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Journal articles on the topic 'Instabilités de type Weibel'

Author: Grafiati

Published: 8 June 2024

Last updated: 31 July 2025

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1

Lazar, M., R. Schlickeiser, R. Wielebinski, and S. Poedts. "COSMOLOGICAL EFFECTS OF WEIBEL-TYPE INSTABILITIES." Astrophysical Journal 693, no. 2 (2009): 1133–41. http://dx.doi.org/10.1088/0004-637x/693/2/1133.

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2

Mirón-Granese, Nahuel, Esteban Calzetta, and Alejandra Kandus. "Primordial Weibel instability." Journal of Cosmology and Astroparticle Physics 2022, no. 01 (2022): 028. http://dx.doi.org/10.1088/1475-7516/2022/01/028.

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Abstract We study the onset of vector instabilities in the post-inflationary epoch of the Universe as a mechanism for primordial magnetic fields amplification. We assume the presence of a charged spectator scalar field arbitrarily coupled to gravity during Inflation in its vacuum de Sitter state. Gravitational particle creation takes place at the transition from Inflation to the subsequent Reheating stage and thus the vacuum field state becomes an excited many particles one. Consequently this state can be described as a real fluid, and we build out the hydrodynamic framework using second order

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3

OKADA, T., I. SAJIKI, and K. SATOU. "Weibel instability by ultraintense laser pulses." Laser and Particle Beams 17, no. 3 (1999): 515–18. http://dx.doi.org/10.1017/s0263034699173191.

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Particle-in-cell (PIC) simulations show that an anisotropic electron velocity distribution is demonstrated by ultraintense laser pulses in underdense plasmas. Recently, it is reported that the anisotropy has been experimentally demonstrated in laser-produced plasmas. It is also pointed out that gigagauss magnetic fields are generated by ultraintense laser pulses. We have already published that the Weibel-type electromagnetic instabilities can be theoretically excited by electrons in a velocity distribution with anisotropic temperature. If these electromagnetic waves are excited, the target may

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4

Baumjohann, W., R. Nakamura, and R. A. Treumann. "Magnetic guide field generation in collisionless current sheets." Annales Geophysicae 28, no. 3 (2010): 789–93. http://dx.doi.org/10.5194/angeo-28-789-2010.

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Abstract. In thin (Δ< few λi) collisionless current sheets in a space plasma like the magnetospheric tail or magnetopause current layer, magnetic fields can grow from thermal fluctuation level by the action of the non-magnetic Weibel instability (Weibel, 1959). The instability is driven by the counter-streaming electron inflow from the "ion diffusion" (ion inertial Hall) region into the inner current (electron inertial) region after thermalisation by the two-stream instability. Under magnetospheric tail conditions it takes ~50 e-folding times (~100 s) for the Weibel field to reach observabl

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5

SUGIE, M., K. OGAWA, and T. OKADA. "DEVELOPMENT OF ELECTROMAGNETIC WEIBEL-TYPE INSTABILITIES IN ANISOTROPIC PLASMAS." International Journal of Modern Physics B 21, no. 03n04 (2007): 637–41. http://dx.doi.org/10.1142/s0217979207042458.

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6

LAZAR, M., A. SMOLYAKOV, R. SCHLICKEISER, and P. K. SHUKLA. "A comparative study of the filamentation and Weibel instabilities and their cumulative effect. I. Non-relativistic theory." Journal of Plasma Physics 75, no. 1 (2009): 19–33. http://dx.doi.org/10.1017/s0022377807007015.

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AbstractA comparative study of the electromagnetic instabilities in anisotropic unmagnetized plasmas is undertaken. The instabilities considered are the filamentation and Weibel instability, and their cumulative effect. Dispersion relations are derived and the growth rates are plotted systematically for the representative cases of non-relativistic counterstreaming plasmas with isotropic or anisotropic velocity distributions functions of Maxwellian type. The pure filamentation mode is attenuated by including an isotropic Maxwellian distribution function. Moreover, it is observed that counterstr

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7

Lazar, M., R. Schlickeiser, and T. Skoda. "Cosmological magnetic field seeds produced by the Weibel instabilities." Proceedings of the International Astronomical Union 6, S271 (2010): 387–88. http://dx.doi.org/10.1017/s1743921311017923.

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AbstractThe source of the cosmological magnetic field is still unknown because the widely invoked dynamo processes are only able to regenerate and amplify some initial magnetic field seeds. In the hot and highly ionized intergalactic matter such magnetic field seeds can easily be produced by the (electro-)magnetic instabilities of Weibel type. Here we discuss suplementary mechanisms that can make these Weibel created fields to evolve at large scales presently observed in galaxies and clusters and can also enhance these magnetic field seeds after the dissipation.

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8

Inglebert, A., A. Ghizzo, T. Reveille, D. Del Sarto, P. Bertrand, and F. Califano. "A multi-stream Vlasov modeling unifying relativistic Weibel-type instabilities." EPL (Europhysics Letters) 95, no. 4 (2011): 45002. http://dx.doi.org/10.1209/0295-5075/95/45002.

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9

Skoutnev, V., A. Hakim, J. Juno, and J. M. TenBarge. "Temperature-dependent Saturation of Weibel-type Instabilities in Counter-streaming Plasmas." Astrophysical Journal 872, no. 2 (2019): L28. http://dx.doi.org/10.3847/2041-8213/ab0556.

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10

Sarrat, M., D. Del Sarto, and A. Ghizzo. "Fluid description of Weibel-type instabilities via full pressure tensor dynamics." EPL (Europhysics Letters) 115, no. 4 (2016): 45001. http://dx.doi.org/10.1209/0295-5075/115/45001.

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11

Doğan, Mustafa, and Kazım Yavuz Ekşi. "Stimulated emission–based model of fast radio bursts." Monthly Notices of the Royal Astronomical Society 494, no. 1 (2020): 876–84. http://dx.doi.org/10.1093/mnras/staa708.

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ABSTRACT Fast radio bursts (FRBs) are bright, short-duration radio transients with very high brightness temperatures implying highly coherent emission. We suggest that the FRBs are caused by the self-focusing of an electron beam interacting with an ambient plasma right beyond the light cylinder radius of a neutron star. The magnetic field at the light cylinder radius is relatively high that can accommodate both young Crab-like systems and old millisecond pulsars addressing the diverse environments of FRBs. At the first stage, the intense pulsed-beam passing through the background plasma causes

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12

Inglebert, A., A. Ghizzo, T. Reveille, D. Del Sarto, P. Bertrand, and F. Califano. "Multi-stream Vlasov model for the study of relativistic Weibel-type instabilities." Plasma Physics and Controlled Fusion 54, no. 8 (2012): 085004. http://dx.doi.org/10.1088/0741-3335/54/8/085004.

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13

Okada, T., T. Shimojo, and K. Niu. "Weibel-type instability of intense ion beam propagation in a reactor chamber." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 278, no. 1 (1989): 97–98. http://dx.doi.org/10.1016/0168-9002(89)91139-x.

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14

Struck, Curtis. "The role of wind driving in OB star bow nebulae." Monthly Notices of the Royal Astronomical Society 494, no. 2 (2020): 1838–47. http://dx.doi.org/10.1093/mnras/staa838.

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ABSTRACT Bow-shaped mid-infrared (mid-IR) emission regions have been discovered in satellite observations of numerous late-type O and early-type B stars with moderate velocities relative to the ambient interstellar medium. Previously, hydrodynamical bow shock models have been used to study this emission. It appears that such models are incomplete in that they neglect kinetic effects associated with long mean free paths of stellar wind particles, and the complexity of Weibel instability fronts. Wind ions are scattered in the Weibel instability and mix with the interstellar gas. However, they do

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15

Emelyanov, N. A., and V. V. Kocharovsky. "Collisional Mechanism of Expanding Wavenumbers Range of Weibel-Type Instability in Magnetoactive Plasma." Fizika plazmy 50, no. 2 (2024): 180–86. http://dx.doi.org/10.31857/s0367292124020032.

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For plasma with anisotropic velocity distribution of particles in the form of two counter-propagating bi-Maxwellian beams, including bi-Maxwellian plasma, in the presence of external magnetic field parallel to the beams, it is shown that in a wide range of parameters, particle collisions lead to the expansion of the wavenumbers range, generally towards the long-wavelength region, and weaken the conditions for the occurrence of the Weibel-type instability. In the specified expanded range, its growth rate, found by means of solving the dispersion equation for the wave vectors orthogonal to the e

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16

Emelyanov, N. A., and V. V. Kocharovsky. "Collisional Mechanism of Expanding Wavenumbers Range of Weibel-Type Instability in Magnetoactive Plasma." Plasma Physics Reports 50, no. 2 (2024): 199–205. http://dx.doi.org/10.1134/s1063780x23602067.

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17

STOCKEM, A., M. LAZAR, P. K. SHUKLA, and A. SMOLYAKOV. "A comparative study of the filamentation and Weibel instabilities and their cumulative effect. II. Weakly relativistic beams." Journal of Plasma Physics 75, no. 4 (2009): 529–43. http://dx.doi.org/10.1017/s002237780800768x.

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AbstractCounterstreaming plasma systems with intrinsic temperature anisotropies are unstable against the excitation of Weibel-type instabilities, namely, filamentation and Weibel instabilities, and their cumulative effect. Here, the analysis is extended to counterstreaming plasmas with weakly relativistic bulk velocities, while the thermal velocities are still considered to be non-relativistic. Such plasma systems are relevant for fusion plasma experiments and the more violent astrophysical phenomena, such as jets in gamma-ray burst sources. Simple analytical forms of the dispersion relations

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18

Lazar, M., R. Schlickeiser, and P. K. Shukla. "Cumulative effect of the Weibel-type instabilities in symmetric counterstreaming plasmas with kappa anisotropies." Physics of Plasmas 15, no. 4 (2008): 042103. http://dx.doi.org/10.1063/1.2896232.

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19

Ghizzo, A. "On the multistream approach of relativistic Weibel instability. II. Bernstein-Greene-Kruskal-type waves in magnetic trapping." Physics of Plasmas 20, no. 8 (2013): 082110. http://dx.doi.org/10.1063/1.4817751.

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20

Garasev, M. A., Vl V. Kocharovsky, A. A. Nechaev, A. N. Stepanov, and V. V. Kocharovsky. "The Coexistence of Orthogonal Current Structures and the Development of Different-Type Weibel Instabilities in Adjacent Regions of a Plasma Transition Layer with a Hot Electron Flow." Геомагнетизм и аэрономия 63, no. 1 (2023): 12–27. http://dx.doi.org/10.31857/s0016794022060050.

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Abstract—By means of particle-in-cell numerical simulations, we find the possibility of the formation andlong-term coexistence of orthogonal current structures in adjacent layers of an inhomogeneous cold plasmapenetrated by a hot electron flow. The formationof these structures is shown to occur in a wide range ofparameters specifying collisionless expansion of high-energy electrons out of a dense plasma into a rarefiedplasma. These structures originate due to the development of Weibel instabilities of two different types thatare associated with qualitatively different anisotropic electron velo

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21

Lazar, M., R. Schlickeiser, and P. K. Shukla. "Erratum: “Cumulative effect of the Weibel-type instabilities in symmetric counterstreaming plasmas with kappa anisotropies” [Phys. Plasmas 15, 042103 (2008)]." Physics of Plasmas 15, no. 7 (2008): 079901. http://dx.doi.org/10.1063/1.2953799.

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22

Garasev, M. A., Vl V. Kocharovsky, A. A. Nechaev, A. N. Stepanov, and V. V. Kocharovsky. "The Coexistence of Orthogonal Current Structures and the Development of Different-Type Weibel Instabilities in Adjacent Regions of a Plasma Transition Layer with a Hot Electron Flow." Geomagnetism and Aeronomy 62, S1 (2022): S10—S24. http://dx.doi.org/10.1134/s0016793222600436.

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23

Haberichter, Sandra L., Elizabeth P. Merricks, Scot A. Fahs, Pamela A. Christopherson, Timothy C. Nichols, and Robert R. Montgomery. "Re-establishment of VWF-dependent Weibel-Palade bodies in VWD endothelial cells." Blood 105, no. 1 (2005): 145–52. http://dx.doi.org/10.1182/blood-2004-02-0464.

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Abstract Type 3 von Willebrand disease (VWD) is a severe hemorrhagic defect in humans. We now identify the homozygous mutation in the Chapel Hill strain of canine type 3 VWD that results in premature termination of von Willebrand factor (VWF) protein synthesis. We cultured endothelium from VWD and normal dogs to study intracellular VWF trafficking and Weibel-Palade body formation. Weibel-Palade bodies could not be identified in the canine VWD aortic endothelial cells (VWD-AECs) by P-selectin, VWFpp, or VWF immunostaining and confocal microscopy. We demonstrate the reestablishment of Weibel-Pal

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24

Tautz, R. C., and I. Lerche. "Nonlinear Weibel-type soliton modes." Journal of Physics A: Mathematical and Theoretical 44, no. 4 (2010): 045501. http://dx.doi.org/10.1088/1751-8113/44/4/045501.

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25

Tautz, R. C., and I. Lerche. "Nonlinear Weibel-type soliton modes." Journal of Physics A: Mathematical and Theoretical 44, no. 16 (2011): 169602. http://dx.doi.org/10.1088/1751-8121/44/16/169602.

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26

Kobayashi, Toshihide, Ulrich M. Vischer, Corinne Rosnoblet, et al. "The Tetraspanin CD63/lamp3 Cycles between Endocytic and Secretory Compartments in Human Endothelial Cells." Molecular Biology of the Cell 11, no. 5 (2000): 1829–43. http://dx.doi.org/10.1091/mbc.11.5.1829.

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In the present study, we show that in human endothelial cells the tetraspanin CD63/lamp3 distributes predominantly to the internal membranes of multivesicular–multilamellar late endosomes, which contain the unique lipid lysobisphosphatidic acid. Some CD63/lamp3 is also present in Weibel–Palade bodies, the characteristic secretory organelle of these cells. We find that CD63/lamp3 molecules can be transported from late endosomes to Weibel–Palade bodies and thus that CD63/lamp3 cycles between endocytic and biosynthetic compartments; however, movement of CD63/lamp3 is much slower than that of P-se

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27

Chauhan, Anil K., Janka Kisucka, Colin B. Lamb, Wofgang Bergmeier, and Denisa D. Wagner. "von Willebrand Factor and Factor VIII Are Independently Required To Form Stable Occlusive Thrombi in Injured Veins." Blood 108, no. 11 (2006): 1789. http://dx.doi.org/10.1182/blood.v108.11.1789.1789.

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Abstract von Willebrand factor (VWF) is a large adhesive glycoprotein synthesized in megakaryocytes and endothelial cells and stored in platelet a-granules and Weibel-Palade bodies respectively. It protects Factor VIII (FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall thus playing an important role in hemostasis and thrombosis. VWF is crucial for the formation of occlusive thrombi at arterial shear rates. However, with only a few conflicting studies published, the role of VWF in venous thrombosis is still unclear. Therefore in order to understa

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28

Hüller, S., and A. Porzio. "Weibull-type speckle distributions as a result of saturation in stimulated scattering processes." Laser and Particle Beams 33, no. 4 (2015): 667–78. http://dx.doi.org/10.1017/s0263034615000713.

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AbstractDuring the propagation of an optically smoothed laser beam through a warm plasma the speckle field pattern and the corresponding speckle intensity distribution are modified in time and along the laser propagation direction. It is shown here that the laser–plasma interaction can change the character of speckle statistics from an initially exponential-type limit law to a Weibull-type law. The Weibull distribution is characterized by a power-law-type behavior in a limited interval of the random variable, which is, in the present case, the speckle intensity. The properties of the speckle d

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29

Chauhan, Anil K., Janka Kisucka, Alexander Brill, Meghan T. Walsh, Friedrich Scheiflinger, and Denisa D. Wagner. "ADAMTS13: a new link between thrombosis and inflammation." Journal of Experimental Medicine 205, no. 9 (2008): 2065–74. http://dx.doi.org/10.1084/jem.20080130.

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von Willebrand factor (VWF) levels are elevated and a disintegrin-like and metalloprotease with thrombospondin type I repeats–13 (ADAMTS13) activity is decreased in both acute and chronic inflammation. We hypothesized that by cleaving hyperactive ultralarge VWF (ULVWF) multimers, ADAMTS13 down-regulates both thrombosis and inflammation. Using intravital microscopy, we show that ADAMTS13 deficiency results in increased leukocyte rolling on unstimulated veins and increased leukocyte adhesion in inflamed veins. Both processes were dependent on the presence of VWF. Depletion of platelets in Adamts

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30

Emeis, J. J., Y. van den Eijnden-Schrauwen, C. M. van den Hoogen, W. de Priester, A. Westmuckett, and F. Lupu. "An Endothelial Storage Granule for Tissue-Type Plasminogen Activator." Journal of Cell Biology 139, no. 1 (1997): 245–56. http://dx.doi.org/10.1083/jcb.139.1.245.

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In previous studies we have shown that, after stimulation by a receptor ligand such as thrombin, tissue-type plasminogen activator (tPA) and von Willebrand factor (vWf) will be acutely released from human umbilical vein endothelial cells (HUVEC). However, the mechanisms involved in the secretion of these two proteins differ in some respects, suggesting that the two proteins may be stored in different secretory granules. By density gradient centrifugation of rat lung homogenates, a particle was identified that contained nearly all tPA activity and antigen. This particle had an average density o

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31

Castaman, Giancarlo, Sofia Helene Giacomelli, Paula M. Jacobi, Tobias Obser, Reinhard Schneppenheim, and Sandra L. Haberichter. "Reduced Von Willebrand Factor Secretion Is Associated with Loss of Weibel-Palade Formation." Blood 116, no. 21 (2010): 541. http://dx.doi.org/10.1182/blood.v116.21.541.541.

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Abstract Abstract 541 Background. Von Willebrand Disease (VWD) is caused by mutations in von Willebrand factor (VWF) that have different pathophysiologic effect in causing low plasma VWF levels. Type 1 VWD includes patients with quantitative plasma VWF deficiency with normal VWF structure and function. Aim of the study. We report three different novel type 1 VWF mutations (A1716P, C2190Y and R2663C) which although located in different VWF domains are associated with reduced secretion and lack of formation of Weibel-Palade body-like granules. Methods. Transient expression of recombinant mutant

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32

Iafrati, Mark D., Olga Vitseva, Kahraman Tanriverdi, et al. "Compensatory mechanisms influence hemostasis in setting of eNOS deficiency." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (2005): H1627—H1632. http://dx.doi.org/10.1152/ajpheart.00819.2004.

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The balance between thrombosis and hemorrhage is carefully regulated. Nitric oxide (NO) is an important mediator of these processes, as it prevents platelet adhesion to the endothelium and inhibits platelet recruitment. Although endothelial NO synthase (eNOS)-deficient mice have decreased vascular reactivity and mild hypertension, enhanced thrombosis in vivo has not been demonstrated. To determine the role of endogenous NO in hemostasis, a model of carotid arterial injury and thrombosis was performed using eNOS-deficient and wild-type mice. Paradoxically, the eNOS-deficient animals had a prolo

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33

Mohamed, Yazidi, Eloutassi Noureddine, Nabih Khadija, Hammi Abdel Hadi, Yazidi Abdelaziz, and Benziane Fouad. "Gestion Des Risques Majeurs Au Maroc: Les Instabilités De Terrain." European Scientific Journal, ESJ 13, no. 12 (2017): 46. http://dx.doi.org/10.19044/esj.2017.v13n12p46.

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Instabilities of the ground is regarded as one of the most serious problems that affect many areas in Morocco. The study is important and beneficial because it concerns various sections of the Rif area. Indeed, certain zones which came at the top have been seriously affected. Disorders are numerous: destruction of homes, loss of agricultural land, and deterioration of infrastructure (roads, railways, and bridges). The aim of this study is focused on the zones where the road network generally is much damaged. This, however, causes a disturbance and even an interruption of the road traffic durin

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34

Groot, Evelyn, Rob Fynheer, Silvie AE Sebastian, Peter J. Lenting, and Philip G. De Groot. "Transition from Non-Platelet-Binding to Platelet-Binding Conformation of Von Willebrand Factor Occurs upon Exocytosis." Blood 112, no. 11 (2008): 3917. http://dx.doi.org/10.1182/blood.v112.11.3917.3917.

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Abstract Introduction Von Willebrand factor (VWF) is a large multimeric glycoprotein that contributes to platelet recruitment at sites of vascular injury. VWF is mainly produced in endothelial cells from where it is secreted directly into the circulation or stored in the rod-shaped organelles called Weibel-Palade bodies. VWF present in the circulation does not bind to platelets. Stimulated endothelial cells secrete VWF that has the capacity to spontaneously interact with platelets. Conversion of the platelet-binding conformation of secreted VWF into the non-binding conformation of plasma VWF i

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35

Rosnoblet, Corinne, Ulrich M. Vischer, Robert D. Gerard, Jean-Claude Irminger, Philippe A. Halban, and Egbert K. O. Kruithof. "Storage of Tissue-Type Plasminogen Activator in Weibel-Palade Bodies of Human Endothelial Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 19, no. 7 (1999): 1796–803. http://dx.doi.org/10.1161/01.atv.19.7.1796.

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36

Monnens, Leo. "Weibel-Palade Bodies-Presumed Role in Clinical Phase of STEC-HUS." Journal of Clinical Haematology 5, no. 1 (2024): 47–51. https://doi.org/10.33696/haematology.5.060.

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In Thrombotic thrombocytopenic purpura ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) activity is deficient and microangiopathy occurs after a second trigger. In Shiga toxin producing Escherichia coli (STEC-HUS) stimulated release of Weibel-Palade bodies (WBP’s) is presumed to be the first hit in damaging Gb3 positive endothelial cells in the diarrhea phase. The objective role of the release of WBP’s components after admission of the patients is not adequately evaluated. Different mechanisms involved in the pathogenesis are discussed and approache

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Barkalow, FJ, MJ Goodman, ME Gerritsen, and TN Mayadas. "Brain endothelium lack one of two pathways of P-selectin-mediated neutrophil adhesion." Blood 88, no. 12 (1996): 4585–93. http://dx.doi.org/10.1182/blood.v88.12.4585.bloodjournal88124585.

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P-selectin, an endothelial leukocyte adhesion receptor, is rapidly translocated to the cell surface upon release from storage granules called Weibel-Palade bodies and is also transcriptionally upregulated upon cytokine stimulation of endothelial cells (ECs). These two pathways of surface expression are coincident with the rapid and cytokine-inducible pathway of neutrophil adhesion to ECs. Constitutive P-selectin expression is largely absent in cultured murine brain microvascular EC (BMEC) monolayers, but interleukin-1beta and tumor necrosis factor-alpha stimulation for 4 hours leads to dramati

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38

Dekker, Rob J., Reinier A. Boon, Mariska G. Rondaij, et al. "KLF2 provokes a gene expression pattern that establishes functional quiescent differentiation of the endothelium." Blood 107, no. 11 (2006): 4354–63. http://dx.doi.org/10.1182/blood-2005-08-3465.

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Abstract The flow-responsive transcription factor KLF2 is acquiring a leading role in the regulation of endothelial cell gene expression. A genome-wide microarray expression profiling is described employing lentivirus-mediated, 7-day overexpression of human KLF2 at levels observed under prolonged flow. KLF2 is not involved in lineage typing, as 42 endothelial-specific markers were unaffected. Rather, KLF2 generates a gene transcription profile (> 1000 genes) affecting key functional pathways such as cell migration, vasomotor function, inflammation, and hemostasis and induces a morphology ch

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39

Dadkhahi, Sara, Julia Gansler, Mona Saffarzadeh, et al. "Expression and localisation of vascular ribonucleases in endothelial cells." Thrombosis and Haemostasis 105, no. 02 (2011): 345–55. http://dx.doi.org/10.1160/th10-06-0345.

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SummaryThe functions of extracellular RNA in the vascular system as new procoagulatory and permeability-increasing factor in vivoand in vitrowere shown to be counteracted by pancreatic type RNase1. Based on the identification of RNase1 in plasma and serum, it is proposed that the enzyme is expressed by vascular cells to contribute in the regulation of extracellular RNA. It is demonstrated that RNase1 and RNase5 (also termed angiogenin) were differentially expressed in various types of endothelial cells, whereby human umbilical vein endothelial cells (HUVEC) expressed and released the highest c

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40

Zeghloul, A., M. Mliha-Touati, and S. Bakir. "Étude des domaines d'existence des instabilités plastiques du type Portevin-Le Chatelier dans l'alliage d'aluminium-magnesium AG3." Journal de Physique III 6, no. 11 (1996): 1467–78. http://dx.doi.org/10.1051/jp3:1996196.

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41

Dieckmann, M. E., J. D. Riordan, and A. Pe'er. "Change of a Weibel-type to an Alfvénic shock in pair plasma by upstream waves." Physics of Plasmas 27, no. 6 (2020): 062107. http://dx.doi.org/10.1063/5.0003596.

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42

Fiedler, Ulrike, Marion Scharpfenecker, Stefanie Koidl, et al. "The Tie-2 ligand Angiopoietin-2 is stored in and rapidly released upon stimulation from endothelial cell Weibel-Palade bodies." Blood 103, no. 11 (2004): 4150–56. http://dx.doi.org/10.1182/blood-2003-10-3685.

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Abstract The angiopoietins Ang-1 and Ang-2 have been identified as ligands with opposing functions of the receptor tyrosine kinase Tie-2 regulating endothelial cell survival and vascular maturation. Ang-1 acts in a paracrine agonistic manner, whereas Ang-2 appears to act primarily as an autocrine antagonistic regulator. To shed further light on the complexity of autocrine/paracrine agonistic/antagonistic functions of the angiopoietin/Tie-2 system, we have studied Ang-2 synthesis and secretion in different populations of wild-type and retrovirally Ang-2–transduced endothelial cells. Endogenous

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43

Haberichter, Sandra L., Paula Jacobi, and Robert R. Montgomery. "Critical independent regions in the VWF propeptide and mature VWF that enable normal VWF storage." Blood 101, no. 4 (2003): 1384–91. http://dx.doi.org/10.1182/blood-2002-07-2281.

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Von Willebrand factor (VWF) is synthesized in endothelial cells, where it is stored in Weibel-Palade bodies. Administration of 1-desamino-8-D-arginine-vasopressin (DDAVP) to patients with type 1 von Willebrand disease and to healthy individuals causes a rapid increase in plasma VWF levels. This increase is the result of stimulated release of VWF from Weibel-Palade bodies in certain beds of endothelial cells. The VWF propeptide (VWFpp) targets VWF to storage granules through a noncovalent association. The nature of the VWFpp/VWF interaction was investigated by using cross-species differences in

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André, Patrick, Cécile V. Denis, Jerry Ware, et al. "Platelets adhere to and translocate on von Willebrand factor presented by endothelium in stimulated veins." Blood 96, no. 10 (2000): 3322–28. http://dx.doi.org/10.1182/blood.v96.10.3322.

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Abstract With the use of intravital microscopy, a new type of platelet–endothelial interaction in mouse mesenteric venules at low shear (80-100 seconds−1) is described. Stimulation of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation without the formation of aggregates. This stop-and-go process reached a maximum in approximately 1 minute, when approximately 25 000 platelets adhered/mm2·s, and then adhesion progressively decreased. This adhesion process was dependent on von Willebr

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45

André, Patrick, Cécile V. Denis, Jerry Ware, et al. "Platelets adhere to and translocate on von Willebrand factor presented by endothelium in stimulated veins." Blood 96, no. 10 (2000): 3322–28. http://dx.doi.org/10.1182/blood.v96.10.3322.h8003322_3322_3328.

Full text

Abstract:

With the use of intravital microscopy, a new type of platelet–endothelial interaction in mouse mesenteric venules at low shear (80-100 seconds−1) is described. Stimulation of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation without the formation of aggregates. This stop-and-go process reached a maximum in approximately 1 minute, when approximately 25 000 platelets adhered/mm2·s, and then adhesion progressively decreased. This adhesion process was dependent on von Willebrand facto

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46

Chauhan, Anil K., Janka Kiucka, Alexander Brill, Meghan T. Walsh, and Denisa D. Wagner. "Deficiency of the VWF-Cleaving Protease ADAMTS13 Results in Increased Leukocyte Rolling and Adhesion in Mice." Blood 110, no. 11 (2007): 290. http://dx.doi.org/10.1182/blood.v110.11.290.290.

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Abstract von Willebrand factor (VWF) is synthesized in megakaryocytes and endothelial cells and stored in a-granules and Weibel-Palade bodies, respectively. VWF levels are elevated in both chronic and acute inflammation. ADAMTS13 (A D isintegrin-like A nd M etalloprotease with T hrombo s pondin type I repeats-13) is a metalloprotease that cleaves ultra large von Willebrand factor (ULVWF) multimers quickly after its release from endothelium. Recent studies have found that VWF promotes leukocyte adhesion in vitro and that ADAMTS13 activity is reduced in inflammation and sepsis. We hypothesized t

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Ewenstein, BM, A. Inbal, JS Pober, and RI Handin. "Molecular studies of von Willebrand disease: reduced von Willebrand factor biosynthesis, storage, and release in endothelial cells derived from patients with type I von Willebrand disease [published erratum appears in Blood 1990 Nov 1;76(9):1901]." Blood 75, no. 7 (1990): 1466–72. http://dx.doi.org/10.1182/blood.v75.7.1466.1466.

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Abstract Endothelial cells were cultured from the umbilical veins of two neonates with type I von Willebrand disease (vWD) and compared with cells cultured in parallel from normal control umbilical veins. In both cases, cultured vWD endothelial cells contained less messenger RNA (mRNA) encoding von Willebrand factor (vWF), and constitutively secreted two- to fourfold less vWF protein than their matched controls. Regulated secretion of stored vWF induced by thrombin or phorbol-12- myristate-13-acetate (PMA) was also diminished in vWD cells. Both the mRNA and protein produced by each of these ty

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48

Ewenstein, BM, A. Inbal, JS Pober, and RI Handin. "Molecular studies of von Willebrand disease: reduced von Willebrand factor biosynthesis, storage, and release in endothelial cells derived from patients with type I von Willebrand disease [published erratum appears in Blood 1990 Nov 1;76(9):1901]." Blood 75, no. 7 (1990): 1466–72. http://dx.doi.org/10.1182/blood.v75.7.1466.bloodjournal7571466.

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Abstract:

Endothelial cells were cultured from the umbilical veins of two neonates with type I von Willebrand disease (vWD) and compared with cells cultured in parallel from normal control umbilical veins. In both cases, cultured vWD endothelial cells contained less messenger RNA (mRNA) encoding von Willebrand factor (vWF), and constitutively secreted two- to fourfold less vWF protein than their matched controls. Regulated secretion of stored vWF induced by thrombin or phorbol-12- myristate-13-acetate (PMA) was also diminished in vWD cells. Both the mRNA and protein produced by each of these type I vWD

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Daidone, Viviana, Giovanni Barbon, Elena Pontara, et al. "Loss of cysteine 584 impairs the storage and release, but not the synthesis of von Willebrand factor." Thrombosis and Haemostasis 112, no. 12 (2014): 1159–66. http://dx.doi.org/10.1160/th14-04-0391.

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SummaryCysteines play a key part in von Willebrand factor (VWF) dimerisation and polymerisation, and their loss may severely affect VWF structure and function. We report on three patients with type 3 von Willebrand disease carrying the new c.1751G>T missense mutation that induces the substitution of cysteine 584 by phenylalanine (C584F), and the deletion of seven nucleotides in exon 7 (c.729_735del), producing a premature stop codon at position 454 (E244Lfs*211). VWF was almost undetectable in the patients’ plasma and platelets, while a single, poorly represented, oligomer emerged on plasma

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Rosnoblet, Corinne, Corinne Di Sanza, Egbert Kruithof, and Michael Pepper. "Synergistic Induction of t-PA by Vascular Endothelial Growth Factor and Basic Fibroblast Growth Factor and Localization of t-PA to Weibel-Palade Bodies in Bovine Microvascular Endothelial Cells." Thrombosis and Haemostasis 86, no. 08 (2001): 702–9. http://dx.doi.org/10.1055/s-0037-1616107.

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SummaryEndothelial cell migration is stimulated by members of the vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) families, and is dependent on extracellular proteolytic activity provided by enzymes of the plasminogen activator (PA) system. Here we report that in bovine microvascular endothelial cells (BME cells), bFGF principally increased urokinase-type PA (u-PA) while tissue-type PA (t-PA) was increased mainly by VEGF. In bovine aortic endothelial cells (BAE cells), bFGF increased u-PA, whereas VEGF had no effect. Co-added bFGF and VEGF increased t-PA mRN

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