Evolutionary origins of stigmatization: The functions of social exclusion.

A reconceptualization of stigma is presented that changes the emphasis from the devaluation of an individual's identity to the process by which individuals who satisfy certain criteria come to be excluded from various kinds of social interactions. The authors propose that phenomena currently placed under the general rubric of stigma involve a set of distinct psychological systems designed by natural selection to solve specific problems associated with sociality. In particular, the authors suggest that human beings possess cognitive adaptations designed to cause them to avoid poor social exchange partners, join cooperative groups (for purposes of between-group competition and exploitation), and avoid contact with those who are differentially likely to carry communicable pathogens. The evolutionary view contributes to the current conceptualization of stigma by providing an account of the ultimate function of stigmatization and helping to explain its consensual nature. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

In vitro antimalarial activity of chalcones and their derivatives

A series of chalcones and their derivatives have been synthesized and identified as novel potential antimalarials using both molecular modeling and in vitro testing against the intact parasite. A large number of chalcones and their derivatives were prepared using one-step Claisen-Schmidt condensations of aldehydes with methyl ketones. These condensates were screened in vitro against both chloroquine-sensitive and chloroquine-resistant strains of Plasmodium falciparum and shown to be active at concentrations in the nanomolar range. The most active chalcone derivative, 1-(2,5-dichlorophenyl)-3-(4-quinolinyl)-2-propen-1-one (7), had an IC50 value of 200 nM against both a chloroquine-resistant strain (W2) and a chloroquine-sensitive strain (D6). The resistance indexes for all compounds were substantially lower than for chloroquine, suggesting that this series will be active against chloroquine-resistant malaria. Structure-activity relationships (SAR) of the chalcones in the context of a homology-based model structure of the malaria trophozoite cysteine protease, the most likely target enzyme, are presented.     

Cystalysin, a 46-kilodalton cysteine desulfhydrase from Treponema denticola, with hemolytic and hemoxidative activities

A 46-kDa hemolytic protein, referred to as cystalysin, from Treponema denticola ATCC 35404 was overexpressed in Escherichia coli LC-67. Both the native and recombinant 46-kDa proteins were purified to homogeneity. Both proteins expressed identical biological and functional characteristics. In addition to its biological function of lysing erythrocytes and hemoxidizing the hemoglobin to methemoglobin, cystalysin was also capable of removing the sulfhydryl and amino groups from selected S-containing compounds (e.g., cysteine) producing H2S, NH3, and pyruvate. This cysteine desulfhydrase resulted in the following Michaelis-Menten kinetics: Km = 3.6 mM and k(cat) = 12 s(-1). Cystathionine and S-aminoethyl-L-cysteine were also substrates for the protein. Gas chromatography-mass spectrometry and high-performance liquid chromatography analysis of the end products revealed NH3, pyruvate, homocysteine (from cystathionine), and cysteamine (from S-aminoethyl-L-cysteine). The enzyme was active over a broad pH range, with highest activity at pH 7.8 to 8.0. The enzymatic activity was increased by beta-mercaptoethanol. It was not inhibited by the proteinase inhibitor TLCK (N alpha-p-tosyl-L-lysine chloromethyl ketone), pronase, or proteinase K, suggesting that the functional site was physically protected or located in a small fragment of the polypeptide. We hypothesize that cystalysin is a pyridoxal-5-phosphate-containing enzyme, with activity of an alphaC-N and betaC-S lyase (cystathionase) type. Since large amounts of H2S have been reported in deep periodontal pockets, cystalysin may also function in vivo as an important virulence molecule.     

Can manipulations of cognitive load be used to test evolutionary hypotheses?

D. DeSteno, M. Y. Bartlett, J. Braverman, and P. Salovey (see record 2002-18731-006) proposed that if sex-differentiated responses to infidelity are evolved, then they should be automatic, and therefore cognitive load should not attenuate them. DeSteno et al. found smaller sex differences in response to sexual versus emotional infidelity among participants under cognitive load, an effect interpreted as evidence against the evolutionary hypothesis. This logic is faulty. Cognitive load probably affects mechanisms involved in simulating infidelity experiences, thus seriously challenging the usefulness of cognitive load manipulations in testing hypotheses involving simulation. The method also entails the assumption that evolved jealousy mechanisms are necessarily automatic, an assumption not supported by theory or evidence. Regardless of how the jealousy debate is eventually settled, cognitive load manipulations cannot rule out the operation of evolved mechanisms. (PsycINFO Database Record (c) 2010 APA, all rights reserved)