Hydrogen Diffusion and Thermal Equilibrium of Electronic States in a-Si:H

1987 ◽  
Vol 95 ◽  
Author(s):  
R. A. Street
Keyword(s):  
Thermal Equilibrium ◽  
Hydrogen Diffusion ◽  
Electronic States ◽  
Thermally Induced ◽  
Rate Limiting Step ◽  
Induced Changes ◽  
Rate Limiting ◽  
Hydrogenated Amorphous ◽  
Diffusion Of Hydrogen

AbstractThis paper reviews the recent evidence for thermal equilibrium effects in the electronic behavior of hydrogenated amorphous silicon, and relates the thermally induced changes to the motion of bonded hydrogen. The electronic properties are studied through measurements of d.c conductivity and-.weep out, and the role of hydrogen is explored through its diffusion. The magnitude and doping dependence of the diffusion coefficient DH matches the data on the equilibration of the electronic states. Furthermore both the diffusibn and the relaxation can be described by the same dispersive time dependence. It is argued that the diffusion of hydrogen is the rate limiting step in the the equilibration mechanisms and determines the kinetics.

Endogenous ACh tonically stimulates ANP secretion in rat atria

2013 ◽  
Vol 305 (7) ◽  
pp. H1050-H1056 ◽  
Author(s):  
Hye Yoom Kim ◽  
Kyung Woo Cho ◽  
Dong Yuan Xu ◽  
Dae Gill Kang ◽  
Ho Sub Lee
Keyword(s):  
Acetylcholinesterase Inhibition ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Rat Atria ◽  
Rate Limiting Step ◽  
Induced Changes ◽  
Rate Limiting ◽  
Muscarinic Ach Receptor ◽  
High Affinity Choline Transporter

Exogenous acetylcholine (ACh) is known to stimulate atrial natriuretic peptide (ANP) secretion concomitantly with a decrease in atrial pulse pressure. However, the role of intrinsic ACh in the regulation of ANP secretion remains unknown. Recently, it was shown that nonneuronal and neuronal ACh is present in the cardiac atria. From this finding we hypothesize that endogenously released ACh is involved in the regulation of ANP secretion in an autocrine or paracrine manner in the atria. Experiments were performed in isolated beating rat atria. ANP was measured using radioimmunoassay. To increase the availability of the ACh in the extracellular space of the atrium, its degradation was inhibited with an inhibitor of acetylcholinesterase. Acetylcholinesterase inhibition with physostigmine increased ANP secretion concomitantly with a decrease in atrial dynamics in a concentration-dependent manner. Inhibitors of M2 muscarinic ACh receptor (mAChR), methoctramine, and ACh-activated K+ (KACh+) channels, tertiapin-Q, abolished the physostigmine-induced changes. The effects were not observed in the atria from rats treated with pertussis toxin. Furthermore, the physostigmine-induced effects were attenuated by an inhibitor of high-affinity choline transporter, hemicholinium-3, which is a rate-limiting step of ACh synthesis. Inhibitors of the mAChR signaling pathway and ACh synthesis also attenuated the basal levels of ANP secretion and accentuated atrial dynamics. These findings suggest that endogenously released ACh tonically stimulates ANP secretion from atrial cardiomyocytes via activation of M2 mAChR-Gi/o-KACh+ channel signaling. It is also suggested that the ACh-ANP signaling is implicated in cardiac physiology and pathophysiology.

scholarly journals Folding initiation sites and protein folding.

1999 ◽  
Vol 46 (3) ◽  
pp. 487-508 ◽  
Author(s):  
M Dadlez
Keyword(s):  
Protein Folding ◽  
Protein Fragments ◽  
Denatured State ◽  
Local Structures ◽  
Rate Limiting Step ◽  
Structural Preferences ◽  
Low Levels ◽  
Rate Limiting ◽  
Transition State Barrier

The paper discusses the role of local structural preferences of protein segments in the folding of proteins. First a short overview of the local, secondary structures detected in peptides, protein fragments, denatured proteins and early folding intermediates is given. Next the discussion of their role in protein folding is presented based on recent literature and data obtained in our laboratory. In conclusion it is pointed out that, during folding, local structures populated at low levels in denatured state may facilitate the crossing of the folding transition state barrier, and consequently accelerate the rate limiting step in folding. However, the data show that this effect does not follow simple rules.

Adenoviral expression of 15-lipoxygenase-1 in rabbit aortic endothelium: role in arachidonic acid-induced relaxation

2007 ◽  
Vol 292 (2) ◽  
pp. H1033-H1041 ◽  
Author(s):  
Nitin T. Aggarwal ◽  
Blythe B. Holmes ◽  
Lijie Cui ◽  
Helena Viita ◽  
Seppo Yla-Herttuala ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Rabbit Aorta ◽  
Epoxyeicosatrienoic Acid ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelium ◽  
Rate Limiting Step ◽  
Immunohistochemical Studies ◽  
Rate Limiting

Endothelium-dependent vasorelaxation of the rabbit aorta is mediated by either nitric oxide (NO) or arachidonic acid (AA) metabolites from cyclooxygenase (COX) and 15-lipoxygenase (15-LO) pathways. 15-LO-1 metabolites of AA, 11,12,15-trihydroxyeicosatrienoic acid (THETA), and 15-hydroxy-11,12-epoxyeicosatrienoic acid (HEETA) cause concentration-dependent relaxation. We tested the hypothesis that in the 15-LO pathway of AA metabolism, 15-LO-1 is sufficient and is the rate-limiting step in inducing relaxations in rabbit aorta. Aorta and rabbit aortic endothelial cells were treated with adenoviruses containing human 15-LO-1 cDNA (Ad-15-LO-1) or β-galactosidase (Ad-β-Gal). Ad-15-LO-1-transduction increased the expression of a 75-kDa protein corresponding to 15-LO-1, detected by immunoblotting with an anti-human15-LO-1 antibody, and increased the production of HEETA and THETA from [14C]AA. Immunohistochemical studies on Ad-15-LO-1-transduced rabbit aorta showed the presence of 15-LO-1 in endothelial cells. Ad-15-LO-1-treated aortic rings showed enhanced relaxation to AA (max 31.7 ± 3.2%) compared with Ad-β-Gal-treated (max 12.7 ± 3.2%) or control nontreated rings (max 13.1 ± 1.6%) ( P < 0.01). The relaxations in Ad-15-LO-1-treated aorta were blocked by the 15-LO inhibitor cinnamyl-3,4-dihydroxy-a-cyanocinnamate. Overexpression of 15-LO-1 in the rabbit aortic endothelium is sufficient to increase the production of the vasodilatory HEETA and THETA and enhance the relaxations to AA. This confirms the role of HEETA and THETA as endothelium-derived relaxing factors.

Role of Hydrogen Microstructure in Amorphous Silicon

1992 ◽  
Vol 258 ◽  
Author(s):  
Sufi Zafar ◽  
E. A. Schiff
Keyword(s):  
Amorphous Silicon ◽  
Hydrogen Evolution ◽  
Hydrogen Diffusion ◽  
Hydrogenated Amorphous Silicon ◽  
Hydrogenated Amorphous ◽  
Unified Description

ABSTRACTA model for correlating the observed properties of hydrogenated amorphous silicon (a-Si:H) with the underlying hydrogen microstructure is reviewed. The model provides a unified description of defect equilibration, hydrogen evolution, rehydrogenation and hydrogen diffusion measurements.

Daily prolactin pulse inhibits the corpus luteum during lactational quiescence in the marsupial, Macropus eugenii

2013 ◽  
Vol 25 (2) ◽  
pp. 456 ◽  
Author(s):  
L. A. Hinds ◽  
C. H. Tyndale-Biscoe
Keyword(s):  
Corpus Luteum ◽  
Tammar Wallaby ◽  
Marked Contrast ◽  
Previous Conclusion ◽  
Macropus Eugenii ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Progesterone Synthesis ◽  
Rate Limiting

The corpus luteum (CL) of the tammar wallaby is inhibited by prolactin during lactation and seasonal quiescence. In seasonal quiescence a daily transient pulse of prolactin (PRL) of less than 2 h duration is sufficient to maintain inhibition. We investigated whether the same inhibition applies in lactation and, if so, how. Our results show that inhibition of the CL during lactation is maintained by a transient pulse of prolactin once a day. They also show that the minimum time without a PRL pulse for the CL to escape inhibition is more than 48 h and less than 72 h. Nevertheless, some animals had a longer refractory period than 72 h, which was reflected in a longer interval to the progesterone peak and birth. These results support the previous conclusion that PRL exercises its effect on a rate-limiting step in progesterone synthesis and secretion rate from the CL, which precedes any increase in its mass. Therefore, we conclude that the role of PRL is to act as a luteostatic agent, an effect that is in marked contrast to its luteotrophic effect in many eutherian species, including rodents.

scholarly journals Hydrogen diffusion and the percolation of austenite in nanostructured bainitic steel

2014 ◽  
Vol 470 (2168) ◽  
pp. 20140108 ◽  
Author(s):  
L. C. D. Fielding ◽  
E. J. Song ◽  
D. K. Han ◽  
H. K. D. H. Bhadeshia ◽  
D.-W. Suh
Keyword(s):  
Hydrogen Diffusion ◽  
Volume Fraction ◽  
Three Dimensional ◽  
Bainitic Ferrite ◽  
Effective Diffusivity ◽  
Steel Sample ◽  
Thin Plates ◽  
Heat Treated ◽  
Diffusion Of Hydrogen

The diffusion of hydrogen in austenite is slower than in ferrite. Experiments have been conducted to study the behaviour of hydrogen in a nanostructured steel sample consisting of a mixture of thin plates of bainitic ferrite and intervening films of retained austenite, with the latter phase present in a quantity larger than the percolation threshold, i.e. it has three-dimensional connectivity. The structure was then heat treated to control the fraction of austenite, and hence to study the role of hydrogen when the austenite decomposes below the value required to sustain percolation. The experiments have involved both thermal desorption analysis and permeation, and when combined with theoretical analysis, indicate a significant influence of percolating austenite in hindering the passage of hydrogen into the steel during hydrogen charging, and its permeation through the composite nanostructure. The effect is not as large as might be expected from a simple comparison of independent data on the diffusivities of hydrogen in the two lattices, because the effective diffusivity in ferrite is found to be much smaller than in the defect-free ferrite, owing to trapping effects. The morphology of the austenite is demonstrated to play a role by comparing with a sample containing a larger volume fraction of austenite but present as isolated grains which are ineffective to the permeation of hydrogen.

scholarly journals Syntaxin-6 SNARE Involvement in Secretory and Endocytic Pathways of Cultured Pancreatic β-Cells

2004 ◽  
Vol 15 (4) ◽  
pp. 1690-1701 ◽  
Author(s):  
Regina Kuliawat ◽  
Elena Kalinina ◽  
Jason Bock ◽  
Lloyd Fricker ◽  
Timothy E. McGraw ◽  
...  
Keyword(s):  
Secretory Granules ◽  
Expression System ◽  
Secretory Cells ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Rate Limiting Step ◽  
Protein Receptor ◽  
Golgi Network ◽  
Rate Limiting

In pancreatic β-cells, the syntaxin 6 (Syn6) soluble N-ethylmaleimide-sensitive factor attachment protein receptor is distributed in the trans-Golgi network (TGN) (with spillover into immature secretory granules) and endosomes. A possible Syn6 requirement has been suggested in secretory granule biogenesis, but the role of Syn6 in live regulated secretory cells remains unexplored. We have created an ecdysone-inducible gene expression system in the INS-1 β-cell line and find that induced expression of a membrane-anchorless, cytosolic Syn6 (called Syn6t), but not full-length Syn6, causes a prominent defect in endosomal delivery to lysosomes, and the TGN, in these cells. The defect occurs downstream of the endosomal branchpoint involved in transferrin recycling, and upstream of the steady-state distribution of mannose 6-phosphate receptors. By contrast, neither acquisition of stimulus competence nor the ultimate size of β-granules is affected. Biosynthetic effects of dominant-interfering Syn6 seem limited to slowed intragranular processing to insulin (achieving normal levels within 2 h) and minor perturbation of sorting of newly synthesized lysosomal proenzymes. We conclude that expression of the Syn6t mutant slows a rate-limiting step in endosomal maturation but provides only modest and potentially indirect interference with regulated and constitutive secretory pathways, and in TGN sorting of lysosomal enzymes.

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