On the role of the weather in the deaths of R. F. Scott and his companions

Robert Falcon Scott and his companions reached the South Pole in January of 1912, only to die on their return journey at a remote site on the Ross Ice Shelf, about 170 miles from their base camp on the coast. Numerous contributing causes for their deaths have been proposed, but it has been assumed that the cold temperatures they reported encountering on the Ross Ice Shelf, near 82–80°S during their northward trek toward safety, were not unusual. The weather in the region where they perished on their unassisted trek by foot from the Pole remained undocumented for more than half a century, but it has now been monitored by multiple automated weather stations for more than a decade. The data recorded by Scott and his men from late February to March 19, 1912, display daily temperature minima that were on average 10 to 20°F below those obtained in the same region and season since routine modern observations began in 1985. Only 1 year in the available 15 years of measurements from the location where Scott and his men perished displays persistent cold temperatures at this time of year close to those reported in 1912. These remarkably cold temperatures likely contributed substantially to the exhaustion and frostbite Scott and his companions endured, and their deaths were therefore due, at least in part, to the unusual weather conditions they endured during their cold march across the Ross Ice Shelf of Antarctica.

The role of antimicrobial peptides in animal defenses

It is becoming clear that the cationic antimicrobial peptides are an important component of the innate defenses of all species of life. Such peptides can be constitutively expressed or induced by bacteria or their products. The best peptides have good activities vs. a broad range of bacterial strains, including antibiotic-resistant isolates. They kill very rapidly, do not easily select resistant mutants, are synergistic with conventional antibiotics, other peptides, and lysozyme, and are able to kill bacteria in animal models. It is known that bacterial infections, especially when treated with antibiotics, can lead to the release of bacterial products such as lipopolysaccharide (LPS) and lipoteichoic acid, resulting in potentially lethal sepsis. In contrast to antibiotics, the peptides actually prevent cytokine induction by bacterial products in tissue culture and human blood, and they block the onset of sepsis in mouse models of endotoxemia. Consistent with this, transcriptional gene array experiments using a macrophage cell line demonstrated that a model peptide, CEMA, blocks the expression of many genes whose transcription was induced by LPS. The peptides do this in part by blocking LPS interaction with the serum protein LBP. In addition, CEMA itself has a direct effect on macrophage gene expression. Because cationic antimicrobial peptides are induced by LPS and are able to dampen the septic response of animal cells to LPS, we propose that, in addition to their role in direct and lysozyme-assisted killing of microbes, they have a role in feedback regulation of cytokine responses. We are currently developing variant peptides as therapeutics against antibiotic-resistant infections.