Black Hole Superradiance in Dynamical Spacetime

We study the superradiant scattering of gravitational waves by a nearly extremal black hole (dimensionless spin $a=0.99$) by numerically solving the full Einstein field equations, thus including backreaction effects. This allows us to study the dynamics of the black hole as it loses energy and angular momentum during the scattering process. To explore the nonlinear phase of the interaction, we consider gravitational wave packets with initial energies up to $10$ of the mass of the black hole. We find that as the incident wave energy increases, the amplification of the scattered waves, as well as the energy extraction efficiency from the black hole, is reduced. During the interaction the apparent horizon geometry undergoes sizable nonaxisymmetric oscillations. The largest amplitude excitations occur when the peak frequency of the incident wave packet is above where superradiance occurs, but close to the dominant quasinormal mode frequency of the black hole.Comment: 5 pages, 4 figures; revised to match PRD versio

Spacetime Dynamics of a Higgs Vacuum Instability During Inflation

A remarkable prediction of the Standard Model is that, in the absence of corrections lifting the energy density, the Higgs potential becomes negative at large field values. If the Higgs field samples this part of the potential during inflation, the negative energy density may locally destabilize the spacetime. We use numerical simulations of the Einstein equations to study the evolution of inflation-induced Higgs fluctuations as they grow towards the true (negative-energy) minimum. These simulations show that forming a single patch of true vacuum in our past light cone during inflation is incompatible with the existence of our Universe; the boundary of the true vacuum region grows outward in a causally disconnected manner from the crunching interior, which forms a black hole. We also find that these black hole horizons may be arbitrarily elongated---even forming black strings---in violation of the hoop conjecture. By extending the numerical solution of the Fokker-Planck equation to the exponentially suppressed tails of the field distribution at large field values, we derive a rigorous correlation between a future measurement of the tensor-to-scalar ratio and the scale at which the Higgs potential must receive stabilizing corrections in order for the Universe to have survived inflation until today.Comment: 36 pages, 11 figures; revised to match published versio

A role for TSPO in mitochondrial Ca2+ homeostasis and redox stress signaling

The 18 kDa translocator protein TSPO localizes on the outer mitochondrial membrane (OMM). Systematically overexpressed at sites of neuroinflammation it is adopted as a biomarker of brain conditions. TSPO inhibits the autophagic removal of mitochondria by limiting PARK2-mediated mitochondrial ubiquitination via a peri-organelle accumulation of reactive oxygen species (ROS). Here we describe that TSPO deregulates mitochondrial Ca2+ signaling leading to a parallel increase in the cytosolic Ca2+ pools that activate the Ca2+-dependent NADPH oxidase (NOX) thereby increasing ROS. The inhibition of mitochondrial Ca2+ uptake by TSPO is a consequence of the phosphorylation of the voltage-dependent anion channel (VDAC1) by the protein kinase A (PKA), which is recruited to the mitochondria, in complex with the Acyl-CoA binding domain containing 3 (ACBD3). Notably, the neurotransmitter glutamate, which contributes neuronal toxicity in age-dependent conditions, triggers this TSPO-dependent mechanism of cell signaling leading to cellular demise. TSPO is therefore proposed as a novel OMM-based pathway to control intracellular Ca2+ dynamics and redox transients in neuronal cytotoxicity

PMI: A Delta Psi(m) Independent Pharmacological Regulator of Mitophagy

Mitophagy is central to mitochondrial and cellular homeostasis and operates via the PINK1/Parkin pathway targeting mitochondria devoid of membrane potential (ΔΨm) to autophagosomes. Although mitophagy is recognized as a fundamental cellular process, selective pharmacologic modulators of mitophagy are almost nonexistent. We developed a compound that increases the expression and signaling of the autophagic adaptor molecule P62/SQSTM1 and forces mitochondria into autophagy. The compound, P62-mediated mitophagy inducer (PMI), activates mitophagy without recruiting Parkin or collapsing ΔΨm and retains activity in cells devoid of a fully functional PINK1/Parkin pathway. PMI drives mitochondria to a process of quality control without compromising the bio-energetic competence of the whole network while exposing just those organelles to be recycled. Thus, PMI circumvents the toxicity and some of the nonspecific effects associated with the abrupt dissipation of ΔΨm by ionophores routinely used to induce mitophagy and represents a prototype pharmacological tool to investigate the molecular mechanisms of mitophagy

Infinite partition monoids

Let $\mathcal P_X$ and $\mathcal S_X$ be the partition monoid and symmetric group on an infinite set $X$. We show that $\mathcal P_X$ may be generated by $\mathcal S_X$ together with two (but no fewer) additional partitions, and we classify the pairs $\alpha,\beta\in\mathcal P_X$ for which $\mathcal P_X$ is generated by $\mathcal S_X\cup\{\alpha,\beta\}$. We also show that $\mathcal P_X$ may be generated by the set $\mathcal E_X$ of all idempotent partitions together with two (but no fewer) additional partitions. In fact, $\mathcal P_X$ is generated by $\mathcal E_X\cup\{\alpha,\beta\}$ if and only if it is generated by $\mathcal E_X\cup\mathcal S_X\cup\{\alpha,\beta\}$. We also classify the pairs $\alpha,\beta\in\mathcal P_X$ for which $\mathcal P_X$ is generated by $\mathcal E_X\cup\{\alpha,\beta\}$. Among other results, we show that any countable subset of $\mathcal P_X$ is contained in a $4$-generated subsemigroup of $\mathcal P_X$, and that the length function on $\mathcal P_X$ is bounded with respect to any generating set

Digital Electronic Communications Between ICU Ventilators and Computers and Printers

journal articleBiomedical Informatic

In search of ‘lost’ knowledge and outsourced expertise in flood risk management

This paper examines the parallel discourses of ‘lost’ local flood expertise and the growing use of commercial consultancies to outsource aspects of flood risk work. We critically examine the various claims and counter-claims about lost, local and external expertise in flood management, focusing on the aftermath of the 2007 floods in East Yorkshire, England. Drawing on interviews with consultants, drainage engineers and others, we caution against claims that privilege ‘local’ floods knowledge as ‘good’ and expert knowledge as somehow suspect. This paper urges carefulness in interpreting claims about local knowledge, arguing that it is important always to think instead of hybrid knowledge formations. We conclude by arguing that experiments in the co-production of flood risk knowledge need to be seen as part of a spectrum of ways for producing shared knowledge