Nonequilibrium velocity distribution and dissociation rate in dissociation of diatomic molecules

1976 ◽  
Vol 64 (9) ◽  
pp. 3784-3790 ◽  
Author(s):  
Katsuhisa Koura
1999 ◽  
Vol 173 ◽  
pp. 45-50
Author(s):  
L. Neslušan

AbstractComets are created in the cool, dense regions of interstellar clouds. These macroscopic bodies take place in the collapse of protostar cloud as mechanically moving bodies in contrast to the gas and miscroscopic dust holding the laws of hydrodynamics. In the presented contribution, there is given an evidence concerning the Solar system comets: if the velocity distribution of comets before the collapse was similar to that in the Oort cloud at the present, then the comets remained at large cloud-centric distances. Hence, the comets in the solar Oort cloud represent a relict of the nebular stage of the Solar system.


2001 ◽  
Vol 19 (1) ◽  
pp. 1-21 ◽  
Author(s):  
FRANK CHAMBERS ◽  
ABDEL AL-SARKHI ◽  
SHENGHONG YAO

1989 ◽  
Vol 86 ◽  
pp. 853-859 ◽  
Author(s):  
Federico Moscardó ◽  
José Pérez-Jordá ◽  
Emilio San-Fabián

1990 ◽  
Vol 64 (04) ◽  
pp. 594-599 ◽  
Author(s):  
Takuya Tomizuka ◽  
Kyohei Yamamoto ◽  
Aizan Hirai ◽  
Yasushi Tamura ◽  
Sho Yoshida

SummaryThe effect of changes in platelet membrane cholesterol content on thromboxane A2 (TXA2)-induced platelet activation was studied. Concentrations of 9,ll-epithio-ll,12-methano-TXA2 (STA2), a stable analogue of TXA2 which can cause half-maximal aggregation and release of [14C]serotonin in cholesterol-rich platelets were significantly lower than those in cholesterol-normal platelets. STA2-induced increase in cytosolic calcium concentration and [32P]phosphatidic acid formation in cholesterol-rich platelets were significantly greater than those in cholesterol-normal platelets. The maximal concentration of binding site (Bmax) for SQ29548 was significantly increased in cholesterol-rich platelets compared with cholesterol-normal platelets, while the equilibrium dissociation rate constant (Kd) for SQ29548 did not differ between cholesterol-rich and cholesterol-normal platelets. The present study suggested that sensitivity to TXA2 was increased by the incorporation of cholesterol into platelet membrane and that the cause of hypersensitivity to TXA2 in cholesterol-rich platelets may be partly explained by an increase in binding capacity for TXA2.


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