scholarly journals Wrench‐Related Dome Formation and Subsequent Orogenic Syntax Bending in a Hot Orogen (Variscan Ibero‐Armorican Arc, the Ouessant Island, France)

Tectonics ◽  
2019 ◽  
Vol 38 (10) ◽  
pp. 3563-3585 ◽  
Author(s):  
Christine Authemayou ◽  
Bernard Le Gall ◽  
Martial Caroff ◽  
Denise Bussien Grosjean
Keyword(s):  
Dome Formation

Dome formation in primary cultured monolayers of alveolar epithelial cells

1982 ◽  
Vol 243 (1) ◽  
pp. C96-C100 ◽  
Author(s):  
B. E. Goodman ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Life Span ◽  
Fluid Balance ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Transport Function ◽  
Dome Formation ◽  
Alveolar Epithelial ◽  
Free Air

We have observed the formation of domes by type II alveolar epithelial cells harvested from rat lungs. The cells were harvested using elastase and grew to confluence in 3-4 days after plating on plastic. Numerous domes were observed in the monolayers 4-18 days after plating, with peak dome density occurring at days 6-9. When trypsin was used instead of elastase as the harvesting enzyme, many fewer domes were formed by the monolayers, with peak dome density observed at day 5 and no domes seen after 8 days. The life span of an individual dome was about 3-4 h. The presence of domes indicates an intact active transport function of the cells in the monolayer, which may represent an important mechanism for the maintenance of fluid-free air spaces and normal alveolar fluid balance in mammalian lungs in vivo.

Mitral Dome Formation in Aortic Valvular Diseases

1967 ◽  
Vol 6 (5) ◽  
pp. 481-486 ◽  
Author(s):  
Kjell Bergström ◽  
Herman Lodin
Keyword(s):  
Dome Formation ◽  
Valvular Diseases

Partial agonist, but not pure antiestrogens stimulate doming, a marker of normal differentiation, in the MCF-7 breast cancer cell line

2012 ◽  
Vol 12 (3) ◽  
Author(s):  
W. Barkley Butler ◽  
Stephen C. D’Amico ◽  
William J. Glassford ◽  
Weizhen Wu
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Partial Agonist ◽  
Trichostatin A ◽  
Calf Serum ◽  
Cancer Cell Line ◽  
Dependent Manner ◽  
Dome Formation ◽  
Mcf 7

AbstractThe mechanisms by which tamoxifen inhibits breast tumor growth are not completely understood. Partial agonist antiestrogens such as tamoxifen may cause the estrogen receptor (ER) to interact with genes different from those activated by ER bound to estradiol. Doming is a property often associated with, and considered a marker of, differentiation in mammary epithelial cells in culture. This study compared the ability of pure and partial agonist antiestrogens to stimulate doming.MCF-7 cells grown in medium with 10% calf serum were treated with antiestrogens. Domes were counted in three rows (width of the 4× field) across the flask.Three partial agonist antiestrogens [4-hydroxytamoxifen (OHT), H1285 and RU 39,411] caused dome formation. None of the pure antiestrogens tested (ICI 164,384, ICI 182,780 and RU 58,668) caused doming. Doming was stimulated in a dose-dependent manner starting at 1 nM OHT with maximum stimulation at 10–100 nM. Estradiol did not stimulate doming, but blocked doming at 1%–10% of the OHT concentration. Trichostatin A (TSA) reduced the level of estrogen receptor alpha (ERα) and adding it 24 h before adding OHT prevented dome formation.OHT and the other partial agonist antiestrogens appear to act through the ER to stimulate doming. The ability of tamoxifen to induce a marker of differentiation may play a role in its inhibition of breast tumors. If so, then the fact that other partial agonist antiestrogens share this ability, but that pure antiestrogens lack it, may be an important consideration in developing new antiestrogens for breast cancer therapy.

scholarly journals Giant rhyolite lava dome formation after 7.3 ka supereruption at Kikai caldera, SW Japan

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Yoshiyuki Tatsumi ◽  
Keiko Suzuki-Kamata ◽  
Tetsuo Matsuno ◽  
Hiroshi Ichihara ◽  
Nobukazu Seama ◽  
...  
Keyword(s):  
Lava Dome ◽  
Dome Formation ◽  
Rhyolite Lava ◽  
Sw Japan

Competition between lensing and dome formation of vortices in Bi2Sr2CaCu2O8+y

2007 ◽  
Vol 463-465 ◽  
pp. 245-250 ◽  
Author(s):  
T. Tamegai ◽  
H. Chiku ◽  
M. Tokunaga
Keyword(s):  
Dome Formation

On the origin of Early Proterozoic gneiss domes and metamorphic nodes, northern Michigan

1996 ◽  
Vol 33 (7) ◽  
pp. 1053-1053 ◽  
Author(s):  
David Schneider ◽  
Daniel Holm ◽  
Daniel Lux
Keyword(s):  
Gravity Anomaly ◽  
Gneiss Dome ◽  
Near Surface ◽  
Dome Formation ◽  
Crustal Shortening ◽  
Gneiss Domes ◽  
History Of ◽  
The Republic ◽  
Different Origins ◽  
Northern Michigan

Biotite 40αr/39αr cooling ages from medium-pressure (500–600 MPa) rocks in the Watersmeet district, northern Michigan, suggest significant cooling–uplift and concomitant deformation during gneiss dome formation at~1755 Ma, well after the close of the 1870–1830 Ma Penokean orogeny. However, an 1822 Ma hornblende plateau date indicates that the isograds surrounding the dome are Penokean in age. We attribute gneiss dome formation and doming of Penokean-aged isograds to an episode of orogenic collapse superimposed on an earlier history of crustal shortening. This contrasts with the compressional origin for gneiss domes preserved in the low-pressure (200–300 MPa) Republic district. The different origins may reflect the fact that collapse was localized along the overthickened region of the orogenic belt. In contrast to the Watersmeet area, hornblende and biotite 40Ar/39Ar ages obtained from the Republic area are 1720–1680 Ma. Given the relatively shallow depth of this region, it is unlikely that temperatures remained above 500 °C for over 100 Ma following collision. We interpret these ages to reflect a major thermal event that may have been responsible for formation of the Republic metamorphic node. This interpretation is supported by the recent identification of an ~1730 Ma pluton that is likely the cause of a large, near-surface, negative gravity anomaly coincident with the node, and by the fact that the metamorphic node crosscuts Penokean structures.

Regulation of transport across pulmonary alveolar epithelial cell monolayers

1984 ◽  
Vol 57 (3) ◽  
pp. 703-710 ◽  
Author(s):  
B. E. Goodman ◽  
S. E. Brown ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Phosphodiesterase Inhibitors ◽  
Beta Agonist ◽  
Type Ii ◽  
Dome Formation ◽  
Cell Monolayers ◽  
Cyclic Monophosphate ◽  
Alveolar Epithelial ◽  
Epithelial Cell Monolayers

Domes are formed in large numbers by primary cultured monolayers of type II alveolar epithelial cells from rat lungs. These fluid-filled structures are formed by active transport of solute from medium to substratum, with water following passively. In the present study, we used dome-forming monolayers to study the regulation of alveolar epithelial transport processes by determining the effects on dome formation of adenosine 3',5'-cyclic monophosphate (cAMP) analogues, phosphodiesterase inhibitors, neurotransmitters, and vasopressin (antidiuretic hormone, ADH). The cAMP analogues (dibutyryl cAMP and 8-bromo-cAMP) and phosphodiesterase inhibitors (theophylline, papaverine, and isobutylmethylxanthine) caused large increases in dome formation by 24 h. ADH and beta-adrenergic agonists (epinephrine, terbutaline, and isoproterenol) also caused significant increases in dome density. The beta-agonist response was completely eliminated in the presence of the beta-blocker propranolol. Dibutyryl guanosine 3',5'-cyclic monophosphate and acetylcholine (cholinergic agonist) had no effect on dome formation, whereas the alpha-adrenergic agonist methoxamine caused a small but significant decrease in dome formation. These findings suggest that the active solute flux resulting in dome formation by type II alveolar epithelial cell monolayers is increased by substances expected to elevate intracellular cAMP (or analogue) concentrations. An attractive speculation having major implications for lung fluid balance is that transepithelial fluxes can be modulated by endogenous, and perhaps exogenous, chemical agents in adult mammalian alveolar epithelium in vivo.

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