The island of New Guinea is located within the deforming zone between the Pacific and Australian plates that converge obliquely at ∼110 mm/yr. New Guinea has been fragmented into a complex array of microplates, some of which rotate rapidly about nearby vertical axes. We present velocities from a network of 38 Global Positioning System (GPS) sites spanning much of the nation of Papua New Guinea (PNG). The GPS‐derived velocities are used to explain the kinematics of major tectonic blocks in the region and the nature of strain accumulation on major faults in PNG. We simultaneously invert GPS velocities, earthquake slip vectors on faults, and transform orientations in the Woodlark Basin for the poles of rotation of the tectonic blocks and the degree of elastic strain accumulation on faults in the region. The data are best explained by six distinct tectonic blocks: the Australian, Pacific, South Bismarck, North Bismarck, and Woodlark plates and a previously unrecognized New Guinea Highlands Block. Significant portions of the Ramu‐Markham Fault appear to be locked, which has implications for seismic hazard determination in the Markham Valley region. We also propose that rapid clockwise rotation of the South Bismarck plate is controlled by edge forces initiated by the collision between the Finisterre arc and the New Guinea Highlands.

The origin of the Papua New Guinea tsunami that killed over 2100 people on 17 July 1998 has remained controversial, as dislocation sources based on the parent earthquake fail to model its extreme run-up amplitude. The generation of tsunamis by submarine mass failure had been considered a rare phenomenon which had aroused virtually no attention in terms of tsunami hazard mitigation. We report on recently acquired high-resolution seismic reflection data which yield new images of a large underwater slump, coincident with photographic and bathymetric evidence of the same feature, suspected of having generated the tsunami. T -phase records from an unblocked hydrophone at Wake Island provide new evidence for the timing of the slump. By merging geological data with hydrodynamic modelling, we reproduce the observed tsunami amplitude and timing in a manner consistent with eyewitness accounts. Submarine mass failure is predicted based on fundamental geological and geotechnical information.

New thermal data from 18–24 Ma lithosphere on the Cocos Plate delineate contrasting subsurface thermal conditions in adjacent sections of crust. Heat flow through seafloor created at the East Pacific Rise is generally suppressed by ∼70% relative to conductive lithospheric cooling models, whereas heat flow through adjacent, similarly‐aged lithosphere generated at the Cocos‐Nazca Spreading Center is consistent with these models. The transition between thermal regimes is remarkably abrupt, only 2–5 km wide, indicating a shallow hydrothermal origin. The transition is more closely associated with differences in the distribution of basement outcrops than with tectonic boundaries, demonstrating the importance of the former in extracting heat from the lithosphere on a regional basis.

As many as one-third of mutations in a gene result in the corresponding enzyme having an increased Michaelis constant, or K(m), (decreased binding affinity) for a coenzyme, resulting in a lower rate of reaction. About 50 human genetic dis-eases due to defective enzymes can be remedied or ameliorated by the administration of high doses of the vitamin component of the corresponding coenzyme, which at least partially restores enzymatic activity. Several single-nucleotide polymorphisms, in which the variant amino acid reduces coenzyme binding and thus enzymatic activity, are likely to be remediable by raising cellular concentrations of the cofactor through high-dose vitamin therapy. Some examples include the alanine-to-valine substitution at codon 222 (Ala222-->Val) [DNA: C-to-T substitution at nucleo-tide 677 (677C-->T)] in methylenetetrahydrofolate reductase (NADPH) and the cofactor FAD (in relation to cardiovascular disease, migraines, and rages), the Pro187-->Ser (DNA: 609C-->T) mutation in NAD(P):quinone oxidoreductase 1 [NAD(P)H dehy-drogenase (quinone)] and FAD (in relation to cancer), the Ala44-->Gly (DNA: 131C-->G) mutation in glucose-6-phosphate 1-dehydrogenase and NADP (in relation to favism and hemolytic anemia), and the Glu487-->Lys mutation (present in one-half of Asians) in aldehyde dehydrogenase (NAD + ) and NAD (in relation to alcohol intolerance, Alzheimer disease, and cancer).