Geophysical imaging of stimulated microbial biomineralization

Understanding how microorganisms influence the physical and chemical properties of the subsurface is hindered by our inability to observe microbial dynamics in real time and with high spatial resolution. Here, we investigate the use of noninvasive geophysical methods to monitor biomineralization at the laboratory scale during stimulated sulfate reduction under dynamic flow conditions. Alterations in sediment characteristics resulting from microbe-mediated sulfide mineral precipitation were concomitant with changes in complex resistivity and acoustic wave propagation signatures. The sequestration of zinc and iron in insoluble sulfides led to alterations in the ability of the pore fluid to conduct electrical charge and of the saturated sediments to dissipate acoustic energy. These changes resulted directly from the nucleation, growth, and development of nanoparticulate precipitates along grain surfaces and within the pore space. Scanning and transmission electron microscopy (SEM and TEM) confirmed the sulfides to be associated with cell surfaces, with precipitates ranging from aggregates of individual 3-5 nm nanocrystals to larger assemblages of up to 10-20 m in diameter. Anomalies in the geophysical data reflected the distribution of mineral precipitates and biomass over space and time, with temporal variations in the signals corresponding to changes in the aggregation state of the nanocrystalline sulfides. These results suggest the potential for using geophysical techniques to image certain subsurface biogeochemical processes, such as those accompanying the bioremediation of metal-contaminated aquifers.

Insulin-stimulated protein kinase B phosphorylation on Ser-473 is independent of its activity and occurs through a staurosporine-insensitive kinase

Full activation of protein kinase B (PKB, also called Akt) requires phosphorylation on two regulatory sites, Thr-308 in the activation loop and Ser-473 in the hydrophobic C-terminal regulatory domain (numbering for PKB alpha /Akt-1), Although 3 ' -phosphoinositide-dependent protein kinase 1 (PDK1) has now been identified as the Thr-308 kinase, the mechanism of the Ser-473 phosphorylation remains controversial. As a step to further characterize the Ser-473 kinase, we examined the effects of a range of protein kinase inhibitors on the activation and phosphorylation of PKB. We found that staurosporine, a broad-specificity kinase inhibitor and inducer of cell apoptosis, attenuated PKB activation exclusively through the inhibition of Thr-308 phosphorylation, with Ser-473 phosphorylation unaffected. The increase in Thr-308 phosphorylation because of overexpression of PDK1 was also inhibited by staurosporine, We further show that staurosporine (CGP 39360) potently inhibited PDK1 activity in vitro with an IC50 of similar to0.22 muM. These data indicate that agonist-induced phosphorylation of Ser-473 of PKB is independent of PDK1 or PKB activity and occurs through a distinct Ser-473 kinase that is not inhibited by staurosporine, Moreover, our results suggest that inhibition of PKB signaling is involved in the proapoptotic action of staurosporine.

Hybrid LMS-LMF algorithm for adaptive echo cancellation

The coefficients of an echo canceller with a near-end section and a far-end section are usually updated with the same updating scheme, such as the LMS algorithm. A novel scheme is proposed for echo cancellation that is based on the minimisation of two different cost functions, i.e. one for the near-end section and a different one for the far-end section. The approach considered leads to a substantial improvement in performance over the LMS algorithm when it is applied to both sections of the echo canceller. The convergence properties of the algorithm are derived. The proposed scheme is also shown to be robust to noise variations. Simulation results confirm the superior performance of the new algorithm.

Cost function adaptation: a stochastic gradient algorithm for data echo cancellation

A family of stochastic gradient algorithms and their behaviour in the data echo cancellation work platform are presented. The cost function adaptation algorithms use an error exponent update strategy based on an absolute error mapping, which is updated at every iteration. The quadratic and nonquadratic cost functions are special cases of the new family. Several possible realisations are introduced using these approaches. The noisy error problem is discussed and the digital recursive filter estimator is proposed. The simulation outcomes confirm the effectiveness of the proposed family of algorithms.

Adaptive data echo cancellation using cost function adaptation

For a digital echo canceller it is desirable to reduce the adaptation time, during which the transmission of useful data is not possible. LMS is a non-optimal algorithm in this case as the signals involved are statistically non-Gaussian. Walach and Widrow (IEEE Trans. Inform. Theory 30 (2) (March 1984) 275-283) investigated the use of a power of 4, while other research established algorithms with arbitrary integer (Pei and Tseng, IEEE J. Selected Areas Commun. 12(9)(December 1994) 1540-1547) or non-quadratic power (Shah and Cowan, IEE.Proc.-Vis. Image Signal Process. 142 (3) (June 1995) 187-191). This paper suggests that continuous and automatic, adaptation of the error exponent gives a more satisfactory result. The family of cost function adaptation (CFA) stochastic gradient algorithm proposed allows an increase in convergence rate and, an improvement of residual error. As special case the staircase CFA algorithm is first presented, then the smooth CFA is developed. Details of implementations are also discussed. Results of simulation are provided to show the properties of the proposed family of algorithms. (C) 2000 Elsevier Science B.V. All rights reserved.

Vasodilator-Stimulated Phosphoprotein Regulates Inside-Out Signaling of beta(2) Integrins in Neutrophils

The monomeric GTPase Rap1 controls functional activation of beta2 integrins in leukocytes. In this article, we describe a novel mechanism by which the chemoattractant fMLP activates Rap1 and inside-out signaling of beta2 integrins. We found that fMLP-induced activation of Rap1 in human polymorphonuclear leukocytes or neutrophils and differentiated PLB-985 cells was blocked by inhibitors of the NO/guanosine-3',5'-cyclic monophosphate-dependent protein kinase (cGKI) pathway [N-(3-(aminomethyl)benzyl)acetamidine, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, DT-3 peptide, 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphothioate, Rp-isomer triethylammonium salt-guanosine-3',5'-cyclic monophosphate], indicating that the downstream signaling events in Rap1 activation involve the production of NO and guanosine-3',5'-cyclic monophosphate, as well as the activation of cGKI. Silencing the expression of vasodilator-stimulated phosphoprotein (VASP), a substrate of cGKI, in resting PLB-985 cells or mice neutrophils led to constitutive activation of Rap1. In parallel, silencing VASP in differentiated PLB-985 cells led to recruitment of C3G, a guanine nucleotide exchange factor for Rap1, to the plasma membrane. Expression of murine GFP-tagged phosphodeficient VASP Ser235Ala mutant (murine serine 235 of VASP corresponds to human serine 239) in PLB-985 cells blunted fMLP-induced translocation of C3G to the membrane and activation of Rap1. Thus, bacterial fMLP triggers cGKI-dependent phosphorylation of human VASP on serine 239 and, thereby, controls membrane recruitment of C3G, which is required for activation of Rap1 and beta2 integrin-dependent antibacterial functions of neutrophils.

Screens, Closets, and Echo-Chambers of the Mind: The Struggle to Represent the Inner Life on Stage

Screens, Closets, and Echo-Chambers of the Mind: The Struggle to Represent the Inner Life on Stage

A Spitzer space telescope study of Sn 2002hh: An infrared echo from a Type IIP supernova

We present late-time ( 590 - 994 days) mid-IR photometry of the normal but highly reddened Type IIP supernova SN 2002hh. Bright, cool, slowly fading emission is detected from the direction of the supernova. Most of this flux appears not to be driven by the supernova event but instead probably originates in a cool, obscured star formation region or molecular cloud along the line of sight. We also show, however, that the declining component of the flux is consistent with an SN-powered IR echo from a dusty progenitor CSM. Mid-IR emission could also be coming from newly condensed dust and/or an ejecta/CSM impact, but their contributions are likely to be small. For the case of a CSM-IR echo, we infer a dust mass of as little as 0.036 M-. with a corresponding CSM mass of 3.6(0.01/ r(dg)) M-., where rdg is the dust-to-gas mass ratio. Such a CSM would have resulted from episodic mass loss whose rate declined significantly about 28,000 years ago. Alternatively, an IR echo from a surrounding, dense, dusty molecular cloud might also have been responsible for the fading component. Either way, this is the first time that an IR echo has been clearly identified in a Type IIP supernova. We find no evidence for or against the proposal that Type IIP supernovae produce large amounts of dust via grain condensation in the ejecta. However, within the CSM-IR echo scenario, the mass of dust derived implies that the progenitors of the most common of core-collapse supernovae may make an important contribution to the universal dust content.