scholarly journals Decay Characteristics of Neutron Excess Sodium Nuclei

Qeios ◽  
2021 ◽  
Author(s):  
Joseph Bevelacqua
Keyword(s):  
2010 ◽  
Vol 86 (4) ◽  
pp. 303-310 ◽  
Author(s):  
Marcia Bitar Portella ◽  
Tania Beninga de Morais ◽  
Mauro Batista de Morais

Author(s):  
Kaname Tagawa ◽  
Yusuke Tsuru ◽  
Katsumi Yokoi ◽  
Takanori Aonuma ◽  
Junichiro Hashimoto

Abstract Background Central pulse pressure is responsible for the hemodynamics of vital organs, and monitoring this parameter is important for cardiovascular disease prevention. Excess sodium intake and (micro)albuminuria (a manifestation of renal microvascular damage) are known to be strong predictors of cardiovascular disease. We sought to investigate the cross-sectional relationships among dietary sodium intake, albuminuria, and central pulse pressure in a general population cohort. Methods The subjects were 933 apparently healthy adults (mean age, 56 ± 10 years). Radial pressure waveforms were recorded with applanation tonometry to estimate mean arterial pressure, central pulse pressure, forward and backward pressure amplitudes, and augmentation index. The urinary sodium/creatinine and albumin/creatinine ratios were measured in spot urine samples. Results Both the urinary sodium/creatinine and albumin/creatinine ratios were positively correlated with central pulse pressure, even after adjusting for mean arterial pressure (P < 0.001). Moreover, both ratios had a synergistic influence on increasing the central pulse pressure independent of age, sex, estimated glomerular filtration rate, hyperlipidemia, and diabetes (interaction P = 0.04). A similar synergistic influence was found on the forward pressure amplitude, but not on the backward pressure amplitude or augmentation index. The overall results were not altered when the urinary albumin/creatinine ratio was replaced with the existence of chronic kidney disease. Conclusion (Micro)albuminuria strengthens the positive association between urinary sodium excretion and central pulse pressure and systolic forward pressure. Excess sodium intake may magnify the cardiovascular risk by widening the aortic pulsatile pressure, particularly in the presence of concomitant chronic kidney disease.


2000 ◽  
Vol 85 (13) ◽  
pp. 2673-2676 ◽  
Author(s):  
George M. Fuller ◽  
Jason Pruet ◽  
Kevork Abazajian

1973 ◽  
Vol 51 (9) ◽  
pp. 1313-1321 ◽  
Author(s):  
Morris J. Robins ◽  
James R. McCarthy Jr. ◽  
Roger A. Jones ◽  
Rudolf Mengel

Reaction of tubercidin (4-amino-7-β-D-ribofuranosylpyrrolo[2,3-d]pyrimidine) (1) with α-acetoxyisobutyryl chloride in the presence of excess sodium iodide in acetonitrile gave an acylated iodo intermediate (2) which was converted into 3′-deoxytubercidin (4) by hydrogenolysis and subsequent saponification.Analogous treatment of formycin (7-amino-3-β-D-ribofuranosylpyrazolo[4,3-d]pyrimidine) (5) gave 3′-deoxyformycin (6) and 2′-deoxyformycin (7) in an approximate ratio of 3:2. These purified nucleosides, 6 and 7 were individually deaminated enzymatically to give 3′-deoxyformycin B (8) and 2′-deoxyformycin B(9).Biological rationale, n.m.r., and mass spectra of these antibiotic-derived deoxynucleosides are discussed.


1991 ◽  
Vol 43 (5) ◽  
pp. 2211-2223 ◽  
Author(s):  
J.-P. Jeukenne ◽  
C. Mahaux ◽  
R. Sartor
Keyword(s):  

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