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Daniel Bernstein - One of the best experts on this subject based on the ideXlab platform.

  • thalidomide treatment prevents Chronic Graft Rejection after aortic transplantation in rats an experimental study
    Transplant International, 2017
    Co-Authors: Katharine K Miller, D Wang, X Hu, T Deuse, Evgenios Neofytou, Thomas Renne, Joachim Velden, Hermann Reichenspurner, S Schrepfer, Daniel Bernstein
    Abstract:

    Background Cardiac alloGraft vasculopathy (CAV) affects approximately 30% of cardiac transplant patients at five years post-transplantation. To date there are few CAV treatment or prevention options, none of which are highly effective. The aim of the study was to investigate the effect of thalidomide on the development of CAV. Methods The effect of thalidomide treatment on Chronic Rejection was assessed in rat orthotopic aortic transplants in allogeneic F344 or syngeneic Lew rats (n=6/group). Animals were left untreated or received thalidomide for 30 days post-transplant, and evidence of Graft CAV was determined by histology (trichrome and immunohistochemistry) and intraGraft cytokine measurements. Results Animals that received thalidomide treatment post-transplant showed markedly reduced luminal obliteration, with concomitant rescue of smooth muscle cells (SMCs) in the aortic media of Grafts. Thalidomide counteracted neointimal hyperplasia by preventing dedifferentiation of vascular SMCs. Measurement of intraGraft cytokine levels after thalidomide treatment revealed down-regulation of matrix metalloproteinase 8 (MMP-8) and monocyte chemotactic protein 1 (MCP-1), cytokines involved in tissue remodeling and inflammation, respectively. Importantly, no negative side effects of thalidomide were observed. Conclusions Thalidomide treatment prevents CAV development in a rodent model and is therefore potentially useful in clinical applications to prevent post-transplant heart Rejection.

  • thalidomide treatment prevents Chronic Graft Rejection after aortic transplantation in rats an experimental study
    Transplant International, 2017
    Co-Authors: Katharine K Miller, D Wang, T Deuse, Evgenios Neofytou, Thomas Renne, Joachim Velden, Hermann Reichenspurner, S Schrepfer, Xiaoqin Hua, Daniel Bernstein
    Abstract:

    Cardiac alloGraft vasculopathy (CAV) affects approximately 30% of cardiac transplant patients at 5 years post-transplantation. To date, there are few CAV treatment or prevention options, none of which are highly effective. The aim of the study was to investigate the effect of thalidomide on the development of CAV. The effect of thalidomide treatment on Chronic Rejection was assessed in rat orthotopic aortic transplants in allogeneic F344 or syngeneic Lew rats (n = 6 per group). Animals were left untreated or received thalidomide for 30 days post-transplant, and evidence of Graft CAV was determined by histology (trichrome and immunohistochemistry) and intraGraft cytokine measurements. Animals that received thalidomide treatment post-transplant showed markedly reduced luminal obliteration, with concomitant rescue of smooth muscle cells (SMCs) in the aortic media of Grafts. Thalidomide counteracted neointimal hyperplasia by preventing dedifferentiation of vascular SMCs. Measurement of intraGraft cytokine levels after thalidomide treatment revealed downregulation of matrix metalloproteinase 8 and monocyte chemotactic protein 1, cytokines involved in tissue remodelling and inflammation, respectively. Importantly, no negative side effects of thalidomide were observed. Thalidomide treatment prevents CAV development in a rodent model and is therefore potentially useful in clinical applications to prevent post-transplant heart Rejection.

Katharine K Miller - One of the best experts on this subject based on the ideXlab platform.

  • thalidomide treatment prevents Chronic Graft Rejection after aortic transplantation in rats an experimental study
    Transplant International, 2017
    Co-Authors: Katharine K Miller, D Wang, X Hu, T Deuse, Evgenios Neofytou, Thomas Renne, Joachim Velden, Hermann Reichenspurner, S Schrepfer, Daniel Bernstein
    Abstract:

    Background Cardiac alloGraft vasculopathy (CAV) affects approximately 30% of cardiac transplant patients at five years post-transplantation. To date there are few CAV treatment or prevention options, none of which are highly effective. The aim of the study was to investigate the effect of thalidomide on the development of CAV. Methods The effect of thalidomide treatment on Chronic Rejection was assessed in rat orthotopic aortic transplants in allogeneic F344 or syngeneic Lew rats (n=6/group). Animals were left untreated or received thalidomide for 30 days post-transplant, and evidence of Graft CAV was determined by histology (trichrome and immunohistochemistry) and intraGraft cytokine measurements. Results Animals that received thalidomide treatment post-transplant showed markedly reduced luminal obliteration, with concomitant rescue of smooth muscle cells (SMCs) in the aortic media of Grafts. Thalidomide counteracted neointimal hyperplasia by preventing dedifferentiation of vascular SMCs. Measurement of intraGraft cytokine levels after thalidomide treatment revealed down-regulation of matrix metalloproteinase 8 (MMP-8) and monocyte chemotactic protein 1 (MCP-1), cytokines involved in tissue remodeling and inflammation, respectively. Importantly, no negative side effects of thalidomide were observed. Conclusions Thalidomide treatment prevents CAV development in a rodent model and is therefore potentially useful in clinical applications to prevent post-transplant heart Rejection.

  • thalidomide treatment prevents Chronic Graft Rejection after aortic transplantation in rats an experimental study
    Transplant International, 2017
    Co-Authors: Katharine K Miller, D Wang, T Deuse, Evgenios Neofytou, Thomas Renne, Joachim Velden, Hermann Reichenspurner, S Schrepfer, Xiaoqin Hua, Daniel Bernstein
    Abstract:

    Cardiac alloGraft vasculopathy (CAV) affects approximately 30% of cardiac transplant patients at 5 years post-transplantation. To date, there are few CAV treatment or prevention options, none of which are highly effective. The aim of the study was to investigate the effect of thalidomide on the development of CAV. The effect of thalidomide treatment on Chronic Rejection was assessed in rat orthotopic aortic transplants in allogeneic F344 or syngeneic Lew rats (n = 6 per group). Animals were left untreated or received thalidomide for 30 days post-transplant, and evidence of Graft CAV was determined by histology (trichrome and immunohistochemistry) and intraGraft cytokine measurements. Animals that received thalidomide treatment post-transplant showed markedly reduced luminal obliteration, with concomitant rescue of smooth muscle cells (SMCs) in the aortic media of Grafts. Thalidomide counteracted neointimal hyperplasia by preventing dedifferentiation of vascular SMCs. Measurement of intraGraft cytokine levels after thalidomide treatment revealed downregulation of matrix metalloproteinase 8 and monocyte chemotactic protein 1, cytokines involved in tissue remodelling and inflammation, respectively. Importantly, no negative side effects of thalidomide were observed. Thalidomide treatment prevents CAV development in a rodent model and is therefore potentially useful in clinical applications to prevent post-transplant heart Rejection.

J K Trinkle - One of the best experts on this subject based on the ideXlab platform.

  • ventilation perfusion inequalities during Graft Rejection in patients undergoing single lung transplantation for primary pulmonary hypertension
    Chest, 1992
    Co-Authors: Stephanie M Levine, C L Bryan, Antonio Anzueto, Cynthia A Zamora, S G Jenkinson, W J Gibbons, John H Calhoon, J K Trinkle
    Abstract:

    We report herein data on single lung transplant (SLT) recipients with primary pulmonary hypertension (PPH). One patient did well following surgery but died on the 30th postoperative day due to cytomegalovirus pneumonia. The remaining two patients initially did well with unlimited exercise tolerance following transplantation, but then developed marked dyspnea on exertion and hypoxemia on postoperative days 144 and 120, respectively. Pulmonary function testing showed marked deterioration of function and transbronchial lung biopsy specimens revealed acute Graft Rejection in one patient and evidence of Chronic Graft Rejection in the second patient. Quantitative ventilation-perfusion lung scanning demonstrated a marked decrease in ventilation to the transplanted lung in both cases associated with only a mild decrease in perfusion. This V/Q mismatch resulted in markedly decreased arterial oxygen saturations, widened alveolar-arterial oxygen gradients, and clinically debilitating dyspnea. We conclude that Rejection may result in significant V/Q mismatch and hypoxemia in PPH patients undergoing SLT, which may limit the use of this specific type of surgery for PPH.

N L Tilney - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Graft Rejection
    Current Opinion in Immunology, 1994
    Co-Authors: H Azuma, N L Tilney
    Abstract:

    Although Chronic Rejection remains the most crucial cause of organ Graft loss over the long term, its etiology is not well defined. Early injury to Graft endothelial cells caused by alloantigen-independent factors, such as ischemia or reperfusion, as well as alloantigen-dependent events, such as acute Rejection, have been implicated. Macrophages and their products, peptide growth factors and adhesion molecules are all thought to play an important role in this process via the cytokine-adhesion molecule cascade. Although new immunosuppressive agents, including RS61443 or rapamycin, may be effective in preventing antigen-driven components of this condition, risk factors for initial non-immune injury must also be considered and, if possible, countered.

Erik G. Larsson - One of the best experts on this subject based on the ideXlab platform.

  • Carvedilol treatment of kidney Graft recipients with Chronic Rejection.
    Clinical Transplantation, 1999
    Co-Authors: Lilija Zezina, Ulla Backman, Bengt Vessby, Erik G. Larsson, Bengt Fellström
    Abstract:

    : Carvedilol is an antihypertensive drug with properties that may be potentially beneficial for kidney Graft recipients. The purpose of the study was to investigate if progression of an established Chronic Rejection may be attenuated or reversed by carvedilol. An open, single-centre, phase II, pilot study, with a 2-yr follow-up, was performed in 25 kidney Graft recipients with Chronic Rejection or accelerated transplant atherosclerosis. Seventeen patients had stable Graft function assessed by serum creatinine levels. Eight patients withdrew from the study due to lack of efficacy (increase in serum creatinine 174-477 micromol/L (46-191%) from the initial levels). However. these patients had higher serum creatinine levels and proteinuria already at the start of the study. Both systolic and diastolic blood pressure, as well as heart rate, were stable in all study patients. Low density lipoprotein (LDL)/high density lipoprotein (HDL) cholesterol ratio decreased from 4.7 +/- 1.9 at 1 month to 3.5 +/- 1.2 at 18 months (p < 0.05), and MDA plasma levels decreased from 0.714 +/- 0.119 to 0.493 +/- 0.073 micromol/L after 3 months of carvedilol treatment (p < 0.05). No attenuation of progression of Chronic Graft Rejection by carvedilol treatment was observed in the study. It is suggested that the process of Chronic Rejection could not be reversed by carvedilol because the patients included in the study already had severe morphological and functional changes of the Graft. In conclusion, our study demonstrated that carvedilol provides a good control of blood pressure in renal transplanted patients. Carvedilol treatment had a beneficial effect on lipid pattern and reduced lipid oxidation, but there was no obvious effect on progression of Chronic Rejection.

  • pathogenesis and treatment perspectives of Chronic Graft Rejection cvr
    Immunological Reviews, 1993
    Co-Authors: Bengt Fellström, Erik G. Larsson
    Abstract:

    Chronic Rejection is a major threat towards the long-term function and survival of transplanted hearts and kidneys. It is characterized by a proliferative remodelling of the Graft vessels along with structural changes of the parenchyma and gradual deterioration of Graft function. The pathogenesis is complex and multifactorial. Since Grafts with Chronic Rejection are also subjected to a more or less intense invasion of immunoreactive cells, an important primary objective is to optimize the immunosuppressive treatment. There is no established means of prevention or treatment of Chronic Rejection. Pharmacological agents interfering with prostaglandin metabolism have been tried most frequently and preliminary results are also available from the use of polyunsaturated fatty acids of the omega-3 series and of heparin derivatives. Based on experimental studies the somatostatin analogue angiopeptin seems very promising today. There will certainly be an increased interest in the use of lipid-reducing agents in the future as well as antioxidant agents acting against the effects of reactive oxygen radicals and oxidative modification of LDL fractions. A strong novel candidate is carvedilol, exerting both antihypertensive, antioxidant and antiproliferative properties.