This should be the name the file is saved as when it is uploaded to our system, and should include the file extension. i.e.: Smith_SourceData_Fig1.xls, or Smith_ Unmodified_Gels_Fig1.pdf Data descriptioni.e.

To determine whether allografts of normal amniotic epithelium might provide a nonimmunogenic cellular source of exogenous lysosomal enzymes, subcutaneous implants of amniotic epithelium were performed in six children with clinically advanced storage diseases. The clinical and the biochemical status of each patient was observed for several weeks after amniotic epithelial cell implantation (AECI). Serial studies of blood samples from each patient in the post-AECI period did not demonstrate any increase in levels of deficient lysosomal hydrolase. In two patients, quantitative urinary excretion of substrate was also studied and did not show consistent alterations after AECI. No patient had objective improvement in clinical or neurodevelopmental status following AECI. Two patients died with progressive disease at 2 1/2 and 3 1/2 mo after AECI; no residual amniotic epithelium was found at postmortem examination. Four patients are alive with progressive disease at 6-14 mo after AECI. We conclude that allografts of normal human amnion do not provide sufficient replacement hydrolases for clinical or biochemical improvement in lysosomal storage diseases.

Burgeoning levels of diabetes are a major concern for dialysis services, as diabetes is now the most common cause of end-stage renal disease in most developed nations. With the rapid rise in diabetes prevalence in developing countries, the burden of end stage renal failure due to diabetes is also expected to rise in such countries. Diabetic patients on dialysis have a high burden of morbidity and mortality, particularly from cardiovascular disease, and a higher societal and economic cost compared to non-diabetic subjects on dialysis. Tight glycaemic and blood pressure control in diabetic patients has an important impact in reducing risk of progression to end stage renal disease. The evidence for improving glycaemic control in patients on dialysis having an impact on mortality or morbidity is sparse. Indeed, many factors make improving glycaemic control in patients on dialysis very challenging, including therapeutic difficulties with hypoglycaemic agents, monitoring difficulties, dialysis strategies that exacerbate hyperglycaemia or hypoglycaemia, and possibly a degree of therapeutic nihilism or inertia on the part of clinical diabetologists and nephrologists. Standard drug therapy for hyperglycaemia (eg, metformin) is clearly not possible in patients on dialysis. Thus, sulphonylureas and insulin have been the mainstay of treatment. Newer therapies for hyperglycaemia, such as gliptins and glucagon-like peptide-1 analogues have become available, but until recently, renal failure has precluded their use. Newer gliptins, however, are now licensed for use in 'severe renal failure', although they have yet to be trialled in dialysis patients. Diabetic patients on dialysis have special needs, as they have a much greater burden of complications (cardiac, retinal and foot). They may be best managed in a multidisciplinary diabetic-renal clinic setting, using the skills of diabetologists, nephrologists, clinical nurse specialists in nephrology and diabetes, along with dietitians and podiatrists.