A novel dianionic surfactant from the reaction of C14-alkenylsuccinic anhydride with sodium isethionate

1994 ◽  
Vol 71 (7) ◽  
pp. 695-703 ◽  
Author(s):  
W. W. Schmidt ◽  
W. Lilienthal ◽  
K. H. Raney ◽  
S. T. Dubey
Keyword(s):  
Alkenylsuccinic Anhydride ◽  
Sodium Isethionate

scholarly journals Paper's resistance to wetting - A review of internal sizing chemicals and their effects

BioResources ◽  
2007 ◽  
Vol 2 (1) ◽  
pp. 106-145 ◽  
Keyword(s):  
Traditional View ◽  
Significant Progress ◽  
Physical Processes ◽  
Contributing Factors ◽  
Cellulosic Fibers ◽  
Modes Of Action ◽  
Alkenylsuccinic Anhydride ◽  
Molecular Scale ◽  
Sizing Agents ◽  
Competing Reactions

This review considers research related to internal sizing agents. Such chemicals, when added as emulsions or in micellar form to slurries of cellulosic fibers before paper is made, can make the product resist water and other fluids. Significant progress has been achieved to elucidate the modes of action of alkylketene dimer (AKD), alkenylsuccinic anhydride (ASA), rosin products, and other sizing chemicals. Recent findings generally support a traditional view that efficient hydrophobation requires that the sizing chemicals contain hydrophobic groups, that they are efficiently retained on fiber surfaces during the papermaking process, that they become well distributed on a molecular scale, and that they need to be chemically anchored. A variety of studies have quantified ways in which internal sizing treatments tend to be inefficient, compared to what is theoretically possible. The inefficient nature of chemical and physical processes associated with internal sizing, as well as competing reactions and some interfering or contributing factors, help to explain apparent inconsistencies between the results of some recent studies.

Photo-Cross-Linked Biodegradable Poly(Ester Anhydride) Networks Prepared from Alkenylsuccinic Anhydride Functionalized Poly(ε-caprolactone) Precursors

2011 ◽  
Vol 12 (7) ◽  
pp. 2806-2814 ◽  
Author(s):  
Risto A. Hakala ◽  
Harri Korhonen ◽  
Ville V. Meretoja ◽  
Jukka V. Seppälä
Keyword(s):  
Alkenylsuccinic Anhydride ◽  
Biodegradable Poly

Drinking after intragastric NaCl without increase in systemic plasma osmolality in rats

1995 ◽  
Vol 269 (5) ◽  
pp. R1085-R1092 ◽  
Author(s):  
F. S. Kraly ◽  
Y. M. Kim ◽  
L. M. Dunham ◽  
R. A. Tribuzio
Keyword(s):  
Sodium Bicarbonate ◽  
Potassium Chloride ◽  
Water Intake ◽  
Packed Cell Volume ◽  
Plasma Osmolality ◽  
Male Rats ◽  
Plasma Sodium ◽  
Sprague Dawley ◽  
Sodium Isethionate ◽  
Hepatic Portal

Drinking after intragastric hypertonic solutions was examined to determine whether increased plasma osmolality always accompanied initiation of drinking. A 2-ml infusion through a gastric catheter was the beginning of tests in Sprague-Dawley male rats. Latency to drink was shorter and 1-h water intake was greater for increasing concentrations of NaCl (600, 1,200, and 1,800 mosmol/kg) compared with baseline (290 mosmol/kg). Although 600, 900, or 1,200 mosmol/kg NaCl elicited drinking, such infusions failed to change systemic plasma osmolality, and 900 mosmol/kg also failed to change plasma sodium, protein, renin activity, or packed cell volume at the initiation of drinking. Intragastric 900 mosmol/kg sodium bicarbonate, sodium isethionate, potassium chloride, lithium chloride, and mannitol differentially increased water intake. Total subdiaphragmatic vagotomy abolished drinking elicited by intragastric NaCl; selective gastric or hepatic vagotomy attenuated intake under some conditions. These results support the hypothesis of a vagally mediated, gastrointestinal and/or hepatic-portal, osmosensitive mechanism for initiation of drinking in advance of postprandial increases in systemic osmolality.

Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport

1991 ◽  
Vol 260 (4) ◽  
pp. F486-F493 ◽  
Author(s):  
J. N. Lorenz ◽  
H. Weihprecht ◽  
J. Schnermann ◽  
O. Skott ◽  
J. P. Briggs
Keyword(s):  
Chloride Transport ◽  
Choline Chloride ◽  
Juxtaglomerular Apparatus ◽  
Positive Control ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renin Release ◽  
Nacl Solution ◽  
Sodium Isethionate ◽  
Ion Substitution

Transport inhibitor and ion substitution studies were performed using perfused, superfused preparations of the isolated rabbit juxtaglomerular apparatus to investigate transport dependency of macula densa-mediated renin secretion. In the first experimental series, tubular perfusion with a high-NaCl solution containing 10(-6) M bumetanide increased renin secretion compared with perfusion with high NaCl alone from 8.7 to 24.6 nano-Goldblatt hog units (nGU)/min. Bath addition of 10(-6) M bumetanide had no effect on renin release. The second series tested ability of luminal addition of 54 mmol/l Na or Cl salts to inhibit renin secretion, starting from a stimulated value produced by low-NaCl perfusion. Perfusion with a high-NaCl solution decreased renin secretion from 58.9 to 14.8 nGU/min, which served as a positive control. Addition of choline chloride decreased renin secretion from 42.7 to 16.6 nGU/min, and RbCl decreased renin secretion from 54.9 to 17.0 nGU/min. In contrast, addition of two different Na salts had no effect on renin release (from 41.7 to 31.6 nGU/min with sodium isethionate and from 14.1 to 13.5 nGU/min with sodium acetate). Also, in the presence of 26 mmol/l Cl, addition of 54 mmol/l Na had no effect on renin secretion (29.9-36.8 nGU/min). These data demonstrate that renin secretion is directly stimulated by luminal application of transport blockers and can be inhibited by increases in Cl concentration at the macula densa but not by changes in Na concentration. These results support the hypothesis that the initiating signal for macula densa control of renin secretion is an inverse change in transport rate via the luminal Na(+)-K(+)-2Cl- cotransporter.

Analysis of sodium isethionate in soap and lye process streams by suppressed ion chromatography

1993 ◽  
Vol 70 (7) ◽  
pp. 733-734 ◽  
Author(s):  
Henrik T. Rasmussen ◽  
Nicholas Omelczenko ◽  
Bruce P. McPherson
Keyword(s):  
Ion Chromatography ◽  
Sodium Isethionate

Splanchnic osmosensation and vasopressin: mechanisms and neural pathways

1991 ◽  
Vol 261 (1) ◽  
pp. E18-E25 ◽  
Author(s):  
S. Choi-Kwon ◽  
A. J. Baertschi
Keyword(s):  
Small Intestine ◽  
Portal Vein ◽  
Plasma Osmolality ◽  
Splanchnic Nerve ◽  
Neural Pathways ◽  
Stomach Tube ◽  
Splanchnic Nerves ◽  
Sodium Isethionate ◽  
Plasma Arginine ◽  
The Right

Hypertonic (2 ml, 598 mosmol/kgH2O) solutions were infused over 4 min via a stomach tube in 12 groups (n = 5-10) of conscious rats with indwelling arterial catheters. Mean changes over 4–21 min of plasma arginine vasopressin (AVP) were 6.1 +/- 0.9 for NaCl (P less than 0.01), 9.3 +/- 3.0 for LiCl (P less than 0.01), 4.5 +/- 1.3 for sodium isethionate (P less than 0.01), 2.8 +/- 0.9 for sucrose (P less than 0.025), 3.9 +/- 2.8 for mannitol (P less than 0.01), and -0.1 +/- 0.1 (SE) pg/ml for urea. The AVP responses to NaCl and sucrose were proportional to the rate of gastrointestinal absorption of radiolabeled NaCl and sucrose, respectively. The AVP response to 598 mosmol/kgH2O NaCl was attenuated by 60.6% (P less than 0.001) in rats with lesion of the side branches of the major splanchnic nerves innervating the mesentery of the upper small intestine and the portal vein area, by 34–37% (P less than 0.05) in rats with right or left splanchnic nerve lesions, and was not affected by subdiaphragmatic vagotomy. Changes in systemic plasma osmolality were small and could not explain the AVP responses. Thus splanchnic receptors are osmosensitive, are situated in the mesentery of the upper small intestine and possibly the portal vein area, and project to the spinal cord via the right and left major splanchnic nerves.

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