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Transplantation Leads (transplantation + lead)
Selected AbstractsLiver cell transplantation leads to repopulation and functional correction in a mouse model of Wilson's diseaseJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2004KATRINA J ALLEN Abstract Background and Aim:, The toxic milk (tx) mouse is a non-fatal animal model for the metabolic liver disorder, Wilson's disease. The tx mouse has a mutated gene for a copper-transporting protein, causing early copper accumulation in the liver and late accumulation in other tissues. The present study investigated the efficacy of liver cell transplantation (LCT) to correct the tx mouse phenotype. Methods:, Congenic hepatocytes were isolated and intrasplenically transplanted into 3,4-month-old tx mice, which were then placed on various copper-loaded diets to examine its influence on repopulation by transplanted cells. The control animals were age-matched untransplanted tx mice. Liver repopulation was determined by comparisons of restriction fragment length polymorphism ratios (DNA and mRNA), and copper levels were measured by atomic absorption spectroscopy. Results:, Repopulation in recipient tx mice was detected in 11 of 25 animals (44%) at 4 months after LCT. Dietary copper loading (whether given before or after LCT, or both) provided no growth advantage for donor cells, with similar repopulation incidences in all copper treatment groups. Overall, liver copper levels were significantly lower in repopulated animals (538 ± 68 µg/g, n = 11) compared to non-repopulated animals (866 ± 62 µg/g, n = 14) and untreated controls (910 ± 103 µg/g, n = 6; P < 0.05). This effect was also seen in the kidney and spleen. Brain copper levels remained unchanged. Conclusion:, Transplanted liver cells can proliferate and correct a non-fatal metabolic liver disease, with some restoration of hepatic copper homeostasis after 4 months leading to reduced copper levels in the liver and extrahepatic tissues, but not in the brain. [source] Quality of life in hepatitis CLIVER INTERNATIONAL, Issue 7 2006Edna Strauss Abstract: A number of different studies have shown a clear reduction in the quality of life of hepatitis C virus (HCV)-related liver-disease patients. Quality of life can be assessed by means of both generic and specific instruments, depending on the aim of the study and the population being studied. The application of a specific instrument to patients with liver diseases provides a broader assessment of different parameters related to hepatic disorders. In hepatitis C, alterations such as the stigma of liver disease, concerns about the disease and symptoms of the disease could be demonstrated with this type of instrument. The impact of the diagnosis of hepatitis C, a potentially serious disease, and the presence of comorbidities such as alcohol and drugs may lead to lower quality of life. Longitudinal studies have proved that, following diagnosis, the stigma of liver disease becomes more apparent over time. Women report worse quality of life than men, supporting that gender differences in hepatitis are also important when assessing quality of life. Alterations in the quality of life of patients submitted to treatment are mainly related to the somatic side effects of Interferon and Ribavirin and are most noticeable in the first weeks of therapy. Early improvement in the quality of life of patients who become HCV-RNA negative suggests that the virus itself plays a biological role. There is no doubt that liver transplantation leads to an improvement in quality of life. Nevertheless, a major concern is the relapse of HCV, with the associated lower quality of life. [source] The natural history of hepatitis C cirrhosis after liver transplantationLIVER TRANSPLANTATION, Issue 9 2009Roberto J. Firpi Hepatitis C after liver transplantation leads to graft cirrhosis in up to 30% of patients within 5 years, but limited data exist regarding the clinical course of cirrhosis after transplantation. The aims of this study were to report the natural history of hepatitis C cirrhosis after liver transplantation and to identify risk factors for decompensation and survival. Hepatitis C patients underwent protocol liver biopsies yearly after liver transplantation. After cirrhosis was identified by biopsy, the outcomes of interest were the development of decompensation, death, or retransplantation for hepatitis C. Kaplan-Meier and Cox regression analysis was used to determine survival and risk factors for decompensation and mortality. Out of 502 liver transplants performed for hepatitis C, 88 patients (18%) had cirrhosis within 3.7 years. Seventy-one patients were compensated at diagnosis. The cumulative probability of decompensation 1 year after cirrhosis was 30%. A Model for End-Stage Liver disease score , 16 was predictive of decompensation and poor survival, whereas successful interferon treatment was found to reduce this risk (relative risk = 0.05). Once decompensation occurred, 1-year survival was 46%. In conclusion, the results confirm an accelerated natural history of hepatitis C cirrhosis after liver transplantation and demonstrate poor survival after decompensation. The Model for End-Stage Liver Disease can stratify risk for decompensation and survival, whereas successful antiviral therapy may be protective. Liver Transpl 15:1063,1071, 2009. © 2009 AASLD. [source] Echocardiographic changes and risk factors for left ventricular hypertrophy in children and adolescents after renal transplantationPEDIATRIC TRANSPLANTATION, Issue 3 2004Amr A. El-Husseini Abstract:, Long-term consequences of cardiac alteration in children with chronic renal failure and after renal transplantation are largely unknown. In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular hypertrophy (LVH) or left ventricular dilatation. The correction of uremic state by renal transplantation leads to normalization of left ventricular contractility, regression of LVH and improvement of cavity volume and so dialysis patients with uremic cardiomyopathy would benefit from renal transplantation. We studied 73 patients, aged 17 yr or less, who underwent renal transplantation in our center. This cross-sectional study was performed 4.6 yr (median) after transplantation. Of the total, 48 were males and 25 were females. Transthoracic echocardiographic examination was performed for all cases. The effects of clinical, demographic, biochemical and therapeutic data on echocardiographic parameters were assessed. Multivariate analysis was used to assess the relation between the risk factors and the left ventricular muscle mass index. The most common echocardiographic abnormalities were the LVH (47.9%), left atrial enlargement (31.5%) and left ventricular dilatation and systolic dysfunction (13.7% for each). The pretransplant dialysis, arteriovenous fistula, acute rejection, cumulative steroid dose per square meter surface area, post-transplant hypertension, anemia and graft dysfunction were significant risk factors for LVH by univariate analysis. The significant factors by multivariate analysis were pretransplant dialysis, post-transplant hypertension and anemia. From this study we may conclude that LVH is a common problem among renal transplant children and adolescents. Early transplantation, control of hypertension and correction of anemia may be beneficial regarding left ventricular function and structure. [source] Blockade of KATP Channels Reduces Endothelial Hyperpolarization and Leukocyte Recruitment upon Reperfusion After HypoxiaAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2009M. Figura Ischemia/reperfusion injury in renal transplantation leads to slow or initial nonfunction, and predisposes to acute and chronic rejection. In fact, severe ischemia reperfusion injury can significantly reduce graft survival, even with modern immunosuppressive agents. One of the mechanisms by which ischemia/reperfusion causes injury is activation of endothelial cells resulting in inflammation. Although several therapies can be used to prevent leukocyte recruitment to ischemic vessels (e.g. antiadhesion molecule antibodies), there have been no clinical treatments reported that can prevent initial immediate neutrophil recruitment upon reperfusion. Using intravital microscopy, we describe abrogation of immediate neutrophil recruitment to ischemic microvessels by the KATP antagonist glibenclamide (GlyburideÔ). Further, we show that glibenclamide can reduce leukocyte recruitment in vitro under physiologic flow conditions. ATP-regulated potassium channels (KATP) are important in the control of cell membrane polarization. Here we describe profound hyperpolarization of endothelial cells during hypoxia, and the reduction of this hyperpolarization using glibenclamide. These findings suggest that control of endothelial membrane potential during ischemia may be an important therapeutic tool in avoiding ischemia/reperfusion injury, and therefore, enhancing transplant long-term function. [source] | ||||||||||