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Coastal plant induced wave attenuation is an important natural process, and its estimation is crucial to model and develop its potential for the emerging field of eco-friendly coastal defense syste...

To date, the best results in life-supporting pig-to-primate renal xenotransplantation have been obtained in recipients exposed to long-term immunosuppression with cyclophosphamide. As this agent is frequently associated with side-effects, we have explored the potential of a mycophenolate sodium-based maintenance immunosuppression in this model. Human decay-accelerating factor (hDAF) transgenic kidneys were transplanted into splenectomized and bilaterally nephrectomized cynomolgus monkeys immunosuppressed with mycophenolate sodium, cyclosporin A and steroids, and exposed to a brief induction course with cyclophosphamide (up to four doses). After transplantation, the primates were monitored daily for biochemical and haematological evaluations and for the measurements of haemolytic anti-pig antibodies (APA). A detailed histological analysis of each explanted graft was also performed. All the animals showed very poor initial graft function but survived for up to 51 days. In contrast to our previous studies in xenograft recipients on long-term immunosuppression with cyclophosphamide, minimal or no circulating xeno-directed antibodies, as measured by the evaluation of APA titres, were detected in this series although some degree of acute humoral rejection was observed in all the explanted grafts and was the primary cause of graft failure. Furthermore, in addition to areas of humorally mediated graft damage, we have observed for the first time areas with exclusive and prominent infiltration by CD2+ and CD8+ mononuclear cells presenting patterns compatible with tubulitis, glomerulitis and arteritis, which we have called acute cellular xenograft rejection (ACXR). In addition, CD68+ infiltrating macrophages and CD20+ B-cells were also present. This study demonstrates that a triple maintenance immunosuppression with mycophenolate sodium, cyclosporin A and steroids is a viable alternative to a cyclophosphamide-based immunosuppression to obtain prolonged survival of porcine organs transplanted into primates. However, a more stringent control of antibody forming cells remains essential to further extend the survival of xenografts in this model. In addition, the use of the immunosuppressive regimen reported here in the primate is associated with the occurrence of a new category of cell-mediated xenograft injury (ACXR) whose significance has yet to be clarified.

A ten-year prospective study of 26 children and adolescents (age range: 3.5 to 15.75 years; mean age 10.25 years) with symptomatic HBsAg-negative chronic aggressive hepatitis is presented. Daily high-dose prednisone therapy was initially prescribed to secure clinical and biochemical remission, and then an alternate-day steroid program was instituted to maintain the state of remission. Azathioprine was added to the regimen (in three children) if remission was not secured after three months of daily prednisone therapy or if frequent relapses precluded reduction of the predanisone dosage. The mean duration of treatment was 19 months. Clinical and biochemical remission was achieved in all children and histologic remission was demonstrated in 17 children. No steroid complications, treatment failures, morbidity, or mortality were noted during this study. Nineteen children have been off therapy for two to 122 months (mean=69 months) and continue to demonstrate clinical and biochemical remission. Therapy is being progressively decreased in the seven remaining patients. We conclude from our study that high-, single-dose prednisone therapy (daily initially, then on alternate days) will effectively suppress HBsAg-negative CAH in children and adolescents without the production of adverse effects of therapy.

To assess the diagnostic accuracy of methods employed for detection of gastroesophageal reflux, 30 infants and children with symptoms of GER were evaluated by upper gastrointestinal series, gastroesophageal scintiscan, measurement of mean resting lower esophageal sphincter pressure, esophageal intraluminal PH measurement (acid reflux test), and endoscopy. Fifteen control patients were also evaluated by the above studies. GER was demonstrated by UGI in 15 and by GE scintiscan in 17 study patients. LESP less than 15 mm Hg was noted in 12 and a positive acid reflux test was obtained in 29 study patients. Esophagitis was detected in two (of 30) study patients radiographically and in 15 (of 21) study patients by upper gastrointestinal endoscopy. Pulmonary aspiration of gastric contents was not detected by the radionuclide method. None of the 15 control patients had GER demonstrated with any of the above methods. These studies indicate that (1) the acid reflux test correlates most closely with symptoms of GER; (2) THE GE scintiscan is complementary to the UGI in the diagnosis of GER, i.e., the combination increases sensitivity; (3) normal LESP does not necessarily exclude GER; and (4) endoscopy is superior to the UGI in detecting the presence of esophagitis.

Treatment of confluent monolayers of human umbilical vein endothelial cells with sublethal concentrations of hydrogen peroxide (H2O2) produces reversible cell retraction that opens gaps between adjacent cells. Despite the retraction, adjacent cells remain in contact through a network of dendrite-like processes. Retraction depends on cellular metabolism but not new protein synthesis or protein kinase C. Shape changes induced by H2O2 are accompanied by partial redistribution of actin filaments from the cell periphery in resting endothelial cells to a tangled network of centrally located filaments in H2O2-treated endothelial cells. This change in actin organization is associated with a loss of the normal distribution pattern of surface protein expression. Specifically, beta 1 and beta 3 integrins partly escape from focal adhesion plaques and migrate to the lateral and apical surface of the cell; PECAM-1 redistributes from the lateral borders to the basal surface; and ICAM-1 and ICAM-2 spread from apical caps to the basal surface and to the dendrite-like processes. The likely consequence of endothelial retraction accompanied by abnormal membrane protein distribution is a loss of normal endothelial cell functions. These changes are best considered manifestations of H2O2-induced sublethal injury that may cause endothelial dysfunction.

A 60-year-old man presented with hypertension, proteinuria and renal failure. He had an IgM lambda plasma and urinary paraprotein, but bone-marrow examination and skeletal survey were normal, and renal biopsy was felt to be consistent with chronic pyelonephritis. Renal failure progressed, and haemodialysis and later cadaveric renal transplantation were performed. He died 7 months after transplantation from pulmonary thromboembolism. Postmortem examination and review with immunohistochemical techniques of his original renal biopsy revealed his renal disease to have been macroglobulinaemic nephropathy which had recurred in his renal allograft.