Comparative Clearance Kinetics of Beat Damaged (Hdrc) and Antibody Coated Red Cells (Igrc)

1982 ◽  
Vol 62 (2) ◽  
pp. 7P-7P ◽  
Author(s):  
A.M. Peters ◽  
M. J. Walport ◽  
K. B. Elkon ◽  
P. P. Ferjencik ◽  
G. R. V. Hughes ◽  
...  
Keyword(s):  
Red Cells ◽  
Clearance Kinetics ◽  
Kinetics Of

The lung clearance kinetics of 57Co3O4 in rats of various ages

1991 ◽  
Vol 22 (4) ◽  
pp. 537-549 ◽  
Author(s):  
C.G. Collier ◽  
A. Hodgson ◽  
S.A. Gray ◽  
J.C. Moody ◽  
A. Ball
Keyword(s):  
Lung Clearance ◽  
Clearance Kinetics ◽  
Kinetics Of

IgA nephropathy: clearance kinetics of IgA-containing immune complexes

2018 ◽  
Vol 40 (6) ◽  
pp. 539-543 ◽  
Author(s):  
Ann Chen ◽  
Sung-Sen Yang ◽  
Tsai-Jung Lin ◽  
Shuk-Man Ka
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Clearance Kinetics ◽  
Kinetics Of

Kinetics of CO2 Uptake by Red Cells

1980 ◽  
pp. 299-305 ◽  
Author(s):  
R. A. B. Holland
Keyword(s):  
Red Cells ◽  
Co2 Uptake ◽  
Kinetics Of

Acetylcholinesterase in Human Erythroid Cells

1973 ◽  
Vol 12 (3) ◽  
pp. 911-923
Author(s):  
R. J. SKAER
Keyword(s):  
Endoplasmic Reticulum ◽  
Nervous System ◽  
Golgi Apparatus ◽  
Red Cells ◽  
The Other ◽  
Red Cell ◽  
Erythroid Cells ◽  
Cell Replacement ◽  
Kinetics Of ◽  
Human Red Cells

Acetylcholinesterase is present in human red cells but cannot be demonstrated by the copper thiocholine test. The enzyme is revealed, however, in the perinuclear cisterna, endoplasmic reticulum and Golgi apparatus of red cell precursors. It is suggested that 2 forms of the enzyme are present, one of which can be demonstrated by the copper thiocholine test, the other cannot; one form may be the precursor of the other. These observations may cast light on the kinetics of red cell replacement and on the interpretation of the results from the copper thiocholine test on other tissues such as the nervous system.

Photographic, stereological and statistical methods in evaluation of aggregation of red cells in disease: Part I: Kinetics of aggregation

Biorheology ◽  
1982 ◽  
Vol 19 (4) ◽  
pp. 567-577 ◽  
Author(s):  
L. Dintenfass ◽  
H. Jedrzejczyk ◽  
A. Willard
Keyword(s):  
Statistical Methods ◽  
Red Cells ◽  
Kinetics Of

scholarly journals Lung inflammation does not affect the clearance kinetics of lipid nanocapsules following pulmonary administration

2016 ◽  
Vol 235 ◽  
pp. 24-33 ◽  
Author(s):  
Aateka Patel ◽  
A. Woods ◽  
Yanira Riffo-Vasquez ◽  
Anna Babin-Morgan ◽  
Marie-Christine Jones ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Lipid Nanocapsules ◽  
Pulmonary Administration ◽  
Clearance Kinetics ◽  
Kinetics Of

scholarly journals Ca2+-Dependent, Stimulus-Specific Modulation of the Plasma Membrane Ca2+ Pump in Hippocampal Neurons

2009 ◽  
Vol 101 (5) ◽  
pp. 2563-2571 ◽  
Author(s):  
Michael J. Ferragamo ◽  
Jessica L. Reinardy ◽  
Stanley A. Thayer
Keyword(s):  
Plasma Membrane ◽  
Neuronal Activity ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Cyclopiazonic Acid ◽  
Synaptic Activity ◽  
Voltage Gated ◽  
Clearance Kinetics ◽  
Transient Elevation ◽  
Kinetics Of

The plasma membrane Ca2+ ATPase (PMCA) plays a major role in restoring Ca2+ to basal levels following transient elevation by neuronal activity. Here we examined the effects of various stimuli that increase [Ca2+]i on PMCA-mediated Ca2+ clearance from hippocampal neurons. We used indo-1-based microfluorimetry in the presence of cyclopiazonic acid to study the rate of PMCA-mediated recovery of Ca2+ elevated by a brief train of action potentials. [Ca2+]i recovery was described by an exponential decay and the time constant provided an index of PMCA-mediated Ca2+ clearance. PMCA function was assessed before and for ≥60 min following a 10-min priming stimulus of either 100 μM N-methyl-d-aspartate (NMDA), 0.1 mM Mg2+ (reduced extracellular Mg2+ induces intense excitatory synaptic activity), 30 mM K+, or control buffer. Recovery kinetics slowed progressively following priming with NMDA or 0.1 mM Mg2+; in contrast, Ca2+ clearance initially accelerated and then slowly returned to initial rates following priming with 30 mM K+-induced depolarization. Treatment with 10 μM calpeptin, an inhibitor of the Ca2+ activated protease calpain, prevented the slowing of kinetics observed following treatment with NMDA but had no affect on the recovery kinetics of control cells. Calpeptin also blocked the rapid acceleration of Ca2+ clearance following depolarization. In calpeptin-treated cells, 0.1 mM Mg2+ induced a graded acceleration of Ca2+ clearance. Thus in spite of producing comparable increases in [Ca2+]i, activation of NMDA receptors, depolarization-induced activation of voltage-gated Ca2+ channels and excitatory synaptic activity each uniquely affected Ca2+ clearance kinetics mediated by the PMCA.

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