scholarly journals The relationship between cobalt binding to tubulin and the stimulation of assembly.

1982 ◽  
Vol 257 (10) ◽  
pp. 5839-5845
Author(s):  
R H Himes ◽  
Y C Lee ◽  
G R Eagle ◽  
K M Haskins ◽  
S D Babler ◽  
...  

It was shown in an earlier paper (7) that if maximal stimulation of either of two different afferent nerves can reflexly excite fractions of a given flexor muscle, there are generally, within the aggregate of neurones which innervate that muscle, motoneurones which can be caused to discharge by either afferent (i. e., motoneurones common to both fractions). The relationship which two such afferents bear to a common motoneurone was shown, by the isometric method of recording contraction, to be such that the activation of one afferent, at a speed sufficient to cause a maximal motor tetanus when trans­mitted to the muscle fibres, caused exclusion of any added mechanical effect when the other afferent was excited concurrently. This default in mechanical effect was called “occlusion.” Occlusion may conceivably be due to total exclusion of the effect of one afferent pathway on the common motoneurone by the activity of the other; but facilitation of the effect of one path by the activation of the other when the stimuli were minimal suggests that, in some circumstances at least, the effect of each could augment and summate with th at of the other at the place of convergence of two afferent pathways. Further investigation, using the action currents of the muscle as indication of the nerve impulses discharged by the motoneurone units, has now given some information regarding the effect of impulses arriving at the locus of convergence by one afferent path when the unit common to both is already discharging in response to impulses arriving by the other afferent path. Our method has been to excite both afferent nerves in overlapping sequence by series of break shocks at a rapid rate and to examine the action currents of the resulting reflex for evidence of the appearance of the rhythm of the second series in the discharge caused by the first when the two series are both reaching the motoneurone.


2001 ◽  
Vol 280 (3) ◽  
pp. C465-C472 ◽  
Author(s):  
Bing Han ◽  
Baoan Ji ◽  
Craig D. Logsdon

In the cholecystokinin (CCK) hyperstimulation model of acute pancreatitis, two early intracellular events, activation of trypsinogen and activation of nuclear factor-κB (NF-κB), are thought to be important in the development of the disease. In this study, the relationship between these two events was investigated. NF-κB activity was monitored by using a DNA binding assay and mob-1 chemokine gene expression. Intracellular trypsin activity was measured by using a fluorogenic substrate. Protease inhibitors including FUT-175, Pefabloc, and E-64d prevented CCK stimulation of intracellular trypsinogen and NF-κB activation. Likewise, the NF-κB inhibitors pyrrolidine dithiocarbamate and N-acetyl-l-cysteine inhibited CCK stimulation of NF-κB and intracellular trypsinogen activation. These results suggested a possible codependency of these two events. However, CCK stimulated NF-κB activation in Chinese hamster ovary-CCKAcells, which do not express trypsinogen, indicating that trypsin is not necessary for CCK activation of NF-κB. Furthermore, adenovirus-mediated expression in acinar cells of active p65 subunits to stimulate NF-κB, or of inhibitory κB-α molecules to inhibit NF-κB, did not affect either basal or CCK-mediated trypsinogen activation. Thus trypsinogen and NF-κB activation are independent events stimulated by CCK.


2016 ◽  
Vol 693 ◽  
pp. 1922-1934
Author(s):  
B. Li ◽  
R. Yi ◽  
T. Li

This paper measured the new urbanization level and the degree of intensive land use in 28 provinces of China from 2006 to 2012 through building index system, and built the economic model by utilizing GMM system to demonstrate the relationship between new urbanization, industrial structure evolution and intensive land use based on panel data. The result indicates that the industrial structure evolution is conducive to intensive land use. The development of new urbanization and the intensive land use generate structural contradictions, but it will promote intensive land use indirectly through stimulation of the industrial structure evolution. At the regional level, new urbanization inhibit the intensive land use in the eastern regions and promote it in the western regions, while the effect in the central region is not significant. Industrial structures in some regions stimulate the intensive land use directly or indirectly.


2002 ◽  
Vol 282 (2) ◽  
pp. G332-G337 ◽  
Author(s):  
Shaheen Hamdy ◽  
John C. Rothwell ◽  
Chris Fraser ◽  
Maxine Power ◽  
David Gow ◽  
...  

To better understand the relationship between cortical plasticity and visceral pain, we developed a pain-induced model of altered esophageal corticobulbar excitability. In eight healthy volunteers, corticoesophageal electromyographic responses were recorded via an intraluminal catheter, following magnetic stimulation of the right sensorimotor cortex using perithreshold intensities. Corticothenar responses were used as control. Responses were assessed both before and for up to 1 h after either painful or nonpainful balloon distension of the esophagus (frequency = 1 Hz, dwell time = 200 ms, duration = 10 min), each being delivered to each subject in random order. Painful esophageal distension (mean volume = 11 ± 3 ml) induced a profound increase in esophageal responses compared with baseline levels (at 30 min: 141 ± 12 vs. 101 ± 9 μV, P < 0.01), whereas nonpainful esophageal distension (mean volume = 4 ± 2 ml) showed a decrease (at 30 min: 72 ± 8 vs. 88 ± 12 μV, P < 0.03). Thenar responses were unaffected. The results show that painful and nonpainful stimuli induce different patterns of esophageal corticobulbar excitability, suggesting a physiological link between cortical plasticity and visceral pain.


1974 ◽  
Vol 61 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Allen W. Schuetz ◽  
Robin A. Wallace ◽  
James N. Dumont

The relationship between blood protein (vitellogenin) incorporation and nuclear maturation was studied in individual amphibian oocytes after in vitro exposure to desoxycorticosterone acetate (DOCA). Isolated Rana pipiens oocytes were incubated in vitro with radioactively labeled oocyte yolk precursor ([3H]vitellogenin) obtained from estrogenized Xenopus laevis. Incorporation of labeled vitellogenin into the oocytes continued over a 24-h period. Oocytes simultaneously exposed to DOCA and to labeled vitellogenin exhibited both inhibition of vitellogenin incorporation and stimulation of nuclear maturation and cortical changes. Inhibition of vitellogenin incorporation was observed after approximately 9 h of incubation and was correlated with the time of nuclear breakdown. Preincubation of oocytes in steroid for 9 h essentially terminated vitellogenin incorporation. Incorporation of vitellogenin occurred after removal of follicle cells from the oocyte by a short treatment with EDTA. These results demonstrate the macromolecular vitellogenin transport system remains operative in oocytes which can undergo nuclear maturation and that the steroid DOCA can affect its function. Evidence suggests that the mechanism of steroid inhibition is in part the result of inhibition of the micropinocytotic process in the oocyte cortex.


1977 ◽  
Vol 40 (1) ◽  
pp. 16-25 ◽  
Author(s):  
D. A. Harris ◽  
E. Henneman

1. Single units of the plantaris pool were isolated in ventral root filaments of decerebrate cats and their critical firing levels (CFLs) were determined. Motoneurons of similar size, as judged by their CFLs and other criteria, were compared in firing rate (FR) during repetitive stimulation of the plantaris nerve. 2. Such units either differed very little or quite widely, suggesting that they were sampled randomly from two populations, one firing rapidly, the other slowly. The relationship between the two rates remained approximately constant, regardless of the intensity or rate of input the units received, as long as both of them discharged rhythmically. 3. In single experiments 10-15 of the smallest units in the pool (all with CFLs in the 0-8% range) were isolated and compared. Statistical analyses and visual inspection of these small samples again suggested the existence of two species of motoneurons. 4. Statistical analyses also indicated that the FRs of units in single experiments were not sampled from any one of a variety of parametric, single-modal distributions. This suggests that the data were sampled from a distribution having more than one mode, indicating the existence of separate populations or species of motoneurons among the small units of the pool (0-8% range of CFL). 5. Pooling of the normalized data from different experiments revealed a bimodal histogram, reinforcing the conclusion that there are two species of small alpha motoneurons in the plantaris pool.


1981 ◽  
Author(s):  
S E Graber ◽  
J Hawiger

Membrane receptor for fibrinogen plays an essential role in adhesion and aggregation of human platelets by allowing fibrinogen to bridge two or more platelets together. Whereas in normal, unstimulated platelets fibrinogen receptor is not available, it becomes mobilized upon stimulation of platelets with thrombin, ADP, and other stimuli. The mechanism(s) regulating availability of membrane receptor for fibrinogen remains unknown. Following our recent demonstration that prostacyclin (PGI2) prevents mobilization of fibrinogen receptor by thrombin and ADP (Nature 1980, 283,195), we investigated the relationship between cAMP levels and fibrinogen receptor availability. Platelets separated from plasma proteins were briefly exposed to a low thrombin concentration (0.05 U/ml) followed by hirudin to inactivate free thrombin. Binding of 125I-fi- brinogen and cAMP levels were determined in parallel samples. A dose-dependent rise in platelet cAMP levels from 3.3 pM to 10.3 pM/108 platelets in response to PGI2 (3×10-9M - 3×108M) was accompanied by a corresponding inhibition of 125I-fibrinogen binding. The degree of the cAMP increment correlated with binding inhibition (r=0.96). The inhibition of 125I-fibrinogen binding by PGI2 was sustained up to 120 min and was paralleled by a persistent rise in cAMP level. Stimulation of platelet cAMP synthesis “from within” by a ribosylation of the nucleotide regulatory component with subunit A1 of cholera toxin also increased cAMP levels and inhibited fibrinogen receptor mobilization.These results provide evidence that “up and down” regulation of fibrinogen receptor in platelets is linked to changes in cAMP levels induced by different types of adenyl cyclase antagonists and agonists.


1969 ◽  
Vol 36 (3) ◽  
pp. 469-478 ◽  
Author(s):  
R. W. Smith ◽  
R. F. Glascock

SummaryA study was made of the changes in the rates of oxidation of the C(1), C(2) and C(6) atoms of glucose and in the pathways of glucose catabolism in sheep udder tissue in vitro which occurred when acetate and pyruvate were added.Whereas in rat mammary tissue the rate of oxidation of the C(1) atom of glucose was very much greater than that of the C(6) atom, the ratio of the rates of oxidation of these 2 atoms in sheep tissue was less than 2 when glucose was the only substrate.The addition of acetate resulted in an unequal stimulation of the oxidation of these 2 atoms, with the result that the ratio of their rates of oxidation was about doubled. The rate of oxidation of the C(2) atom was also increased.Acetate also increased the participation of the pentose phosphate pathway in glucose catabolism as measured by the incorporation of the C(1) and C(6) atoms of glucose into fatty acids, lactic acid and glycerol.Pyruvate produced little effect on the rate of oxidation of the C(1) atom but somewhat depressed that of the C(6) atom of glucose. At the same time, it caused a large increase in the participation of the pentose phosphate pathway.These results are discussed with reference to re-cycling of glucose carbon in the pentose phosphate pathway and to the relationship between that pathway and fatty acid synthesis. It is noted that the incorporation of glucose carbon into the 3 intermediates used gave values for the participation of that pathway which were in better agreement than was obtained in rat tissue. It is concluded that triose phosphates are more nearly in equilibrium in sheep than in rat mammary tissue.


1993 ◽  
Vol 265 (6) ◽  
pp. G1039-G1044 ◽  
Author(s):  
F. Hollande ◽  
J. P. Bali ◽  
R. Magous

Histamine plays an important role in the control of gastric acid secretion by activating H2 receptors located on parietal cells. In gastric mucosa, histamine is stored both in mast cells and in enterochromaffin-like cells, especially in rodents. It has been proposed that histamine may regulate its own synthesis and/or release through receptors pharmacologically distinct from H1- and H2-receptor subtypes. In this article, we studied the regulation by histamine of histidine decarboxylase (HDC) activity (enzyme responsible for the formation of histamine by decarboxylation of L-histidine) in a fraction of isolated rabbit gastric mucosal cells enriched in mucous and endocrine cells. Histamine and (R)-alpha-methylhistamine (H3 receptor agonist) dose dependently inhibited HDC activity with the same potency (mean effective concn: 32.2 +/- 0.7 and 50.5 +/- 3.1 pM, respectively) and efficacy (35 and 36% inhibition, respectively). In contrast, the H2 agonist dimaprit was devoid of effect. The H3 antagonist thioperamide was found to decrease the histamine- or (R)-alpha-methylhistamine-induced inhibition of HDC activity (mean ineffective concn = 28.3 +/- 1.8 and 9.87 +/- 0.8 nM, respectively), whereas H1 (promethazine) and H2 (ranitidine) antagonists were unable to affect HDC activity. Moreover, high concentrations of thioperamide (1-10 microns) increased histamine release from these cells. All these results allowed us to conclude that, in gastric mucosa, histamine downregulates its own synthesis (and perhaps release) through the stimulation of autoreceptors with pharmacological characteristics of H3 receptors. However, the relationship between histamine synthesis and release remains unclear and needs further investigation.


1995 ◽  
Vol 269 (5) ◽  
pp. C1317-C1325 ◽  
Author(s):  
G. Nowak ◽  
R. G. Schnellmann

This study examined the relationship between alterations in cellular metabolism and induction of proliferation in renal proximal tubular cells (RPTC) after epidermal growth factor (EGF) exposure. EGF treatment (10 ng/ml) of confluent RPTC cultures for 6 consecutive days increased monolayer DNA content 3.3-fold. EGF-stimulated proliferation of RPTC was preceded by a rapid (within 4 h) induction of glycolysis and a decrease in basal and ouabain-sensitive oxygen consumption (20 and 30%, respectively). EGF stimulated the pentose cycle by 58% and decreased gluconeogenesis by 48%. Supplementation of the culture medium with ribose-5-phosphate or ribose abolished the stimulation of glycolysis and the pentose cycle by EGF but had no effect on proliferation. These results show that EGF rapidly stimulates the pentose cycle, shifts glucose metabolism from gluconeogenesis to glycolysis, and decreases oxygen consumption before any increase in proliferation. The lack of an EGF effect on the pentose cycle and glycolysis in the presence of exogenous precursors for DNA synthesis suggests that the stimulation of these pathways before proliferation is due to increased demands for ribose for subsequent nucleic acid synthesis.


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