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Guidelines for Parenteral Nutrition were prepared by the German Society for Nutritional Medicine (http://www.dgem.de/), in collaboration with other medical associations to provide guidance for quality assurance for parenteral nutrition (PN) practice, and to promoting health and quality of life of patients concerned. A coordination team proposed topics, working group leaders who along with working group members performed systematic literatur searches and drafted recommendations in a nominal group process. Recommendations were discussed and agreed upon in a structured consensus conference process, followed by a Delphi consensus. The current English version of the guidelines was written and updated during the period between the last quarter of 2007 and the first quarter of 2009. The recommendations of the guidelines should be reviewed, and if necessary updated five years after publication.

The aim of this study is to evaluate the temperature effect on the mechanical properties and damage mechanisms of a Glass/Elium 150 laminate composite. Quasi-static indentation tests are carried out at different temperatures to highlight the temperature dependency of different parameters of the samples (stiffness, maximum load, stored elastic energy, and applied energy). The different damage mechanisms involved in the collapse of the composite are observed at the macro-, meso-, and micro-scopic scales using optical and scanning electron microscopy. The influence of temperature on these damage mechanisms is discussed based on post-mortem observations. It has been highlighted that the kind and the severity of damage are strongly temperature dependent. Below 20℃, fiber breakage, strand failure, intra- and inter-laminar crack propagation are identified. At 60℃, plastic flow of the polymer matrix is observed, which modifies micro-crack propagation at the fiber/matrix interface. Above 90℃, only intra-laminar micro-cracking occurs. To conclude, based on all these observations the kinetics of damage appearance are discussed. [ABSTRACT FROM AUTHOR]

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Context: Fabry disease is a metabolic disorder without a specific treatment, caused by a deficiency of the lysosomal enzyme alpha-galactosidase A (alpha-gal A). Most patients experience debilitating neuropathic pain and premature mortality because of renal failure, cardiovascular disease, or cerebrovascular disease.Objective: To evaluate the safety and efficacy of intravenous alpha-gal A for Fabry disease.Design and Setting: Double-blind placebo-controlled trial conducted from December 1998 to August 1999 at the Clinical Research Center of the National Institutes of Health.Patients: Twenty-six hemizygous male patients, aged 18 years or older, with Fabry disease that was confirmed by alpha-gal A assay.Intervention: A dosage of 0.2 mg/kg of alpha-gal A, administered intravenously every other week (12 doses total).Main Outcome Measure: Effect of therapy on neuropathic pain while without neuropathic pain medications measured by question 3 of the Brief Pain Inventory (BPI).Results: Mean (SE) BPI neuropathic pain severity score declined from 6.2 (0.46) to 4.3 (0.73) in patients treated with alpha-gal A vs no significant change in the placebo group (P =.02). Pain-related quality of life declined from 3.2 (0.55) to 2.1 (0.56) for patients receiving alpha-gal A vs 4.8 (0.59) to 4.2 (0.74) for placebo (P =.05). In the kidney, glomeruli with mesangial widening decreased by a mean of 12.5% for patients receiving alpha-gal vs a 16.5% increase for placebo (P =.01). Mean inulin clearance decreased by 6.2 mL/min for patients receiving alpha-gal A vs 19.5 mL/min for placebo (P =.19). Mean creatinine clearance increased by 2.1 mL/min (0.4 mL/s) for patients receiving alpha-gal A vs a decrease of 16.1 mL/min (0.3 mL/s) for placebo (P =.02). In patients treated with alpha-gal A, there was an approximately 50% reduction in plasma glycosphingolipid levels, a significant improvement in cardiac conduction, and a significant increase in body weight.Conclusion: Intravenous infusions of alpha-gal A are safe and have widespread therapeutic efficacy in Fabry disease. [ABSTRACT FROM AUTHOR]

The efficacy of sodium fluoride therapy for osteoporosis remains controversial. Evidence from clinical studies and from animals receiving fluoride has suggested that fluoride might act on bone to increase osteoblast numbers and matrix synthesis. In order to examine the hypothesis that fluoride has a direct mitogenic or anabolic action on the osteoblast, we tested the effect of fluoride on first passage human osteoblastic bone cells grown from collagenase-treated trabecular bone fragments. Under a variety of culture conditions, including both medium supplementation with serum and with a chemically defined medium, fluoride in doses ranging from 10(-6) to 10(-3) M did not alter cell proliferation as measured either by thymidine incorporation or by direct cell counting. Furthermore, exposure to fluoride under conditions of low serum supplementation did not alter either the total protein synthesis of the cells or their biosynthetic profile. These data suggest that fluoride does not act in vitro upon differentiated osteoblastic bone cells derived from adult human patients. [ABSTRACT FROM AUTHOR]