275 research outputs found
Regulation of Calcium-Permeable TRPV2 Channel by Insulin in Pancreatic β-Cells
OBJECTIVE—Calcium-permeable cation channel TRPV2 is expressed in pancreatic β-cells. We investigated regulation and function of TRPV2 in β-cells
Comments on black holes I: The possibility of complementarity
We comment on a recent paper of Almheiri, Marolf, Polchinski and Sully who
argue against black hole complementarity based on the claim that an infalling
observer 'burns' as he approaches the horizon. We show that in fact
measurements made by an infalling observer outside the horizon are
statistically identical for the cases of vacuum at the horizon and radiation
emerging from a stretched horizon. This forces us to follow the dynamics all
the way to the horizon, where we need to know the details of Planck scale
physics. We note that in string theory the fuzzball structure of microstates
does not give any place to 'continue through' this Planck regime. AMPS argue
that interactions near the horizon preclude traditional complementarity. But
the conjecture of 'fuzzball complementarity' works in the opposite way: the
infalling quantum is absorbed by the fuzzball surface, and it is the resulting
dynamics that is conjectured to admit a complementary description.Comment: 34 pages, 6 figures, v3: clarifications & references adde
Staphylococcus aureus Induces Eosinophil Cell Death Mediated by α-hemolysin
Staphylococcus aureus, a major human pathogen, exacerbates allergic disorders, including atopic dermatitis, nasal polyps and asthma, which are characterized by tissue eosinophilia. Eosinophils, via their destructive granule contents, can cause significant tissue damage, resulting in inflammation and further recruitment of inflammatory cells. We hypothesised that the relationship between S. aureus and eosinophils may contribute to disease pathology. We found that supernatants from S. aureus (SH1000 strain) cultures cause rapid and profound eosinophil necrosis, resulting in dramatic cell loss within 2 hours. This is in marked contrast to neutrophil granulocytes where no significant cell death was observed (at equivalent dilutions). Supernatants prepared from a strain deficient in the accessory gene regulator (agr) that produces reduced levels of many important virulence factors, including the abundantly produced α-hemolysin (Hla), failed to induce eosinophil death. The role of Hla in mediating eosinophil death was investigated using both an Hla deficient SH1000-modified strain, which did not induce eosinophil death, and purified Hla, which induced concentration-dependent eosinophil death via both apoptosis and necrosis. We conclude that S. aureus Hla induces aberrant eosinophil cell death in vitro and that this may increase tissue injury in allergic disease
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