13 research outputs found
Non-extremal Black Hole Microstates: Fuzzballs of Fire or Fuzzballs of Fuzz ?
We construct the first family of microstate geometries of near-extremal black
holes, by placing metastable supertubes inside certain scaling supersymmetric
smooth microstate geometries. These fuzzballs differ from the classical black
hole solution macroscopically at the horizon scale, and for certain probes the
fluctuations between various fuzzballs will be visible as thermal noise far
away from the horizon. We discuss whether these fuzzballs appear to infalling
observers as fuzzballs of fuzz or as fuzzballs of fire. The existence of these
solutions suggests that the singularity of non-extremal black holes is resolved
all the way to the outer horizon and this "backwards in time" singularity
resolution can shed light on the resolution of spacelike cosmological
singularities.Comment: 34 pages, 10 figure
Metastable Supertubes and non-extremal Black Hole Microstates
We study the dynamics of supertubes in smooth bubbling geometries with three
charges and three dipole charges that can describe black holes, black rings and
their microstates. We find the supertube Hamiltonian in these backgrounds and
show that there exist metastable supertube configurations, that can decay into
supersymmetric and non-supersymmetric ones via brane-flux annihilation. We also
find stable non-supersymmetric configurations. Both the metastable and the
stable non-supersymmetric configuration are expected to describe microstate
geometries for non-extremal black holes, and we discuss the implication of
their existence for the fuzzball proposal.Comment: 25 pages, 9 figure
Mitochondria Are a Subset of Extracellular Vesicles Released by Activated Monocytes and Induce Type I IFN and TNF Responses in Endothelial Cells.
Extracellular vesicles, including microvesicles, are increasingly recognized as important mediators in cardiovascular disease. The cargo and surface proteins they carry are considered to define their biological activity, including their inflammatory properties. Monocyte to endothelial cell signaling is a prerequisite for the propagation of inflammatory responses. However, the contribution of microvesicles in this process is poorly understood. OBJECTIVE: To elucidate the mechanisms by which microvesicles derived from activated monocytic cells exert inflammatory effects on endothelial cells. METHODS AND RESULTS: LPS (lipopolysaccharide)-stimulated monocytic cells release free mitochondria and microvesicles with mitochondrial content as demonstrated by flow cytometry, quantitative polymerase chain reaction, Western Blot, and transmission electron microscopy. Using RNAseq analysis and quantitative reverse transcription-polymerase chain reaction, we demonstrated that both mitochondria directly isolated from and microvesicles released by LPS-activated monocytic cells, as well as circulating microvesicles isolated from volunteers receiving low-dose LPS-injections, induce type I IFN (interferon), and TNF (tumor necrosis factor) responses in endothelial cells. Depletion of free mitochondria significantly reduced the ability of these microvesicles to induce type I IFN and TNF-dependent genes. We identified mitochondria-associated TNFα and RNA from stressed mitochondria as major inducers of these responses. Finally, we demonstrated that the proinflammatory potential of microvesicles and directly isolated mitochondria were drastically reduced when they were derived from monocytic cells with nonrespiring mitochondria or monocytic cells cultured in the presence of pyruvate or the mitochondrial reactive oxygen species scavenger MitoTEMPO. CONCLUSIONS: Mitochondria and mitochondria embedded in microvesicles constitute a major subset of extracellular vesicles released by activated monocytes, and their proinflammatory activity on endothelial cells is determined by the activation status of their parental cells. Thus, mitochondria may represent critical intercellular mediators in cardiovascular disease and other inflammatory settings associated with type I IFN and TNF signaling