Pertussis toxin S1 mutant with reduced enzyme activity and a conserved protective epitope

Pertussis toxin (PTX) is a major virulence factor in whooping cough and can elicit protective antibodies. Amino acid residues 8 to 15 of PTX subunit S1 are important for the adenosine diphosphate-ribosyltransferase activity associated with the pathobiological effects of PTX. Furthermore, this region contains at least a portion of an epitope that elicits both toxin-neutralizing and protective antibody responses in mice. The gene encoding the S1 subunit was subjected to site-specific mutagenesis in this critical region. A mutant containing a single amino acid substitution (Arg9----Lys) had reduced enzymatic activity (approximately 0.02% of control) while retaining the protective epitope. This analog S1 molecule may provide the basis for a genetically detoxified PTX with potential for use as a component of an acellular vaccine against whooping cough.     

Guest-dependent spin crossover in a nanoporous molecular framework material

The nanoporous metal-organic framework Fe2(azpy)4(NCS)4.(guest) (azpy is trans-4,4'-azopyridine) displays reversible uptake and release of guest molecules and contains electronic switching centers that are sensitive to the nature of the sorbed guests. The switching of this material arises from the presence of iron(II) spin crossover centers within the framework lattice, the sorbed phases undergoing "half-spin" crossovers, and the desorbed phase showing no switching property. The interpenetrated framework structure displays a considerable flexibility with guest uptake and release, causing substantial changes in the local geometry of the iron(II) centers. The generation of a host lattice that interacts with exchangeable guest species in a switchable fashion has implications for the generation of previously undeveloped advanced materials with applications in areas such as molecular sensing.     

Radiocarbon Dating: Fictitious Results with Mollusk Shells

Evidence is presented to show that modern mollusk shells from rivers can have anomalous radiocarbon ages, owing mainly to incorporation of inactive (carbon-14-deficient) carbon from humus, probably through the food web, as well as by the pathway of carbon dioxide from humus decay. The resultant effect, in addition to the variable contributions of atmospheric carbon dioxide, fermentative carbon dioxide from bottom muds, and, locally, of carbonate carbon from dissolving limestones, makes the initial carbon-14-activity of ancient fresh-water shell indeterminate, but within limits. Consequent errors of shell radiocarbon dates may be as large as several thousand years for river shells.