Prevention of irreversible aggregation of whey soy proteins in their foam fractionation from soy whey wastewater

Rui Li; Zhaoliang Wu; Yanji Wang; Linlin Ding; Wei Liu

doi:10.1002/apj.1994

Pilot study of recovery of whey soy proteins from soy whey wastewater using batch foam fractionation

Journal of Food Engineering ◽

10.1016/j.jfoodeng.2014.05.004 ◽

2014 ◽

Vol 142 ◽

pp. 201-209 ◽

Cited By ~ 32

Author(s):

Rui Li ◽

Zhaoliang Wu ◽

Yanji Wang ◽

Wei Liu

Keyword(s):

Pilot Study ◽

Soy Proteins ◽

Foam Fractionation

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A Monoclonal Antibody to the Human Platelet Glycoprotein II b/III a Complex Induces Platelet Activation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647637 ◽

1988 ◽

Vol 60 (01) ◽

pp. 068-074 ◽

Cited By ~ 33

Author(s):

Piet W Modderman ◽

Han G Huisman ◽

Jan A van Mourik ◽

Albert E G Kr von dem Borne

Keyword(s):

Human Platelet ◽

Adenosine Diphosphate ◽

Dense Granule ◽

Platelet Glycoprotein ◽

Activated Platelets ◽

Complex Functions ◽

Slow Aggregation ◽

Irreversible Aggregation ◽

Platelet Release ◽

Aggregation Of Platelets

SummaryThe platelet glycoprotein (GP) IIb/IIIa complex functions as the receptor for fibrinogen on activated platelets. The effects of two anti-GPIIb/IIIa monoclonal antibodies on platelet function were studied. These antibodies, 6C9 and C17, recognized different epitopes, which were exclusively present on the undissociated GPIIb/IIIa complex. Whereas C17 inhibited the binding of fibrinogen to platelets and platelet aggregation induced by adenosine diphosphate (ADP) or collagen, 6C9 caused irreversible aggregation of platelets, both in the presence and absence of extracellular fibrinogen. When incubated with unstirred (nonaggregating) platelets, 6C9 induced release of alpha and dense granule-constituents as well as binding of 125I-fibrinogen to platelets. The latter was evidently mediated in part by platelet-derived ADP, since it was inhibited to a large extent by apyrase, the ADP-hydrolyzing enzyme. F(ab’)2 fragments of 6C9 did not induce platelet-release reactions but caused (slow) aggregation of platelets in the presence of extracellular fibrinogen.These results indicate that binding of an antibody to a specific site on the platelet GPIIb/IIIa complex may cause fibrinogen-mediated aggregation. The Fc part of the platelet-bound antibody appears to be involved in the induction of platelet release.

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Transmembrane Calcium Influx Associated with von Willebrand Factor Binding to GP Ib in the Initiation of Shear-Induced Platelet Aggregation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651640 ◽

1993 ◽

Vol 69 (05) ◽

pp. 496-502 ◽

Cited By ~ 123

Author(s):

Yasuo Ikeda ◽

Makoto Handa ◽

Tetsuji Kamata ◽

Koichi Kawano ◽

Yohko Kawai ◽

...

Keyword(s):

Shear Force ◽

Calcium Influx ◽

Fold Increase ◽

Intracellular Camp ◽

Recombinant Fragment ◽

Transmembrane Flux ◽

Irreversible Aggregation ◽

Von Willebrand ◽

Willebrand Factor ◽

Camp Levels

SummaryWe found that the binding of multimeric vWF to GP Ib under a shear force of 108 dynes/cm2 resulted in the transmembrane flux of Ca2+ ions with a two-to three-fold increase in their intracellular concentration ([Ca2+]i). The blockage of this event, obtained by inhibiting the vWF-GP Ib interaction, suppressed aggregation. In contrast, the blockage of vWF binding to GP IIb-IIIa, as well as the prevention of activation caused by increased intracellular cAMP levels, inhibited aggregation but had no significant effect on [Ca2+]i increase. A monomeric recombinant fragment of vWF containing the GP Ib-binding domain of the molecule (residues 445-733) prevented all effects mediated by multimeric vWF but, by itself, failed to support the increase in [Ca2+]i and aggregation. These results suggest that the binding of multimeric vWF to GP Ib initiates platelets aggregation induced by high shear stress by mediating a transmembrane flux of Ca2+ ions, perhaps through a receptor-dependent calcium channel. The increase in [Ca2+]i may act as an intracellular message and cause the activation of GP IIb-IIIa; the latter receptor then binds vWF and mediates irreversible aggregation.

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Aggregation of Cat Platelets in Vitro

Thrombosis and Haemostasis ◽

10.1055/s-0038-1654191 ◽

1970 ◽

Vol 23 (03) ◽

pp. 601-620 ◽

Cited By ~ 14

Author(s):

Th. B Tschopp

Keyword(s):

Adenosine Monophosphate ◽

Blood Collection ◽

Base Line ◽

Reversible Aggregation ◽

Low Concentrations ◽

Irreversible Aggregation ◽

High Concentrations ◽

Two Phases ◽

Improved Technique

SummaryAggregation of cat platelets in the citrated plasma is examined by means of Born’s absorptiometer. A marked tendency of the platelets of this species to spontaneous aggregation necessitated first of all the development of an improved technique of blood collection.A hypothesis according to which 5-HT is released from the platelets, explains the absence of oscillations on the base line of the absorptiometer, the absence of platelet swelling, when ADP is added, and the effect of stirring on the aggregation curves in cat PRP. The average volume of cat platelets amounts to 10.46 μ3 when directly fixed in the blood, when fixed from PRP to 12.17 μ3, when fixed from stirred PRP to 13.51 μ3.In low concentrations (0.3-2 μM) ADP produce reversible aggregation; in narrowly restricted, individually dissimilar mean concentrations irreversible aggregation in two phases and in high concentrations, irreversible aggregation in one phase. Like ADP serotonin produces 2 phase irreversible aggregation in concentrations of 3-10 μM, but unlike ADP, the aggregation velocity decreases again with high 5-HT concentrations (>100 μM). Adrenaline does not produce aggregation and it is likely that adenosine and adenosine monophosphate inhibit the aggregation by serotonin but not by ADP. Species differences in the aggregation of human, rabbit and cat platelets are discussed.

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FOAM FRACTIONATION

A-to-Z Guide to Thermodynamics Heat and Mass Transfer and Fluids Engineering ◽

10.1615/atoz.f.foafra ◽

2006 ◽

Vol f ◽

Author(s):

R. Lemlich

Keyword(s):

Foam Fractionation

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Soybean proteins counteract heart remodeling in wistar rats fed a high sodium chloride diet

Nephrology (Saint-Petersburg) ◽

10.36485/1561-6274-2019-236-92-99 ◽

2019 ◽

Vol 23 (6) ◽

pp. 92-99

Author(s):

I. G. Kayukov ◽

O. N. Beresneva ◽

M. M. Parastaeva ◽

G. T. Ivanova ◽

A. N. Kulikov ◽

...

Keyword(s):

Blood Pressure ◽

Sodium Chloride ◽

Cardiac Remodeling ◽

Wistar Rats ◽

Salt Intake ◽

Left Ventricular ◽

High Salt ◽

Soy Proteins ◽

High Sodium ◽

Heart Remodeling

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.

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