Porphyry-copper ore shells form at stable pressure-temperature fronts within dynamic fluid plumes.

Porphyry-type ore deposits are major resources of copper and gold, precipitated from fluids expelled by crustal magma chambers. The metals are typically concentrated in confined ore shells within vertically extensive vein networks, formed through hydraulic fracturing of rock by ascending fluids. Numerical modeling shows that dynamic permeability responses to magmatic fluid expulsion can stabilize a front of metal precipitation at the boundary between lithostatically pressured up-flow of hot magmatic fluids and hydrostatically pressured convection of cooler meteoric fluids. The balance between focused heat advection and lateral cooling controls the most important economic characteristics, including size, shape, and ore grade. This self-sustaining process may extend to epithermal gold deposits, venting at active volcanoes, and regions with the potential for geothermal energy production.

The structure and dynamics of mid-ocean ridge hydrothermal systems.

Sub-seafloor hydrothermal convection at mid-ocean ridges transfers 25% of the Earth's heat flux and can form massive sulfide ore deposits. Their three-dimensional (3D) structure and transient dynamics are uncertain. Using 3D numerical simulations, we demonstrated that convection cells self-organize into pipelike upflow zones surrounded by narrow zones of focused and relatively warm downflow. This configuration ensures optimal heat transfer and efficient metal leaching for ore-deposit formation. Simulated fluid-residence times are as short as 3 years. The concentric flow geometry results from nonlinearities in fluid properties, and this may influence the behavior of other fluid-flow systems in Earth's crust.

Negative regulation of N-cadherin-mediated cell-cell adhesion by the estrogen receptor signaling pathway in rat pituitary GH3 cells.

The ability of the estrogen receptor signaling pathway to regulate cell-cell adhesion, and N-cadherin and beta-catenin expression was examined in rat somatolactotropic GH3 cells cultured in serum-free, phenol red-free medium (SFM). Estradiol-17beta (E2) promoted a nonadherent phenotype, whereas the steroidal antiestrogen, ICI 182,780, induced the formation of tightly adherent aggregates of cells. The antiestrogen-induced cell-cell adhesion was associated with the presence of adherens junctions, and was Ca2+-dependent. E2 reduced surface N-cadherin protein to barely detectable levels, whereas ICI 182,780-treated cells displayed abundant punctate immunoreactive N-cadherin. Antiestrogen failed to induce adhesion in the presence of a blocking antibody to N-cadherin. ICI 182,780 increased the protein levels for N-cadherin and the cadherin-binding protein, beta-catenin, by twofold over SFM controls or E2-treated samples. ICI 182,780 also increased the mRNA levels for N-cadherin and beta-catenin by two- to fivefold. In GH3 cells cultured in growth medium, ICI 182,780 increased N-cadherin and beta-catenin levels by twofold over untreated controls, and inhibited cell proliferation by 53%. These results provide the first demonstration of the regulation of N-cadherin-mediated cell-cell adhesion by the estrogen receptor (ER) signaling pathway in pituitary somatolactotrophs through the coordinate regulation of N-cadherin and beta-catenin expression. The inverse relationship between ICI 182,780-induced adhesion and proliferation raises the possibility that these two processes are functionally related.

Behavioral modification of colonic function. Can constipation be learned?

We challenged the two hypotheses: first, that defecation can be suppressed for an extended time, and second, if so, that this has an effect on upper colonic motility. Thus we studied 12 male volunteers with conditions of identical nutrition and patterns of physical activity over a two-week period, where one week with normal defecation and one week with voluntary prolonged suppression of defecation followed each other in randomized order. Frequencies of defecation, stool weights, total and segmental colonic transit times (using radiopaque markers) were compared. Frequency of defecations and stool weights were lower during suppressed defecation [8.9 +/- 0.66 vs 3.7 +/- 0.41 (mean +/- SE) bowel movements per week, P = 0.003, and 1.30 +/- 0.09 vs 0.98 +/- 0.13 kg/week, P = 0.01]. Total transit times were increased from 28.8 +/- 4.4 to 53.1 +/- 4.3 hr, P = 0.004. Segmental transit times were increased in the rectosigmoid (from 8.83 +/- 3.6 to 32.1 +/- 5.6 hr, P = 0.04) and right hemicolon (from 14.5 +/- 0.9 hr to 19.7 +/- 1.5 hr, P = 0.02) by suppression of defecation. We conclude that defecation habits may induce changes in colonic function such as those seen in constipation and that functional anorectal outlet obstruction may, probably by reflex mediation, affect the right colon.