Appraisal as a Pervasive Determinant of Anger.

L. Berkowitz and E. Harmon-Jones (see record 2004-15096-001) challenge appraisal theories of emotion by describing 2 sets of conditions (physical discomfort and anger-related muscle actions) in which anger appears to be elicited in the absence of theoretically predicted appraisals. In response, the authors discuss the ability of the specific appraisal model they have developed (e.g., C. A. Smith & L. D. Kirby, 2000, 2001; C. A. Smith & R. S. Lazarus, 1990) to account for such instances of anger. First, a number of issues are clarified relevant to the authors' model, including the nature of both the cognitive operations underlying appraisal and the specific appraisals hypothesized to evoke anger. The authors then describe how their model can account for the instances of anger described by L. Berkowitz and E. Harmon-Jones and how both accounts might be tested. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Anti-inflammatory action of dapsone: inhibition of neutrophil adherence is associated with inhibition of chemoattractant-induced signal transduction

Dapsone has clinical utility as an anti-inflammatory agent but the mechanism of this action remains unknown. We have previously reported that dapsone inhibits beta2 integrin (CD11b/CD18)-mediated adherence of human neutrophils in vitro and now describe studies designed to discover how dapsone-mediated inhibition of this neutrophil function occurs. Results indicate that dapsone interferes with the activation or function of the G-protein (Gi type) that initiates the signal transduction cascade common to chemotactic stimuli. They also show that dapsone-mediated suppression of this pathway inhibits the generation of second messengers essential to the activation of beta2 integrin molecules, as well as respiratory and secretory functions of neutrophils exposed to chemoattractants. We propose that the inhibition of chemoattractant-induced signal transduction by dapsone suppresses neutrophil recruitment and local production of toxic respiratory and secretory products in the affected skin of dermatitis herpetiformis and other neutrophilic dermatoses.     

Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors

Volatile anaesthetics have historically been considered to act in a nonspecific manner on the central nervous system. More recent studies, however, have revealed that the receptors for inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine are sensitive to clinically relevant concentrations of inhaled anaesthetics. The function of GABA(A) and glycine receptors is enhanced by a number of anaesthetics and alcohols, whereas activity of the related GABA rho1 receptor is reduced. We have used this difference in pharmacology to investigate the molecular basis for modulation of these receptors by anaesthetics and alcohols. By using chimaeric receptor constructs, we have identified a region of 45 amino-acid residues that is both necessary and sufficient for the enhancement of receptor function. Within this region, two specific amino-acid residues in transmembrane domains 2 and 3 are critical for allosteric modulation of both GABA(A) and glycine receptors by alcohols and two volatile anaesthetics. These observations support the idea that anaesthetics exert a specific effect on these ion-channel proteins, and allow for the future testing of specific hypotheses of the action of anaesthetics.     

NMR structure and mutagenesis of the FADD (Mort1) death-effector domain

When activated, membrane-bound receptors for Fas and tumour-necrosis factor initiate programmed cell death by recruiting the death domain of the adaptor protein FADD to the membrane. FADD then activates caspase 8 (also known as FLICE or MACH) through an interaction between the death-effector domains of FADD and caspase 8. This ultimately leads to the apoptotic response. Death-effector domains and homologous protein modules known as caspase-recruitment domains have been found in several proteins and are important regulators of caspase (FLICE) activity and of apoptosis. Here we describe the solution structure of a soluble, biologically active mutant of the FADD death-effector domain. The structure consists of six antiparallel, amphipathic alpha-helices and resembles the overall fold of the death domains of Fas and p75. Despite this structural similarity, mutations that inhibit protein-protein interactions involving the Fas death domain have no effect when introduced into the FADD death-effector domain. Instead, a hydrophobic region of the FADD death-effector domain that is not present in the death domains is vital for binding to FLICE and for apoptotic activity.     

Breaking the Nyquist barrier

The author discusses the concept that data sampled beyond the Nyquist frequency is meaningless. A simple signal processing scheme to extend resolution to nearly twice the Nyquist without the problem of alias emerged. It starts by placing one-dimensional signals into a simulated sample-and-hold process in a Mathcad application     

The Study of Heterogeneous Catalysts by High-Resolution Transmission Electron MicroscoDV

Advances in instrumentation have made it possible in recent years to study the microstructure of inorganic materials at atomic resolution using the technique of high-resolution electron microscopy (HREM). Details of instrumentation have been described elsewhere [l], and applications and trends for HREM have recently been reviewed [2]. Although HREM is primarily a technique for studying bulk defects, it is increasingly also being applied in the profile-imaging mode to derive information about surfaces [3]. The high spatial resolution of the electron microscope makes it a valuable tool for the characterization of heterogeneous catalysts. This is evidenced by the growing number of studies wherein electron micrographs are being used to describe the morphology of a particular catalyst. Profile imaging is proving particularly useful in this regard for following changes in surface structure as a function of treatment conditions [4].     

Effects of viscosity on the bitterness and astringency of grape seed tannin

To examine the separate effects of viscosity and sweetness on astringency, aqueous solutions of grape seed tannin (GST) were thickened with carboxymethyl cellulose (CMC) from 2 to 45 cP (experiment 1) or sweetened with 0 to 1.8 g/L aspartame (experiment 2). Trained subjects continuously rated astringency and bitterness in duplicate. Subjects were categorized by the salivary flow induced by citric acid and ability to taste n-propyl thiouracil (PROP). In experiment 1, maximum intensity and total duration of astringency were significantly decreased as viscosity rose, although time to maximum intensity of astringency was not affected. Maximum intensity and total duration of bitterness were not significantly affected by increasing viscosity; however, the onset of bitterness was significantly delayed. In experiment 2, increasing sweetness had no affect on any astringency parameter, although maximum intensity of bitterness was significantly decreased. Neither PROP nor salivary flow-status had any effect on perception of bitterness or astringency in either experiment.