16:0 PA (sodium salt)
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16:0 PA (sodium salt)

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DPPA is a glycerophospholipid used in the characterization of polymer-stabilized liposome system.

Category
Peptide Synthesis Reagents
Catalog number
BAT-006383
CAS number
169051-60-9
Molecular Formula
C35H68NaO8P
Molecular Weight
670.87
16:0 PA (sodium salt)
Size Price Stock Quantity
100 mg $199 In stock
IUPAC Name
sodium;[(2R)-2,3-di(hexadecanoyloxy)propyl] phosphate
Synonyms
1,2-DPPA; 1,2-dipalmitoyl-sn-glycero-3-phosphate (sodium salt); DPPA-Na
Related CAS
7091-44-3 (free acid)
Appearance
Crystalline solid.
Purity
99%
Melting Point
161-165°C
Boiling Point
706.9°C
Storage
Store at -20°C
Solubility
Chloroform: 1.6 mg/ml.
InChI
InChI=1S/C35H69O8P.Na/c1-3-5-7-9-11-13-15-17-19-21-23-25-27-29-34(36)41-31-33(32-42-44(38,39)40)43-35(37)30-28-26-24-22-20-18-16-14-12-10-8-6-4-2;/h33H,3-32H2,1-2H3,(H2,38,39,40);/q;+1/p-1/t33-;/m1./s1
InChI Key
BMBWFDPPCSTUSZ-MGDILKBHSA-M
Canonical SMILES
CCCCCCCCCCCCCCCC(=O)OCC(COP(=O)(O)[O-])OC(=O)CCCCCCCCCCCCCCC.[Na+]
1. Non-iodized salt consumption among women of reproductive age in sub-Saharan Africa: a population-based study
Duanping Liao, Kristen H Kjerulff, Ping Du, Paddy Ssentongo, Djibril M Ba Public Health Nutr . 2020 Oct;23(15):2759-2769. doi: 10.1017/S1368980019003616.
Objective:To identify countries in sub-Saharan Africa (SSA) that have not yet achieved at least 90 % universal salt iodization and factors associated with the consumption of non-iodized salt among women of reproductive age.Design:A cross-sectional study using data from Demographic and Health Surveys (DHS). The presence of iodine in household salt (iodized or non-iodized), which was tested during the survey process, was the study outcome. Multivariable logistic regression models were used to determine independent factors associated with the consumption of non-iodized salt among women of reproductive age.Setting:There were eleven countries in SSA that participated in the DHS since 2015 and measured the presence of iodine in household salt.Participants:Women (n 108 318) aged 15-49 years.Results:Countries with the highest rate of non-iodized salt were Senegal (29·5 %) followed by Tanzania (21·3 %), Ethiopia (14·0 %), Malawi (11·6 %) and Angola (10·8 %). The rate of non-iodized salt was less than 1 % in Rwanda (0·3 %), Uganda (0·5 %) and Burundi (0·8 %). Stepwise multivariable logistic regression showed that women were more likely to be using non-iodized salt (adjusted OR; 95 % CI) if they were poor (1·62; 1·48, 1·78), pregnant (1·16; 1·04, 1·29), aged 15-24 years (v. older: 1·14; 1·04, 1·24) and were not literate (1·14; 1·06, 1·23).Conclusions:The use of non-iodized salt varies among SSA countries. The higher level of use of non-iodized salt among poor, young women and pregnant women is particularly concerning.
2. Role of the aldosterone system in the salt-sensitivity of patients with benign essential hypertension
Y Uehara, M Takagi, T Ikeda, S Murao, Y Hirata, K Atarashi, H Matsuoka, M Ishii, T Igari, T Takeda Jpn Heart J . 1983 Jan;24(1):79-90. doi: 10.1536/ihj.24.79.
This study compared responses of blood pressure, plasma concentrations of norepinephrine (PNE) and aldosterone (PA), plasma renin activity (PRA) and urinary excretion of aldosterone during a 5-day period of high salt intake in 11 untreated patients with essential hypertension and 11 age-matched normotensive control subjects. The hypertensive patients all had blood pressures that had been above 160 systolic and/or 90 mmHg diastolic before admission and had decreased to below 150/90 mmHg with only bed-rest and mild salt restriction (6 Gm per day). Sodium balance was also measured before and after high salt intake (16 Gm per day). The hypertensive patients showed both a significant reduction in blood pressure after hospitalization and a significant blood pressure elevation when salt intake was increased. In contrast, no obvious changes in blood pressure were observed in the normotensive subjects. Sodium retention and decreases in PNE and PRA during the high salt period were similar in both groups. However, the reduction in PA and urinary aldosterone excretion in response to excessive salt intake was less pronounced in the hypertensive patients than in the normotensive subjects. The ratio of percentage changes in PA to percentage changes in PRA after salt loading was significantly lower in the hypertensive patients than in the normotensive subjects. In addition, the changes in PA during salt loading were inversely proportional to changes in blood pressure (r = 0.66, p less than 0.01). Thus, it is suggested that the sensitivity of blood pressure to increased dietary salt intake in hypertensive patients may be related to altered aldosterone dynamics, and that the blunt responses of the PA and urinary excretion of aldosterone can be attributed to reduced sensitivity of the adrenal cortex to changes in circulating angiotensin.
3. Ca2+ sparks induced by Na/Ca exchange
Hideyuki Ishida, Kenneth W Spitzer, Zhi Sui, Michael Ritter, Kenneth D Philipson, William H Barry, Fenghua Li Cell Calcium . 2003 Jul;34(1):11-7. doi: 10.1016/s0143-4160(03)00017-4.
Whether Ca(2+) influx on the Na/Ca exchanger (NCX) can trigger elementary sarcoplasmic reticulum (SR) Ca(2+) release events (Ca(2+) sparks) is controversial. We imaged [Ca(2+)](i) (Nipkow confocal microscope and fluo-3) in left ventricular myocytes isolated from wild type (WT) and transgenic (TG) mice overexpressing NCX 2.5-fold. Sudden activation of Ca(2+) influx via NCX induced by abrupt exposure to "0" [Na(+)](o)/normal [Ca(2+)](o) solution by means of a rapid solution switcher-induced Ca(2+) sparks in NCX TG myocytes in 425+/-17 ms, n=21. The diameter and amplitude (F/F(0)) of these sparks (2.74+/-0.14 microm, F/F(0)=2.16+/-0.06, n=18) were similar to those induced by field stimulation of myocytes in the presence of 20 microM nifedipine (2.70+/-0.10 microm, F/F(0)=1.98+/-0.08, n=17). In WT myocytes no Ca(2+) sparks were observed within the first 600 ms after abrupt removal of extracellular Na. In parallel experiments, voltage clamp current measurements (-80 mV) showed that the Na/Ca exchange current (I(NCX)) began within 60 ms of activation of the switcher, and peaked at 312+/-57 pA in TG myocytes within 300-500 ms. I(Ca,L) in 20 microM nifedipine was 10.3+/-4.3 pA, n=7. These results indicate that Ca(2+) entering the myocyte via NCX can cause Ca(2+) sparks which are similar to those elicited by electrical stimulation. However, Ca(2+) influx on NCX is much less efficient in inducing Ca(2+) sparks than Ca(2+) influx via I(Ca,L).
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