Kinetic model of hybridoma cultures for the identification of rate limiting factors and process optimisation

1996 ◽  
Vol 42 (2-3) ◽  
pp. 197-205
Author(s):  
A. Lourenço da Silva ◽  
A. Marc ◽  
J.M. Engasser ◽  
J.L. Goergen
1996 ◽  
Vol 41 (7) ◽  
pp. S5-S13 ◽  
Author(s):  
Jean-Marie Danion ◽  
Herbert Weingartner ◽  
Leonard Singer

Objective: To examine the strengths and weaknesses of cognitive psychopathology through the specific examples of the memory impairments associated with the administration of benzodiazepines, with schizophrenia, and with depression. Method: These examples are analyzed with reference to a model of memory based on the principle of division between specialized and central processing structures. A basic contention is that it is useful to consider 2 broad classes of processes—automatic, associative, or sensory/perceptual processes on the one hand and intentional, strategic, or reflective processes on the other hand—as being separate. Results: The functional mechanisms of the memory impairments associated with these conditions are beginning to be identified, and there is preliminary evidence that a deficit in an elementary computation may have dramatic consequences on highest cognitive functions. There is also evidence that certain memory impairments are linked to specific dysfunctional outcomes in everyday life. By showing that specific rate-limiting factors of cognitive performance can be identified and are amenable to cognitive interventions, existing data open the door for theoretically and empirically based cognitive remediation of mental disorders. Conclusion: The bulk of available evidence (albeit limited) makes the enterprise of cognitive psychopathology quite plausible and convincing.


2018 ◽  
Vol 165 (3) ◽  
pp. A525-A533 ◽  
Author(s):  
Byoung-Sun Lee ◽  
Zhaohui Wu ◽  
Victoria Petrova ◽  
Xing Xing ◽  
Hee-Dae Lim ◽  
...  

1960 ◽  
Vol 198 (1) ◽  
pp. 108-112 ◽  
Author(s):  
Basil I. Hirschowitz ◽  
D. K. O'Leary ◽  
I. N. Marks

Simultaneous measurements of gastric juice pepsin and stomach mucosal pepsinogen were made in groups of pylorus-ligated rats at intervals from 2 to 24 hours to examine the effects of atropine sulfate (20 mg/100 gm/8 hrs.) on pepsinogen secretion and synthesis. Animals given subcutaneous injections of water served as controls. Atropine caused a marked reduction in pepsinogen secretion and a concomitant accumulation of pepsinogen in the mucosa which increased with time to a plateau; pylorus ligation had the opposite effect, indicating that atropine effected the reduction in secretion of pepsinogen by blocking the release of pepsinogen from peptic cells. In untreated rats the hematocrit increased proportionately to presumed body water loss, but in the atropine-treated rats the hematocrit failed to increase to the same degree for equivalent body water loss. Indirect evidence is presented to suggest that the rate of water secretion may be one of the rate-limiting factors in pepsinogen secretion. Although synthesis of pepsinogen can proceed without secretion, correlation of the rates of synthesis with those of secretion suggested that the rate of synthesis could be increased by an increased rate of secretion.


1992 ◽  
pp. 283-285
Author(s):  
Toshiya Takeda ◽  
Minoru Seki ◽  
Shintaro Furusaki ◽  
Tsutomu Furuya

2016 ◽  
Vol 9 ◽  
pp. IJTR.S37984 ◽  
Author(s):  
Katsumi Shibata ◽  
Tsutomu Fukuwatari

The aim of this article is to report the organ-specific correlation with tryptophan (Trp) metabolism obtained by analyses of tryptophan 2,3-dioxygenase knockout (TDO-KO) and quinolinic acid phosphoribosyltransferase knockout (QPRT-KO) mice models. We found that TDO-KO mice could biosynthesize the necessary amount of nicotinamide (Nam) from Trp, resulting in the production of key intermediate, 3-hydroxyanthranilic acid. Upstream metabolites, such as kynurenic acid and xanthurenic acid, in the urine were originated from nonhepatic tissues, and not from the liver. In QPRT-KO mice, the Trp to quinolinic acid conversion ratio was 6%; this value was higher than expected. Furthermore, we found that QPRT activity in hetero mice was half of that in wild-type (WT) mice. Urine quinolinic acid levels remain unchanged in both hetero and WT mice, and the conversion ratio of Trp to Nam was also unaffected. Collectively, these findings show that QPRT was not the rate-limiting enzyme in the conversion. In conclusion, the limiting factors in the conversion of Trp to Nam are the substrate amounts of 3-hydroxyanthranilic acid and activity of 3-hydroxyanthranilic acid 3,4-dioxygenase in the liver.


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