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This study investigated the growth-dependent role of algal organic matters (AOMs) to achieve high removal efficiency (R.E) of microalgae. The results showed that the microalgae cells produced 96 ± 2% of total AOMs as loose bound AOMSS (LB-AOMs) and 4 ± 1% as cell-bound (CB-AOMs) in exponential phase. In stationary phase, LB-AOMs and CB-AOMs were 46 ± 0.7percentage and 54 ± 0.2 percentage, respectively. The R.Es in exponential and stationary phase were 83 ± 2.6% and 66 ± 1.2%, respectively. It is found that the difference of biomass concentration (between exponential and stationary phase) had no significant impact on the R.E (P > 0.01). Further investigations revealed that LB-AOMs inhibit flocculation in exponential and CB-AOMs in stationary phase; however, CB-AOMs showed stronger inhibition than the LB-AOMs (P < 0.01). The provision of calcium (17 ± 0.9 mg/L) to the culture reduced the AOMs inhibition and improved the R.E from 66 ± 1.2% (in control) to 90 ± 4.2%. An increase in R.E was attributed to the interaction of calcium with AOMs and subsequently acting as a flocculant. The findings of this study can be valuable to improve the performance of auto-flocculation technology, which is mainly limited by the presence of AOMs. [ABSTRACT FROM AUTHOR]

The specific binding of Ca2+ to synthetic hexasaccharide models of modified heparin has been investigated by NMR and molecular modeling and compared with previous results on a model of regular heparin. These two models represent the regular region of heparin lacking one type of O-sulfate group, either at C-6 of glucosamine or at C-2 of iduronate. The NMR experiments show different responses to the presence of Ca2+. In the case of the compound lacking O-sulfate groups at C-2, the results are indicative of specific binding similar to that observed for the regular heparin, while the model lacking sulfate groups in position 6 interacts more weakly with Ca2+. In order to understand the basis of this difference, a molecular modeling study based on a rigid body docking approach of the interaction of these carbohydrates with Ca2+ and Na+ was performed. We have found that the results are strongly dependent on the starting orientation of the lateral side chains of the charged groups of the carbohydrate, and that the best agreement with the experimental results is obtained when the starting conformations are taken from previous simulations in the presence of Ca2+. [Copyright &y& Elsevier]

To determine whether an “atherogenic” diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n=12) or the cholesterol- and fat-rich experimental diet (CH-F, n=12) for 111 ± 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins >100 kD and a deficit of proteins >30–50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies. [ABSTRACT FROM AUTHOR]

The muscle mechanical and haemodynamic effects of adriamycin were investigated in guinea pigs and rats by use of isolated myocardium (isometric contractions of papillary muscles of guinea pigs and rats) and in situ preparations (haemodynamic parameters in thoracotomized rats). [ABSTRACT FROM AUTHOR]