878,311 research outputs found
Natural history and outcome in systemic AA amyloidosis
No full textBACKGROUND:Deposition of amyloid fibrils derived from circulating acute-phase reactant serum amyloid A protein (SAA) causes systemic AA amyloidosis, a serious complication of many chronic inflammatory disorders. Little is known about the natural history of AA amyloidosis or its response to treatment.METHODS:We evaluated clinical features, organ function, and survival among 374 patients with AA amyloidosis who were followed for a median of 86 months. The SAA concentration was measured serially, and the amyloid burden was estimated with the use of whole-body serum amyloid P component scintigraphy. Therapy for inflammatory diseases was administered to suppress the production of SAA.RESULTS:Median survival after diagnosis was 133 months; renal dysfunction was the predominant disease manifestation. Mortality, amyloid burden, and renal prognosis all significantly correlated with the SAA concentration during follow-up. The risk of death was 17.7 times as high among patients with SAA concentrations in the highest eighth, or octile, (greater/equal 155 mg per liter) as among those with concentrations in the lowest octile (< 4 mg per liter); and the risk of death was four times as high in the next-to-lowest octile (4 to 9 mg per liter). The median SAA concentration during follow-up was 6 mg per liter in patients in whom renal function improved and 28 mg per liter in those in whom it deteriorated (P < 0.001). Amyloid deposits regressed in 60% of patients who had a median SAA concentration of less than 10 mg per liter, and survival among these patients was superior to survival among those in whom amyloid deposits did not regress (P=0.04).CONCLUSIONS:The effects of renal dysfunction dominate the course of AA amyloidosis, which is associated with a relatively favorable outcome in patients with SAA concentrations that remain in the low-normal range (< 4 mg per liter)
Eprodisate for the treatment of renal disease in AA amyloidosis
No full textBackground: Amyloid A (AA) amyloidosis is a complication of chronic inflammatory conditions that develops when proteolytic fragments of serum amyloid A protein (SAA) are deposited in tissues as amyloid fibrils. Amyloid deposition in the kidney causes progressive deterioration in renal function. Eprodisate is a member of a new class of compounds designed to interfere with interactions between amyloidogenic proteins and glycosaminoglycans and thereby inhibit polymerization of amyloid fibrils and deposition of the fibrils in tissues.
Methods: We performed a multicenter, randomized, double-blind, placebo-controlled trial to evaluate the efficacy and safety of eprodisate in patients with AA amyloidosis and kidney involvement. We randomly assigned 183 patients from 27 centers to receive eprodisate or placebo for 24 months. The primary composite end point was an assessment of renal function or death. Disease was classified as worsened if any one of the following occurred: doubling of the serum creatinine level, reduction in creatinine clearance by 50% or more, progression to end-stage renal disease, or death.
Results: At 24 months, disease was worsened in 24 of 89 patients who received eprodisate (27%) and 38 of 94 patients given placebo (40%, P=0.06); the hazard ratio for worsening disease with eprodisate treatment was 0.58 (95% confidence interval, 0.37 to 0.93; P=0.02). The mean rates of decline in creatinine clearance were 10.9 and 15.6 ml per minute per 1.73 m2 of body-surface area per year in the eprodisate and the placebo groups, respectively (P=0.02). The drug had no significant effect on progression to end-stage renal disease (hazard ratio, 0.54; P=0.20) or risk of death (hazard ratio, 0.95; P=0.94). The incidence of adverse events was similar in the two groups.
Conclusions: Eprodisate slows the decline of renal function in AA amyloidosis
Renal AA-amyloidosis in intravenous drug users - a role for HIV-infection?
No full textBackground: Chronic renal disease is a serious complication of long-term intravenous drug use (IVDU). Recent reports have postulated a changing pattern of underlying nephropathy over the last decades.
Methods: Retrospective investigation including all patients with prior or present IVDU that underwent renal biopsy because of chronic kidney disease between 01.04.2002 and 31.03.2012 in the city of Frankfurt/Main, Germany.
Results: Twenty four patients with IVDU underwent renal biopsy because of progressive chronic kidney disease or proteinuria. Renal AA-amyloidosis was the predominant cause of renal failure in 50% of patients. Membranoproliferative glomerulonephritis (GN) was the second most common cause found in 21%. Patients with AA-amyloidosis were more likely to be HIV infected (67 vs.17%; p=0.036) and tended to have a higher rate of repeated systemic infections (92 vs. 50%; p=0.069). Patients with AA-amyloidosis presented with progressive renal disease and nephrotic-range proteinuria but most patients had no peripheral edema or systemic hypertension. Development of proteinuria preceded the decline of GFR for approximately 1--2 years.
Conclusions: AA-amyloidosis was the predominant cause of progressive renal disease in the last 10 years in patients with IVDU. The highest rate of AA-amyloidosis observed was seen in HIV infected patients with IVDU. We speculate that chronic HIV-infection as well as the associated immunosuppression might promote development of AA-amyloidosis by increasing frequency and duration of infections acquired by IVDU
95% confidence interval (CI) plots of R<sub>AD</sub>, R<sub>AA</sub> and R<sub>AL</sub>. R<sub>AD</sub>: The correlation coefficient of Asymmetric acceleration index (AAI) and saccade duration; R<sub>AA</sub>: The correlation coefficient of AAI and saccade amplitude; R<sub>AL</sub>: The correlation coefficient of AAI and saccade latency.
No full text<p>95% confidence interval (CI) plots of R<sub>AD</sub>, R<sub>AA</sub> and R<sub>AL</sub>. R<sub>AD</sub>: The correlation coefficient of Asymmetric acceleration index (AAI) and saccade duration; R<sub>AA</sub>: The correlation coefficient of AAI and saccade amplitude; R<sub>AL</sub>: The correlation coefficient of AAI and saccade latency.</p
THE ABSORPTION SPECTRUM OF SODIUM VAPOR FROM 1040{\AA} TO 3500 {\AA}
No full textR. W. Ditchburn and R. D. Hudson, Proc, Roy. SOC. A256, 53 (1960). R. W. Ditchburn, P. J. Jutsum and G. V. Marr, Proc. Roy. Soc. A219, 89 (1953).Author Institution: Space Physics Laboratory, Aerospace Corporation“The absorption of ultraviolet radiation by sodium vapor, and the associated ionization, has been investigated from 1040{\AA} to 3500{\AA} using a two-metre McPherson normal incidence spectrometer and an absorption chamfer of the type described by Ditchburn and The atomic cross section at the series limit (2412 {\AA}) was found to be , in good agreement with the previous result obtained by Ditchburn, Jutsum and The atomic cross section decreases to a minimum at 1900{\AA} and then increases again towards shorter wavelengths. Continuous molecular absorption was observed from 3500{\AA} to 1700{\AA} and ion chamber measurement indicate that this absorption is due to an ionization continuum. Ion current peaks were also seen between 2413{\AA} and 3500{\AA} at wavelengths corresponding to the series absorption lines of the sodium atom. Curves will be presented showing the variation with wavelength of both the atomic cross section and the relative molecular cross section.
Does vitamin E improve the outcomes of pediatric nonalcoholic fatty liver disease? A systematic review and meta-analysis
No full textBackground and Aims: To systemically evaluate the efficacy of adjuvant vitamin E on the outcomes of nonalcoholic fatty liver disease (NAFLD) and/or nonalcoholic steatohepatitis (NASH) in children. Materials and Methods: We searched MEDLINE, PUBMED, EMBASE, the Cochrane Central Register Controlled Trials, and the Cochrane Database of Systematic Reviews over the period between January 1980 and September 2012 for the studies that examined the role of adjuvant vitamin E given at any dose or duration, alone or in combination with other interventions, on the outcome of pediatric NAFLD. The outcomes are alanine aminotransferase (ALT) normalization and histological improvement. Results: Five randomized trials were eligible to be included in our analysis, with a total of 270 participants. There was no statistically significant difference in the effect of adjuvant vitamin E on normalizing serum ALT [risk ratio (RR) =1.18, confidence interval (CI) =0.92-1.53, P = 0.77 for heterogeneity, I 2 = 0%]. Sensitivity analysis showed that using higher doses of vitamin E, a longer duration of therapy or adding vitamin C did not change the effect on the measured outcome. Only two studies looked at histological changes as an outcome. We observed substantial heterogeneity between the two studies. Conclusions: Our meta-analysis did not find a significant effect of adjuvant vitamin E over placebo in normalizing serum ALT. Data on the long-term effect of adjuvant vitamin E on histological improvements in NAFLD patients are still lacking. Larger, well-designed randomized controlled trials (RCTs) in children with histological endpoints are still needed to answer this question
ROTATIONAL ANALYSIS OF THE 6125 \AA \ REGION
No full text C. G. Stevens and R. N, Zare, J. Mol. Spectrosc. 56, 167 (1975). R. E. Smalley, L. Wharton, and D. H. Levy, J. Chem. Phys. 63, 4977 (1975).Author Institution: Department of Chemistry, Columbia University; Department of Chemistry, Columbia University, New yorkThe 6125 \AA \ region wag chosed for investigation, because of the strength of the transitions and because of the seeming simplicity of this region. From an analysis of the rotationally resolved fluorescence of excited by a narrow band (0.03 \AA) \ tunable dye quantum numbers have been assigned to 150 transitions in the 6125 \AA \ region. Four vibronic bands are observed in a 20 \AA \ interval, two of which have been previously A rotational analysis of the 6125 \AA \ and 6126 \AA \ bands is presented, while the small number of transitions assigned to the 6117 \AA \ and 6119 \AA \ bands precludes analysis
Kitab fi misahat al-mujassamat al-mukafiya
No full textpage, (left) folio 118 r, drawing of a dome profile; (right) fol. 119v, drawings of dome profile
Optimal solution of the nearest correlation matrix problem by minimization of the maximum norm
No full textThe nearest correlation matrix problem is to find a valid (positive semidefinite) correlation matrix, R(m,m), that is nearest to a given invalid (negative semidefinite) or pseudo-correlation matrix, Q(m,m); m larger than 2. In the literature on this problem, 'nearest' is invariably defined in the sense of the least Frobenius norm. Research works of Rebonato and Jaeckel (1999), Higham (2002), Anjos et al. (2003), Grubisic and Pietersz (2004), Pietersz, and Groenen (2004), etc. use Frobenius norm explicitly or implicitly. However, it is not necessary to define 'nearest' in this conventional sense. The thrust of this paper is to define 'nearest' in the sense of the least maximum norm (LMN) of the deviation matrix (R-Q), and to obtain R nearest to Q. The LMN provides the overall minimum range of deviation of the elements of R from those of Q. We also append a computer program (source codes in FORTRAN) to find the LMN R from a given Q. Presently we use the random walk search method for optimization. However, we suggest that more efficient methods based on the Genetic algorithms may replace the random walk algorithm of optimization.Nearest correlation matrix problem; Frobenius norm; maximum norm; LMN correlation matrix; positive semidefinite; negative semidefinite; positive definite; random walk algorithm; Genetic algorithm; computer program; source codes; FORTRAN; simulation
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