in the graft, and especially the number of macrophages, was significantly reduced by DFO. Portal inflammation and bile duct destruction were also significantly reduced. In the untreated group, the bile duct epithelial cells were found to be strongly positive for tumor necrosis factor-alpha and this expression was clearly decreased by DFO. In addition, DFO significantly inhibited vascular cell adhesion molecule-1 expression on sinusoidal endothelial cells. CONCLUSIONS: Our in vivo transplant study strongly supports the inhibitory effects of metal chelators on CMV infection and their possible usefulness in the treatment of CMV-induced pathogenic changes.

Adjuvants, Immunologic↗
PubMed1999

Time-related effects of cytomegalovirus infection on the development of chronic renal allograft rejection in a rat model.

Cytomegalovirus (CMV) infection is a risk factor for chronic allograft rejection. The histological findings of chronic renal allograft rejection include inflammation, vascular intimal thickening, glomerulosclerosis, tubular atrophy and fibrosis. We have developed a rat model of renal transplantation in which transplants, after an early inflammatory episode, end up with chronic rejection within 60 days. During the early phase of the process in this model, CMV increased and prolonged the inflammatory response, the expression of adhesion molecules, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 and their ligands, lymphocyte function antigen-1 and very late antigen-4 in the graft. Simultaneously, the production of various growth factors, such as transforming growth factor beta, platelet-derived growth factor and connective tissue growth factor was upregulated, which induce smooth muscle cell proliferation in the vascular wall and collagen synthesis by fibroblasts. Chronic rejection developed within 20 days in CMV-infected grafts. In summary, CMV infection accelerated and enhanced the early immune response, the induction of growth factors and collagen synthesis, and the development of chronic rejection in renal allografts.

Animals↗
PubMed1998

Cytomegalovirus infection is associated with increased inflammation and severe bile duct damage in rat liver allografts.

It has been suggested that cytomegalovirus (CMV) infection is involved in allograft rejection. In liver transplantation, it has been suggested that CMV is associated with the development of vanishing bile duct syndrome (VBDS), and persistent CMV has been found in liver grafts that develop chronic rejection. In this experimental study, the effect of rat CMV (RCMV) infection on intragraft changes was investigated in a rat model of acute liver allograft rejection. Liver transplantations were performed in a rat strain combination of PVG (RT1c) --> BN (RT1n). No immunosuppression was given. One group of animals was infected with RCMV Maastricht Strain (10(5) plaque-forming units, intraperitoneally), and another group was left uninfected. The grafts were examined histologically after the rats were killed on postoperative days 7 through 9 at the early phase and days 20 through 30 at the late phase of rejection. Immunohistochemical studies were performed to demonstrate the immunological activation markers major histocompatibility complex class II and interleukin 2 receptors, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and their ligands. RCMV infection was demonstrated from the grafts by culture and direct antigen detection. In liver allografts undergoing acute rejection, CMV significantly increased portal inflammation and caused more severe bile duct damage than in the uninfected grafts. CMV was also linked to the induction of VCAM-1 in the endothelial cells. The ongoing infection was found to vary over time in the different structures of the liver grafts, including the vascular endothelium and bile ducts. Our results support an association between CMV infection and the immunological mechanisms of rejection, as well as the role of CMV in the development of bile duct damage in liver allografts.

Animals↗
PubMed1997

Effect of cytomegalovirus on an experimental model of chronic renal allograft rejection under triple-drug treatment in the rat.

BACKGROUND: Cytomegalovirus (CMV) infection is thought to be a risk factor of chronic rejection. In clinical studies and animal models, mainly concerning graft vasculopathy, CMV has been demonstrated to enhance allograft arteriosclerosis. In this study we have investigated the effect of CMV on the early inflammatory response and graft histology in an experimental model of renal transplantation in a rat strain combination that develops chronic rejection under triple-drug immunosuppression. METHODS: Renal transplantations were performed in a rat strain combination of DA-->BN receiving triple-drug treatment (2 mg/kg methylprednisolone, 2 mg/kg azathioprine, 5 mg/kg cyclosporine daily subcutaneously). One group of immunosuppressed animals was infected with rat CMV, the Maastricht strain (10(5) plaque-forming units intraperitoneally), and the other group was left uninfected. As a positive control for alloresponse, one group of recipients received neither immunosuppression nor virus. Syngenic transplantations with triple-drug treatment and CMV were used as negative controls. The grafts were monitored by frequent ultrasound-guided fine-needle aspiration biopsies, and the intragraft inflammation was quantified in detail by the increment method and expressed in corrected increment units (CIU). Graft histology was performed in parallel. RESULTS: Nonimmunosuppressed animals developed acute rejection with a high peak of inflammation (7.9+/-3.2 CIU), a typical blast response, and lymphocytosis followed by infiltration of macrophages and necrosis within 7 days. Triple drug-treated animals had a short, mild inflammatory response (3.3+/-1.4 CIU at the peak) in the graft 3-5 days after transplantation but ended up with histological changes characteristic of chronic rejection with vasculopathy and fibrosis 40-60 days later. Triple drug-treated animals with CMV demonstrated a significantly stronger inflammation (4.5+/-1.8 CIU, P<0.01) than those without, and lymphoid activation continued longer and was followed by infiltration of macrophages in the graft. CMV infection of the graft was demonstrated by viral culture and antigen detection. In histology, chronic rejection with intimal thickening of arteries and arterioles and medial necrosis of large arteries was seen at 14 days, ending up with remarkable graft fibrosis within 20 days after transplantation. CONCLUSION: CMV prolonged and increased graft inflammation and accelerated chronic rejection of renal allografts under triple-drug treatment.

Animals↗
PubMed1997

Cytomegalovirus infection-enhanced cardiac allograft vasculopathy is abolished by DHPG prophylaxis in the rat.

BACKGROUND: A wealth of clinical and experimental evidence exists for cytomegalovirus (CMV) infection as an accelerating factor in the development of cardiac allograft vasculopathy. In this study, the impact of 9-(1,3-dihydroxy-2-propoxymethyl) guanine (DHPG) on rat CMV infection-enhanced cardiac allograft vasculopathy is investigated. METHODS AND RESULTS: Heterotopic rat cardiac allografts were performed from the DA to the WF rat strain, and the recipients were immunosuppressed with cyclosporine A 2 mg.kg-1.d-1 s.c. for a period of 90 days until the end of experiment. Two groups of recipients were infected intraperitoneally with 10(5) plaque-forming units of rat CMV, whereas one group was left noninfected and used as controls. One group of rat CMV-infected rats was treated with DHPG with an initial dose of 20 mg/kg i.p. and a maintenance dose of 10 mg/kg i.p. twice a day from 1 day before transplantation to 30 days after transplantation. Compared with noninfected rats, rat CMV infection was associated with a significant increase in intimal thickening, from 0.68 +/- 0.10 to 1.30 +/- 0.12 score units (P < .01), and double the number of vessels affected (P < .01). DHPG treatment significantly reduced intimal thickening in rat CMV-infected rats, from 1.30 +/- 0.12 to 0.68 +/- 0.13 score units (P < .01), and halved the number of vessels affected (P < .01). CONCLUSIONS: The present results demonstrate that DHPG prophylaxis entirely abolishes the accelerating effect of rat CMV infection on cardiac allograft vasculopathy in immunosuppressed rat recipients, which is consistent with our earlier findings demonstrating a similar effect in nonimmunosuppressed rat aortic allografts. Taken together, these results suggest that DHPG might be useful in the prevention of CMV-accelerated cardiac allograft vasculopathy among heart transplant recipients.

Animals↗
PubMed1996

Cytomegalovirus infection accelerates obliterative bronchiolitis of rat tracheal allografts.

A cascade of inflammation and injury of the airway wall followed by a fibroproliferative process that results in airway obstruction has been suggested as the explanation of the process of obliterative bronchiolitis (OB) in lung allograft recipients. To determine the impact of rat cytomegalovirus (RCMV) infection on the development of OB, heterotopic rat tracheal allografts were transplanted from DA donors to WF recipients immunosuppressed with 2 mg/kg per day cyclosporine A. Chronic RCMV infection was similarly established 8 weeks before transplantation in donors alone (D+/R-), recipients alone (D-/R+), and both donors and recipients (D+/R+). The control rats were left non-infected, but were similarly immunosuppressed. The results of this study demonstrate that both acute and chronic recipient RCMV infection, but not donor infection, amplify the development of experimental OB in the rat and suggest that RCMV infection-associated immune response, rather than the viral load in the graft, is essential for the development of the accelerated form of OB.

Animals↗
PubMed1995

Cytomegalovirus antigen expression, endothelial cell proliferation, and intimal thickening in rat cardiac allografts after cytomegalovirus infection.

BACKGROUND: Cardiac allograft arteriosclerosis is the primary cause of late death in heart transplant recipients. Clinical studies have suggested that humoral and cellular immune response, hyperlipidemia, and cytomegalovirus (CMV) infection may amplify the disease. In this study, the role of CMV infection in the development of rat cardiac allograft arteriosclerosis is investigated. METHODS AND RESULTS: Heterotopic rat cardiac allografts were performed from the DA to the WF rat strains. To prevent rejection, the recipients received triple-drug (cyclosporine A 20 mg.kg-1.d-1, azathioprine 2 mg.kg-1.d-1, and methylprednisolone 0.5 mg.kg-1.d-1) immunosuppression postoperatively. Recipient rats were infected intraperitoneally (n = 21) with 10(5) plaque-forming units of rat CMV (RCMV) 1 day after transplantation or were left uninfected and used as controls (n = 18). The grafts were removed 7 and 14 days and 1 and 3 months after transplantation. In 42% (9 of 21) of cardiac allografts in RCMV-infected rats, an intramural, mononuclear cell inflammation of small intramyocardial arterioles was observed compared with none in uninfected rats (P = .005). Acute RCMV infection was associated with an early perivascular inflammatory cell response of helper T (W3/25), cytotoxic T (OX8), and NK (3.2.3) cells, macrophages (OX42), and major histocompatibility complex class II expression around small intramyocardial arterioles and capillaries. No upregulation of interleukin-2 receptor expression was seen. In arteries and small intramyocardial arterioles, RCMV infection was associated with a significant endothelial cell proliferation and a clear increase in intimal thickening. Significant endothelial cell proliferation was also observed in the capillaries after RCMV infection. Immunohistochemistry revealed specific focal RCMV early and late antigen expression in epicardial and interstitial ED1-immunoreactive mononuclear cell infiltrates and around small arterioles of RCMV-infected cardiac allografts. Occasionally, media cells of stenosed small intramyocardial arterioles also showed strong focal RCMV antigen expression. In addition, infectious RCMV could be recovered by plaque assay in cardiac allografts expressing RCMV antigens. CONCLUSIONS: These results demonstrate a productive RCMV infection in cardiac allograft structures and suggest that RCMV infection accelerates cardiac allograft arteriosclerosis, particularly in small intramyocardial arterioles mediated by inflammatory responses in the vascular wall and perivascular space.

Animals↗