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Plasma Albumin (plasma + albumin)
Selected AbstractsBeta-2-Microglobulin in nocturnal hemodialysis , A comparative study in low and high flux dialysersHEMODIALYSIS INTERNATIONAL, Issue 1 2005A.B. Reid In end-stage renal failure, impaired renal catabolism leads to retention of beta 2 microglobulin (ß2M), identified as the major constituent of hemodialysis (HD) related amyloidosis. It has been previously shown that, while using a high flux (HF) HD membrane, nocturnal hemodialysis (NHD) with its increased time and frequency provides a much higher clearance of ß2M compared to conventional HD. We compared serum ß2M levels between low flux (LF) and HF in a group of 9 NHD patients who dialyse 8 hours 6 nights/week. Fresenius polysulfone LF membrane size F6-F8 HPS dialyser were used for the first 15 months (mth) of NHD (SA 1.3,1.8 m2). Subsequently, polysulfone HF FX80 dialyzer were used (SA 1.8 m2). Blood flow and dialysate flow rates were unchanged throughout the study. ß2M levels were measured at 6, 12, 15 mth on LF and at 6, 12 mth on HF. Albumin, homocysteine (Hcy), and phosphate (Phos) levels were also recorded at these times. ß2M levels trended upwards during the 15 mth on LF (36.6 ± 10.57 at 6 mth vs 47.1 ± 11.7 at 15 mth). On introduction of HF, there was a significant fall in ß2M at 6 mth to 12.4 ± 3.5 (p < 0.003), while ß2M levels were unchanged at 12 mth of HF. A downward trend in Hcy levels with the use of HF was noted (12.9 ± 2.9 at 0 mth Vs 11.1 ± 3.7 at 12 mth). Plasma albumin and Phos levels remained unchanged as did the use of Phos supplementation. Levels of ß2M continued to rise on NHD with LF, indicating inadequate clearance. With the introduction of HF there was a significant fall in ß2M levels consistent with improved clearance. The implications of this are that ß2M clearance may be time and frequency dependent only if dialyser membrane flux is adequate. [source] New concepts in bilirubin encephalopathyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2003J. D. Ostrow Abstract Revised concepts of bilirubin encephalopathy have been revealed by studies of bilirubin toxicity in cultured CNS cells and in congenitally jaundiced Gunn rats. Bilirubin neurotoxicity is related to the unbound (free) fraction of unconjugated bilirubin (Bf), of which the dominant species at physiological pH is the protonated diacid, which can passively diffuse across cell membranes. As the binding affinity of plasma albumin for bilirubin decreases strikingly as albumin concentration increases, previously reported Bf values were underestimated. Newer diagnostic tests can detect reversible neurotoxicity before permanent damage occurs from precipitation of bilirubin (kernicterus). Early toxicity can occur at Bf only modestly above aqueous saturation and affects astrocytes and neurons, causing mitochondrial damage, resulting in impaired energy metabolism and apoptosis, plus cell-membrane perturbation, which causes enzyme leakage and hampers transport of neurotransmitters. The concentrations of unbound bilirubin in the cerebro-spinal fluid and CNS cells are probably limited mainly by active export of bilirubin back into plasma, mediated by ABC transporters present in the brain capillary endothelium and choroid plexus epithelium. Intracellular bilirubin levels may be diminished also by oxidation, conjugation and binding to cytosolic proteins. These new concepts may explain the varied susceptibility of neonates to develop encephalopathy at any given plasma bilirubin level and the selective distribution of CNS lesions in bilirubin encephalopathy. They also can suggest better strategies for predicting, preventing and treating this syndrome. [source] Attenuation of half sulfur mustard gas-induced acute lung injury in ratsJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2006Shannon D. McClintock Abstract Airway instillation into rats of 2-chloroethyl ethyl sulfide (CEES), the half molecule of sulfur mustard compound, results in acute lung injury, as measured by the leak of plasma albumin into the lung. Morphologically, early changes in the lung include alveolar hemorrhage and fibrin deposition and the influx of neutrophils. Following lung contact with CEES, progressive accumulation of collagen occurred in the lung, followed by parenchymal collapse. The co-instillation with CEES of liposomes containing pegylated (PEG)-catalase (CAT), PEG-superoxide dismutase (SOD), or the combination, greatly attenuated the development of lung injury. Likewise, the co-instillation of liposomes containing the reducing agents, N-acetylcysteine (NAC), glutathione (GSH), or resveratrol (RES), significantly reduced acute lung injury. The combination of complement depletion and airway instillation of liposomes containing anti-oxidant compounds maximally attenuated CEES-induced lung injury by nearly 80%. Delayed airway instillation of anti-oxidant-containing liposomes (containing NAC or GSH, or the combination) significantly diminished lung injury even when instillation was delayed as long as 1 h after lung exposure to CEES. These data indicate that CEES-induced injury of rat lungs can be substantially diminished by the presence of reducing agents or anti-oxidant enzymes delivered via liposomes. Copyright © 2005 John Wiley & Sons, Ltd. [source] Albumin-bound low molecular weight thiols analysis in plasma and carotid plaques by CEJOURNAL OF SEPARATION SCIENCE, JSS, Issue 1 2010Angelo Zinellu Abstract We describe a new method for the quantification of low molecular weight thiols, as homocysteine, cysteine, cysteinylglycine, glutamylcysteine and glutathione bound to human plasma albumin. After albumin isolation and purification by SDS-PAGE, thiols were freed from protein with tri- n -butylphosphine and successively derivatized with 5-iodoacetamidofluorescein. Samples were then injected and quantified in about 18,min by CE with laser induced fluorescence detection. Precision tests indicate a good repeatability of the method both for migration times (RSD<0.63%) and areas (RSD<2.98%). The method allows to measure all five low molecular weight thiols released from just 3,,g of albumin thus improving the other described methods in which only three or four thiols were detected. Due to the elevated sensitivity (LOD of 0.3,pM for all thiols), also low molecular weight thiols bound to albumin filtered in tissues could be quantified. [source] C677T polymorphism of methylenetetrahydrofolate reductase gene affects plasma homocysteine level and is a genetic factor of late-onset Alzheimer's diseasePSYCHOGERIATRICS, Issue 1 2004Tomoyuki KIDA Abstract Background:, Elevated plasma homocysteine levels are known as a risk for atherosclerotic vascular disease and venous thrombosis and have been shown as a risk for late-onset Alzheimer's disease (LOAD). Method:, To examine the effect of genetic factors predisposing to elevated plasma homocysteine levels on the occurrence of LOAD, we determined the genotype of a C677T polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene and a variable number tandem repeat (VNTR) spanning exon 13,intron 13 boundary of cystathionine ,-synthase (CBS) gene in patients with LOAD and community-based control subjects. Results:, Logistic regression indicated that the MTHFR-T allele was a risk for LOAD (P < 0.05), independently from apolipoprotein E-,4 (APOE-,4) allele. Kaplan,Meier tests showed that in APOE-,4 non-carriers, individuals with the MTHFR-TT genotype have occurences of LOAD earlier than those with the MTHFR-CC genotype (P < 0.05). Multiple regression analysis indicates that MTHFR-T allele increases plasma homocysteine levels (P = 0.0002), while the number of X chromosomes decreases (P = 0.01). Plasma homocysteine level was not correlated with age, plasma albumin reflecting nutritional condition, and the dose of APOE-,4 allele. The CBS-20 VNTR allele showed the same trend to increase plasma homocysteine level as the MTHFR-T allele, but a risk effect for LOAD was not evident. Conclusion:, A genetic propensity for elevated plasma homocysteine levels, explained by the MTHFR-T allele encoding defective enzymatic function, is involved in the development of LOAD, particularly in APOE-,4 non-carriers, and that homocysteine metabolism could be a preventive target to LOAD in the elderly. [source] Complications and mortality in older surgical patients in Australia and New Zealand (the REASON study): a multicentre, prospective, observational study,ANAESTHESIA, Issue 10 2010D. A. Story Summary We conducted a prospective study of non-cardiac surgical patients aged 70 years or more in 23 hospitals in Australia and New Zealand. We studied 4158 consecutive patients of whom 2845 (68%) had pre-existing comorbidities. By day 30, 216 (5%) patients had died, and 835 (20%) suffered complications; 390 (9.4%) patients were admitted to the Intensive Care Unit. Pre-operative factors associated with mortality included: increasing age (80,89 years: OR 2.1 (95% CI 1.6,2.8), p < 0.001; 90+ years: OR 4.0 (95% CI 2.6,6.2), p < 0.001); worsening ASA physical status (ASA 3: OR 3.1 (95% CI 1.8,5.5), p < 0.001; ASA 4: OR 12.4 (95% CI 6.9,22.2), p < 0.001); a pre-operative plasma albumin < 30 g.l,1 (OR: 2.5 (95% CI 1.8,3.5), p < 0.001); and non-scheduled surgery (OR 1.8 (95% CI 1.3,2.5), p < 0.001). Complications associated with mortality included: acute renal impairment (OR 3.3 (95% CI 2.1,5.0), p < 0.001); unplanned Intensive Care Unit admission (OR 3.1 (95% CI 1.9,4.9), p < 0.001); and systemic inflammation (OR 2.5 (95% CI 1.7,3.7), p < 0.001). Patient factors often had a stronger association with mortality than the type of surgery. Strategies are needed to reduce complications and mortality in older surgical patients. [source] The short-term effect of hyperoncotic albumin, given alone or with furosemide, on oxygenation in sepsis-induced Acute Respiratory Distress SyndromeANAESTHESIA, Issue 3 2007M. Kuper Summary Two prospective non-randomised interventional case series were conducted consecutively at a single university hospital mixed intensive care unit, in patients with severe sepsis and acute respiratory distress syndrome. The first series describes the administration of 200 ml of 20% human albumin solution over 120 s in 13 patients, examining the hypothesis that raising plasma albumin should improve oxygenation. The second series describes the effect of administering 30 mg of furosemide intravenously along with the albumin in 15 patients, exploring whether this would produce more sustained improvement in oxygenation than albumin only. Oxygenation and haemodynamic parameters were measured for 4 h, during the period of peak oncotic effect. Hyperoncotic albumin given alone or with furosemide produced only transient improvement in oxygenation and haemodynamics, which was statistically significant only in the patients given albumin alone. Although the plasma albumin remained significantly elevated at 4 h in both series, no sustained improvement in oxygenation was seen. [source] Seminal plasma albumin: origin and relation to the male reproductive parametersANDROLOGIA, Issue 2 2007S. Elzanaty Summary We wanted to investigate the origin of seminal plasma albumin and its relation to the male reproductive parameters. Semen samples from 916 men, under infertility assessment, were analysed according to guidelines of the World Health Organization. Seminal plasma constituents, i.e. albumin, markers of the epididymal (neutral , -glucosidase, NAG), prostatic (prostate-specific antigen, PSA, and zinc) and seminal vesicle function (fructose), as well as levels of reproductive hormones in plasma were measured. The sperm chromatin structure assay (SCSA) was applied on 267 of the 916 samples. A negative correlation was seen for seminal albumin and plasma follicle-stimulating hormone (r = ,0.1, P = 0.02) and a positive correlation for seminal albumin and serum inhibin B (r = 0.2, P = 0.004). Albumin exhibited positive correlations with the epididymal marker, NAG (r = 0.5, P < 0.001) and with the prostatic markers, PSA and zinc (r = 0.1, P = 0.001; r = 0.2, P < 0.001 respectively) as well as with age (r = 0.2, P < 0.001). A negative significant association was seen for seminal albumin and semen volume (, = ,0.60; 95% CI ,0.80 to ,0.30). The opposite trend was found regarding sperm concentration (, = 0.34; 95% CI 0.30,0.40), total sperm count (, = 0.30; 95% CI 0.20,0.40), and percentage morphologically normal spermatozoa (, = 0.70; 95% CI 0.10,1.0). No association was found between albumin and sperm motility, SCSA parameters, or fructose, the marker of seminal vesicles. Our results suggest testicular, epididymal and prostatic origin of seminal plasma albumin, in addition to the contribution from blood. This is the first study to demonstrate an association between seminal plasma albumin and sperm morphology. Further studies are needed to elucidate the role of seminal albumin in sperm morphology. [source] | |||||||||||||