122,707 research outputs found
Combustion and Society: A Fire-Centred History of Energy Use
Get PDFFire is a force that links everyday human activities to some of the most powerful energetic movements of the Earth. Drawing together the energy-centred social theory of Georges Bataille, the fire-centred environmental history of Stephen Pyne, and the work of a number of ‘pyrotechnology’ scholars, the paper proposes that the generalized study of combustion is a key to contextualizing human energetic practices within a broader ‘economy’ of terrestrial and cosmic energy flows. We examine the relatively recent turn towards fossil-fuelled ‘internal combustion’ in the light of a much longer human history of ‘broadcast’ burning of vegetation and of artisanal pyrotechnologies – the use of heat to transform diverse materials. A combustion-centred analysis, it is argued, brings human collective life into closer contact with the geochemical and geologic conditions of earthly existence, while also pointing to the significance of explorative, experimental and even playful dispositions towards energy and matter. © 2014, SAGE Publications. All rights reserved
On the Power of Regular and Permutation Branching Programs
Get PDFWe give new upper and lower bounds on the power of several restricted classes of arbitrary-order read-once branching programs (ROBPs) and standard-order ROBPs (SOBPs) that have received significant attention in the literature on pseudorandomness for space-bounded computation.
- Regular SOBPs of length n and width ⌊w(n+1)/2⌋ can exactly simulate general SOBPs of length n and width w, and moreover an n/2-o(n) blow-up in width is necessary for such a simulation. Our result extends and simplifies prior average-case simulations (Reingold, Trevisan, and Vadhan (STOC 2006), Bogdanov, Hoza, Prakriya, and Pyne (CCC 2022)), in particular implying that weighted pseudorandom generators (Braverman, Cohen, and Garg (SICOMP 2020)) for regular SOBPs of width poly(n) or larger automatically extend to general SOBPs. Furthermore, our simulation also extends to general (even read-many) oblivious branching programs.
- There exist natural functions computable by regular SOBPs of constant width that are average-case hard for permutation SOBPs of exponential width. Indeed, we show that Inner-Product mod 2 is average-case hard for arbitrary-order permutation ROBPs of exponential width.
- There exist functions computable by constant-width arbitrary-order permutation ROBPs that are worst-case hard for exponential-width SOBPs.
- Read-twice permutation branching programs of subexponential width can simulate polynomial-width arbitrary-order ROBPs
Ann Pyne : une poétique de l'indistinct
No full textGrimal Claude. Ann Pyne : une poétique de l'indistinct. In: Cahiers Charles V, n°29, décembre 2000. États-Unis : formes récentes de l’imagination littéraire (Travaux de l’Observatoire de Littérature Américaine -ODELA) pp. 159-165
Bradykinin-stimulated phosphatidate and 1,2-diacylglycerol accumulation in guinea-pig airway smooth muscle: evidence for regulation 'down-stream' of phospholipases
No full textBradykinin-treatment of cultured airway smooth muscle (ASM) induced the formation of [3H]1,2-diacylglycerol ([3H]1,2-DG), [3H]1,3-diacylglycerol ([3H]1,3-DG) and [3H]phosphatidic acid ([3H]PtdOH) in [3H]palmitate-labelled cells and of [3H]choline in [3H]methyl choline-labelled cells. [3H]1,2-DG and [3H]1,3-DG responses were biphasic with an initial transient phase from 0-2 min and a second sustained phase to 10 min. In contrast, [3H]PtdOH accumulation plateaued at 2 min stimulation as did [3H]choline formation. The bradykinin-stimulated [3H]1,2-DG and [3H]PtdOH responses exhibited similar concentration dependencies (EC50 values: [3H]1,2-DG 5.14 +/- 2.82 nM; [3H]1,3-DG 4.95 +/- 1.12 nM; [3H]PtdOH 1.52 +/- 0.82 nM). In contrast, PMA elicited a [3H]PtdOH response, but was without effect upon [3H]DG levels. Bradykinin-induced accumulation of [3H]1,2-DG and [3H]PtdOH was insensitive to blockade by a bradykinin B2-receptor antagonist, NPC567 (40 microM) and the B1-receptor agonist, Des-Arg9-bradykinin, (10 microM) failed to elicit a response. These observations are similar to those obtained previously for bradykinin-stimulated phospholipase D activity in ASM (Pyne S. and Pyne N. J., Br. J. Pharmac. 110, 477-481, 1993). Thus, both bradykinin-stimulated 1,2-DG and PtdOH accumulation may also be regulated via a novel B3-receptor. Bradykinin-stimulated formation of [3H]PtdOH was partially inhibited by butan-1-ol (by 47.25 +/- 12.7%, n = 3) which had no effect upon basal or bradykinin-stimulated levels of [3H]1,2-DG or upon basal [3H]PtdOH
Hitting Sets for Regular Branching Programs
Get PDFWe construct improved hitting set generators (HSGs) for ordered (read-once) regular branching programs in two parameter regimes. First, we construct an explicit ε-HSG for unbounded-width regular branching programs with a single accept state with seed length Õ(log n ⋅ log(1/ε)), where n is the length of the program. Second, we construct an explicit ε-HSG for width-w length-n regular branching programs with seed length Õ(log n ⋅ (√{log(1/ε)} + log w) + log(1/ε)). For context, the "baseline" in this area is the pseudorandom generator (PRG) by Nisan (Combinatorica 1992), which fools ordered (possibly non-regular) branching programs with seed length O(log(wn/ε) ⋅ log n). For regular programs, the state-of-the-art PRG, by Braverman, Rao, Raz, and Yehudayoff (FOCS 2010, SICOMP 2014), has seed length Õ(log(w/ε) ⋅ log n), which beats Nisan’s seed length when log(w/ε) = o(log n). Taken together, our two new constructions beat Nisan’s seed length in all parameter regimes except when log w and log(1/ε) are both Ω(log n) (for the construction of HSGs for regular branching programs with a single accept vertex).
Extending work by Reingold, Trevisan, and Vadhan (STOC 2006), we furthermore show that an explicit HSG for regular branching programs with a single accept vertex with seed length o(log² n) in the regime log w = Θ(log(1/ε)) = Θ(log n) would imply improved HSGs for general ordered branching programs, which would be a major breakthrough in derandomization. Pyne and Vadhan (CCC 2021) recently obtained such parameters for the special case of permutation branching programs
Pseudodistributions That Beat All Pseudorandom Generators (Extended Abstract)
Get PDFA recent paper of Braverman, Cohen, and Garg (STOC 2018) introduced the concept of a weighted pseudorandom generator (WPRG), which amounts to a pseudorandom generator (PRG) whose outputs are accompanied with real coefficients that scale the acceptance probabilities of any potential distinguisher. They gave an explicit construction of WPRGs for ordered branching programs whose seed length has a better dependence on the error parameter ε than the classic PRG construction of Nisan (STOC 1990 and Combinatorica 1992).
In this work, we give an explicit construction of WPRGs that achieve parameters that are impossible to achieve by a PRG. In particular, we construct a WPRG for ordered permutation branching programs of unbounded width with a single accept state that has seed length Õ(log^{3/2} n) for error parameter ε = 1/poly(n), where n is the input length. In contrast, recent work of Hoza et al. (ITCS 2021) shows that any PRG for this model requires seed length Ω(log² n) to achieve error ε = 1/poly(n).
As a corollary, we obtain explicit WPRGs with seed length Õ(log^{3/2} n) and error ε = 1/poly(n) for ordered permutation branching programs of width w = poly(n) with an arbitrary number of accept states. Previously, seed length o(log² n) was only known when both the width and the reciprocal of the error are subpolynomial, i.e. w = n^{o(1)} and ε = 1/n^{o(1)} (Braverman, Rao, Raz, Yehudayoff, FOCS 2010 and SICOMP 2014).
The starting point for our results are the recent space-efficient algorithms for estimating random-walk probabilities in directed graphs by Ahmadenijad, Kelner, Murtagh, Peebles, Sidford, and Vadhan (FOCS 2020), which are based on spectral graph theory and space-efficient Laplacian solvers. We interpret these algorithms as giving WPRGs with large seed length, which we then derandomize to obtain our results. We also note that this approach gives a simpler proof of the original result of Braverman, Cohen, and Garg, as independently discovered by Cohen, Doron, Renard, Sberlo, and Ta-Shma (these proceedings)
Pseudorandom Linear Codes Are List-Decodable to Capacity
Get PDFWe introduce a novel family of expander-based error correcting codes. These codes can be sampled with randomness linear in the block-length, and achieve list decoding capacity (among other local properties). Our expander-based codes can be made starting from any family of sufficiently low-bias codes, and as a consequence, we give the first construction of a family of algebraic codes that can be sampled with linear randomness and achieve list-decoding capacity. We achieve this by introducing the notion of a pseudorandom puncturing of a code, where we select n indices of a base code C ⊂ _q^m in a correlated fashion. Concretely, whereas a random linear code (i.e. a truly random puncturing of the Hadamard code) requires O(n log(m)) random bits to sample, we sample a pseudorandom linear code with O(n + log (m)) random bits by instantiating our pseudorandom puncturing as a length n random walk on an exapnder graph on [m]. In particular, we extend a result of Guruswami and Mosheiff (FOCS 2022) and show that a pseudorandom puncturing of a small-bias code satisfies the same local properties as a random linear code with high probability. As a further application of our techniques, we also show that pseudorandom puncturings of Reed-Solomon codes are list-recoverable beyond the Johnson bound, extending a result of Lund and Potukuchi (RANDOM 2020). We do this by instead analyzing properties of codes with large distance, and show that pseudorandom puncturings still work well in this regime
Role of sphingosine 1-phosphate receptors, sphingosine kinases and sphingosine in cancer and inflammation
Get PDFSphingosine kinase (there are two isoforms, SK1 and SK2) catalyses the formation of sphingosine 1-phosphate (S1P), a bioactive lipid that can be released from cells to activate a family of G protein-coupled receptors, termed S1P1-5. In addition, S1P can bind to intracellular target proteins, such as HDAC1/2, to induce cell responses. There is increasing evidence of a role for S1P receptors (e.g. S1P4) and SK1 in cancer, where high expression of these proteins in ER negative breast cancer patient tumours is linked with poor prognosis. Indeed, evidence will be presented here to demonstrate that S1P4 is functionally linked with SK1 and the oncogene HER2 (ErbB2) to regulate mitogen-activated protein kinase pathways and growth of breast cancer cells. Although much emphasis is placed on SK1 in terms of involvement in oncogenesis, evidence will also be presented for a role of SK2 in both T-cell and B-cell acute lymphoblastic leukemia. In patient T-ALL lymphoblasts and T-ALL cell lines, we have demonstrated that SK2 inhibitors promote T-ALL cell death via autophagy and induce suppression of c-myc and PI3K/AKT pathways. We will also present evidence demonstrating that certain SK inhibitors promote oxidative stress and protein turnover via proteasomal degradative pathways linked with induction of p53-and p21-induced growth arrest. In addition, the SK1 inhibitor, PF-543 exacerbates disease progression in an experimental autoimmune encephalomyelitis mouse model indicating that SK1 functions in an anti-inflammatory manner. Indeed, sphingosine, which accumulates upon inhibition of SK1 activity, and sphingosine-like compounds promote activation of the inflammasome, which is linked with multiple sclerosis, to stimulate formation of the pro-inflammatory mediator, IL-1β. Such compounds could be exploited to produce antagonists that diminish exaggerated inflammation in disease. The therapeutic potential of modifying the SK-S1P receptor pathway in cancer and inflammation will therefore, be reviewed
Local Access to Random Walks
Get PDFFor a graph G on n vertices, naively sampling the position of a random walk of at time t requires work Ω(t). We desire local access algorithms supporting position_G(t) queries, which return the position of a random walk from some fixed start vertex s at time t, where the joint distribution of returned positions is 1/poly(n) close to those of a uniformly random walk in ₁ distance.
We first give an algorithm for local access to random walks on a given undirected d-regular graph with Õ(1/(1-λ)√n) runtime per query, where λ is the second-largest eigenvalue of the random walk matrix of the graph in absolute value. Since random d-regular graphs G(n,d) are expanders with high probability, this gives an Õ(√n) algorithm for a graph drawn from G(n,d) whp, which improves on the naive method for small numbers of queries.
We then prove that no algorithm with subconstant error given probe access to an input d-regular graph can have runtime better than Ω(√n/log(n)) per query in expectation when the input graph is drawn from G(n,d), obtaining a nearly matching lower bound. We further show an Ω(n^{1/4}) runtime per query lower bound even with an oblivious adversary (i.e. when the query sequence is fixed in advance).
We then show that for families of graphs with additional group theoretic structure, dramatically better results can be achieved. We give local access to walks on small-degree abelian Cayley graphs, including cycles and hypercubes, with runtime polylog(n) per query. This also allows for efficient local access to walks on polylog degree expanders. We show that our techniques apply to graphs with high degree by extending or results to graphs constructed using the tensor product (giving fast local access to walks on degree n^ε graphs for any ε ∈ (0,1]) and Cartesian product
Bradykinin stimulates cAMP synthesis via mitogen-activated protein kinase-dependent regulation of cytosolic phospholipase A2 and prostaglandin E2 release in airway smooth muscle
No full textBradykinin stimulates cAMP synthesis in cultured airway smooth muscle (ASM) cells. This occurs via a pathway that involves: (1) the protein kinase C (PKC)-dependent activation of mitogen-activated protein kinase (MAPK); (2) the MAPK-dependent phosphorylation and activation of cytosolic phospholipase A2 (cPLA2) and (3) the utilization of cPLA2-derived arachidonate by the cyclo-oxygenase pathway to produce prostaglandin E2 (PGE2). PGE2 is released and binds to cell surface receptors to stimulate intracellular cAMP synthesis. The signalling pathway was confirmed by the use of PD098059 [the inhibitor of MAPK kinase-1 (MEK-1) activation], AACOCF3 (an inhibitor of cPLA2) and indomethacin (an inhibitor of cyclo-oxygenase), which all reduced bradykinin-stimulated cAMP synthesis. Bradykinin also elicits the inhibition of approx. 60% of the total cAMP phosphodiesterase activity in the cell [Stevens, Pyne, Grady and Pyne (1994) Biochem. J. 297, 233-239]. This is likely to decrease the rate of cAMP degradation markedly and therefore to potentiate PGE2-stimulated cAMP synthesis. Acute treatment of ASM cells with PMA (a direct activator of PKC) also stimulated the MAPK-dependent phosphorylation of cPLA2. However, in contrast with bradykinin, PMA did not stimulate arachidonate release, suggesting that additional signals (e.g. Ca2+ ions) are required for phosphorylation by MAPK to activate cPLA2. PMA was also without effect on PGE2 release and cAMP synthesis. Evidence that PKC can also directly regulate adenylate cyclase was obtained by using cells pretreated with cholera toxin. Under these conditions, PMA stimulated cAMP synthesis independently of arachidonate metabolites. Furthermore the combined treatment of cells with PMA (to activate PKC) and PGE2 (to activate Gs) stimulated synergistic cAMP synthesis. This might be due to the presence of the type 2 adenylate cyclase, which is synergistically activated by Gs and PKC
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