Micellar Effects in Steady-State Radiation Induced Reactions

1973 ◽  
pp. 53-71 ◽  
Author(s):  
J. H. Fendler ◽  
G. W. Bogan ◽  
E. J. Fendler ◽  
G. A. Infante ◽  
P. Jirathana
1985 ◽  
Vol 88 (2) ◽  
pp. 655-662 ◽  
Author(s):  
G. S. Mingalevv ◽  
A. P. Tyutnev ◽  
A. V. Vannikov ◽  
V. I. Arkhipov ◽  
A. I. Rudenko ◽  
...  

2018 ◽  
Vol 65 (1) ◽  
pp. 111-118 ◽  
Author(s):  
A. Morana ◽  
I. Planes ◽  
S. Girard ◽  
C. Cangialosi ◽  
S. Delepine-Lesoille ◽  
...  

2010 ◽  
Vol 56 (197) ◽  
pp. 384-394 ◽  
Author(s):  
Natalya Reznichenko ◽  
Tim Davies ◽  
James Shulmeister ◽  
Mauri McSaveney

AbstractHere we report a laboratory study of the effects of debris thickness, diurnally cyclic radiation and rainfall on melt rates beneath rock-avalanche debris and sand (representing typical highly permeable supraglacial debris). Under continuous, steady-state radiation, sand cover >50 mm thick delays the onset of ice-surface melting by >12 hours, but subsequent melting matches melt rates of a bare ice surface. Only when diurnal cycles of radiation are imposed does the debris reduce the longterm rate of ice melt beneath it. This is because debris >50 mm thick never reaches a steady-state heat flux, and heat acquired during the light part of the cycle is partially dissipated to the atmosphere during the nocturnal part of the cycle, thereby continuously reducing total heat flux to the ice surface underneath. The thicker the debris, the greater this effect. Rain advects heat from high-permeability supraglacial debris to the ice surface, thereby increasing ablation where thin, highly porous material covers the ice. In contrast, low-permeability rock-avalanche material slows water percolation, and heat transfer through the debris can cease when interstitial water freezes during the cold/night part of the cycle. This frozen interstitial water blocks heat advection to the ice–debris contact during the warm/day part of the cycle, thereby reducing overall ablation. The presence of metre-deep rock-avalanche debris over much of the ablation zone of a glacier can significantly affect the mass balance, and thus the motion, of a glacier. The length and thermal intensity of the diurnal cycle are important controls on ablation, and thus both geographical location and altitude significantly affect the impact of debris on glacial melting rates; the effect of debris cover is magnified at high altitude and in lower latitudes.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 180-180
Author(s):  
Scott A Peslak ◽  
Jesse Wenger ◽  
Amali P Epa ◽  
Jeffrey C Bemis ◽  
Paul D Kingsley ◽  
...  

Abstract Abstract 180 Erythropoiesis is a robust process of cellular expansion and maturation that occurs in the bone marrow and spleen of mice. Following clastogenic injury such as total body irradiation (TBI), erythroblasts are severely depleted in these organs, resulting in loss of reticulocyte output and the development of a mild anemia (Peslak et al., Exp. Hematol. 2011). However, the mechanistic and microenvironmental factors underlying erythroid recovery following sublethal TBI are poorly understood. To this end, we utilized colony assays to quantify erythroid progenitors, which consist of immature d7 erythroid burst-forming units (BFU-E) and more mature d3 BFU-E and erythroid colony forming units (CFU-E). Imaging flow cytometry was used to quantify erythroblast precursors. We found that d7 BFU-E undergo a slow, incomplete recovery during the first 10 days post-4 Gy TBI of C57Bl/6 mice. In contrast, d3 BFU-E exhibit a robust recovery beginning at 4 days post-TBI that is immediately followed by a rapid increase in CFU-E numbers to over 200 percent of steady-state levels. This initial erythroid progenitor recovery is followed by a wave of erythroid precursor maturation and red cell formation that occurs in close association with macrophages in the bone marrow. These erythroblast islands undergo a rapid synchronous expansion that peaks at 6 days post-TBI, suggesting that the bone marrow microenvironment plays a role in the recovery of the erythron from sublethal TBI. We hypothesized that erythropoietin (EPO), the primary regulator of erythroid survival and proliferation, mediates the rapid, specific expansion of late-stage erythroid progenitors following radiation injury. We found that plasma EPO levels increase 13-fold 4 days after 4 Gy TBI, temporally correlated with expansion of d3 BFU-E. Furthermore, maintenance of steady-state hematocrit levels following TBI prevented EPO induction and blocked expansion of late-stage erythroid progenitors, while exogenous EPO administered at 1 hour post-radiation specifically advanced recovery of late-stage progenitors. These data indicate that EPO is required for expansion of d3 BFU-E and CFU-E following radiation-induced marrow depletion. During times of acute hypoxia, such as the severe anemia induced by bleeding or phenylhydrazine exposure, EPO production is rapidly upregulated and splenic stress erythropoiesis is induced. Surprisingly, splenic erythropoiesis is absent during the rapid initial recovery of erythropoiesis in the bone marrow at 4–6 days post-TBI. However, a massive expansion of CFU-E begins at 7–8 days post-4 Gy TBI in spleen. EPO administration at 4 days following 4 Gy TBI significantly enhances late-stage progenitor recovery exclusively in the marrow, indicating that erythroid progenitors are not present in spleen at the time of rapid bone marrow expansion and that late-stage erythroid progenitor recovery initiates in the marrow and subsequently proceeds to the spleen. Furthermore, we found that erythroid progenitors transiently emerge in the bloodstream at 6–8 days post-TBI, following marrow recovery and prior to initiation of splenic erythropoiesis. These data are consistent with endogenous migration of the erythron from the bone marrow to the spleen during recovery from radiation-induced erythroid injury. Taken together, our data indicate that recovery from sublethal irradiation injury is regulated primarily by the EPO-induced expansion of late-stage erythroid progenitors in the bone marrow. This form of clastogenic injury is critically different from bleeding or hemolysis, which preserve bone marrow and splenic erythroblasts and induce expansion of splenic erythroid stress progenitors. Sublethal irradiation injury thus provides a unique model for the in vivo study of endogenous erythroid recovery. This model may be clinically useful for the functional evaluation of therapeutic factors that regulate or modulate erythroid cell maturation. Disclosures: Bemis: Litron Laboratories: Employment, Patents & Royalties.


Polimery ◽  
1986 ◽  
Vol 31 (06) ◽  
pp. 200-203 ◽  
Author(s):  
JANINA ZURAKOWSKA-ORSZAGH ◽  
JOZEF BARTNIK ◽  
КRZYSZTOF MIROWSKI ◽  
ADAM CHAJEWSKI

2001 ◽  
Vol 27 (7-8) ◽  
pp. 765-773 ◽  
Author(s):  
L. H. Luthjens ◽  
M. S. Frahn ◽  
R. D. Abellon ◽  
M. L. Hom ◽  
J. M. Warman

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