Unialgal cultures were used to investigate relationships between cell volume and the carbon and nitrogen content of nondiatomaceous marine nanophytoplankton. Cell dimensions were determined by image-analyzed epifluorescence microscopy and particulate C and N by high-temperature dry combustion. Volumes were calculated by direct integration with published algorithms (biovolume), but could be estimated equally well from linear dimensions as prolate spheres. Preservation with 0.5% glutaraldehyde reduced cell volumes 29% on average. Correlations were highly significant between biovolume of preserved cells and C and N contents. Nonlinear regression models appeared most appropriate because smaller cells contained more C and N per unit volume than did larger cells. Suggested general C densities for estimating cell C from preserved volume were 0.36 pg pm-3 for 10' pm3 cells, 0.24 pg pm-3 for lo2 pm3 cells, and 0.16 pg C pm-3 for lo3 pm3 cells. Previous regression models substantially underestimated the C densities of nanophytoplankton of lo*-lo3 l.cm3. The explanation for these differences includes the method of determining mean population volumes, the use of preservatives, and the occurrence of significant vacuolar volume in larger phytoplankton.

Metformin, one of the most commonly used drugs for the treatment of type II diabetes, was recently found to exert its therapeutic effects, at least in part, by activating the AMP-activated protein kinase (AMPK). However, the site of its action, as well as the mechanism to activate AMPK, remains elusive. Here we report how metformin activates AMPK. In cultured bovine aortic endothelial cells, metformin dose-dependently activated AMPK in parallel with increased detection of reactive nitrogen species (RNS). Further, either depletion of mitochondria or adenoviral overexpression of superoxide dismutases, as well as inhibition of nitric-oxide synthase, abolished the metformin-enhanced phosphorylations and activities of AMPK, implicating that activation of AMPK by metformin might be mediated by the mitochondria-derived RNS. Furthermore, administration of metformin, which increased 3-nitrotyrosine staining in hearts of C57BL6, resulted in parallel activation of AMPK in the aorta and hearts of C57BL6 mice but not in those of endothelial nitric-oxide synthase (eNOS) knockout mice in which metformin had no effect on 3-nitrotyrosine staining. Because the eNOS knockout mice expressed normal levels of AMPK-␣ that was activated by 5-aminoimidazole-4-carboxamide riboside, an AMPK agonist, these data indicate that RNS generated by metformin is required for AMPK activation in vivo. In addition, metformin significantly increased the coimmunoprecipitation of AMPK and its upstream kinase, LKB1, in C57BL6 mice administered to metformin in vivo. Using pharmacological and genetic inhibitors, we found that inhibition of either c-Src or PI3K abolished AMPK that was enhanced by metformin. We conclude that activation of AMPK by metformin might be mediated by mitochondria-derived RNS, and activation of the c-Src/PI3K pathway might generate a metabolite or other molecule inside the cell to promote AMPK activation by the LKB1 complex.

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Two-dimensional cusped interfaces are line singularities of curvature. We create such cusps by rotating a cylinder half immersed in liquid. A liquid film is dragged out of the reservoir on one side and is plunged in at the other, where it forms a cusp at finite speeds, if the conditions are right. Both Newtonian and non-Newtonian fluids form cusps, but the transition from a rounded interface to a cusp is gradual in Newtonian liquids and sudden in non-Newtonian liquids. We present an asymptotic analysis near the cusp tip for the case of zero surface tension, and we make some remarks about the effects of a small surface tension. We also present the results of numerical simulations showing the development of a cusp. In those simulations, the fluid is filling an initially rectangular domain with a free surface on top. The fluid enters from both sides and is sucked out through a hole in the bottom.

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Our data, in conjunction with that of others, suggest that Meniere's disease may predispose patients to intractable BPPV. Hydropically induced damage to the maculae of the utricle and saccule or partial obstruction of the membranous labyrinth may be possible mechanisms that explain the coexistence of Meniere's disease and BPPV.

A coherent plume from the Mississippi River was detected in MODIS imagery in July–October 2004 extending from the eastern Gulf of Mexico into the Florida Straits (FS), and reaching the Gulf Stream (GS) off Georgia. The plume was sampled from ships in the FS and the GS. In early August, the plume was about 10–20 km wide in the western FS and about 50 km wide off Georgia. The FS ship survey (16–26 August) documented a 50 km, 10–20 m deep band with anomalies in surface salinity (−0.8), temperature (0.5°C), and surface chlorophyll concentration (2×) relative to FS waters outside the plume. Nutrient concentrations were only slightly higher in the FS plume and there was no apparent increase in colored dissolved organic matter. We estimate that the plume carried some 23% (∼2778 m3 s−1) of the Mississippi River discharge between July and September 2004 into the GS.