The static deformation of an elastic half‐space by surface pressure is reviewed. A brief mention is made of methods for solving the problem when the medium is plane stratified, but the major emphasis is on the solution for spherical, radially stratified, gravitating earth models. Love‐number calculations are outlined, and from the Love numbers, Green's functions are formed for the surface mass‐load boundary‐value problem. Tables of mass‐load Green's functions, computed for realistic earth models, are given, so that the displacements, tilts, accelerations, and strains at the earth's surface caused by any static load can be found by evaluating a convolution integral over the loaded region.

An exact method is presented for calculating the changes in sea level that occur when ice and water masses are rearranged on the surface of elastic and viscoelastic non-rotating Earth models. The method is used to calculate the instantaneous elastic and delayed vi scoelastic sea level changes following the partial melting of late Quaternary ice sheets. We find that there can be large errors in the usual assumption that changes in sea level are uniform over the ocean basins. If a quantity of ice equivalent to a uniform 100-m rise in sea level melts from the Laurentide and Fennoscandian ice sheets, then in the South Pacific the instantaneous rise in sea level can be as large as 120m. In the North Atlantic the instantaneous rise is always less than 100 m. There is a zone in the North Atlantic with almost no sea level change and near Greenland and Norway the sea level falls, rather than rises, by over 100 m. One thousand years after the melting a forebulge migrating towards the ice loads causes water to flow from the South Pacific into the North Pacific suggesting that raised beaches should occur in the South Pacific. The gravitational attraction of an ice mass upon a nearby ocean tends to hold sea level high in the vicinity of the ice. This extra load near the ice may have a significant influence on postglacial isostatic adjustment.

BACKGROUND Increased secretion of growth hormone leads to gigantism in children and acromegaly in adults; the genetic causes of gigantism and acromegaly are poorly understood. METHODS We performed clinical and genetic studies of samples obtained from 43 patients with gigantism and then sequenced an implicated gene in samples from 248 patients with acromegaly. RESULTS We observed microduplication on chromosome Xq26.3 in samples from 13 patients with gigantism; of these samples, 4 were obtained from members of two unrelated kindreds, and 9 were from patients with sporadic cases. All the patients had disease onset during early childhood. Of the patients with gigantism who did not carry an Xq26.3 microduplication, none presented before the age of 5 years. Genomic characterization of the Xq26.3 region suggests that the microduplications are generated during chromosome replication and that they contain four protein-coding genes. Only one of these genes, GPR101, which encodes a G-protein–coupled receptor, was overexpressed in patients’ pituitary lesions. We identified a recurrent GPR101 mutation (p.E308D) in 11 of 248 patients with acromegaly, with the mutation found mostly in tumors. When the mutation was transfected into rat GH3 cells, it led to increased release of growth hormone and proliferation of growth hormone–producing cells. CONCLUSIONS We describe a pediatric disorder (which we have termed X-linked acrogigantism [X-LAG]) that is caused by an Xq26.3 genomic duplication and is characterized by early-onset gigantism resulting from an excess of growth hormone. Duplication of GPR101 probably causes X-LAG. We also found a recurrent mutation in GPR101 in some adults with acromegaly. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and others.)

The sea-level rise due to ice-sheet melting since the last glacial maximum was not uniform everywhere because of the deformation of the Earth's surface and its geoid by changing ice and water loads. A numerical model is employed to calculate global changes in relative sea level on a spherical viscoelastic Earth as northern hemisphere ice sheets melt and fill the ocean basins with meltwater. Predictions for the past 16,000 years explain a large proportion of the global variance in the sea-level record, particularly during the Holocene. Results indicate that the oceans can be divided into six zones, each of which is characterized by a specific form of the relative sea-level curve. In four of these zones emerged beaches are predicted, and these may form even at considerable distance from the ice sheets themselves. In the remaining zones submergence is dominant, and no emerged beaches are expected. The close agreement of these predictions with the data suggests that, contrary to the beliefs of many, no net change in ocean volume has occurred during the past 5000 years. Predictions for localities close to the ice sheets are the most in error, suggesting that slight modifications of the assumed melting history and/or the rheological model of the Earth's interior are necessary.

Each differentiated cell type has its own epigenetic signature, which reflects its genotype, developmental history, and environmental influences, and is ultimately reflected in the phenotype of the cell and organism. Some cells undergo major epigenetic 'reprogramming' during fetal development. The proper, or improper, handling of these highly sensitive periods may have significant short-term and long-term effects on the newborn and his/her progeny. This review highlights the impact of environmental and nutritional factors on the epigenome and the potential effect of epigenetic dysregulation on maternal and fetal pregnancy outcomes, as well as possible long-term implications.