Interaction of eddies and mean zonal flow on Jupiter as inferred from Voyager 1 and 2 images

Voyager 1 and 2 narrow-angle frames were used to obtain displacements of features at resolutions of 130 km over time intervals of 1 Jovian rotation. The zonal velocity ū was constant to 1.5% during the 4 months between the Voyager 1 and 2 encounters. The latitudes of the zonal jet maxima (extrema of ū) are the same as inferred from earth-based observations extending over the past 80 years. The curvature of the velocity profile d²ū/dy² varies with latitudinal coordinate y in the range from −3β to +2β, where β is the planetary vorticity gradient. The barotropic stability criterion is violated at about 10 latitudes between ±60°. The eddy momentum flux variation with latitude (u'ν')(overbar) is positively correlated with dū/dy for both Voyager 1 and 2 data. The rate of conversion {K'K(overbar)} of eddy kinetic energy into zonal mean kinetic energy is in the range 1.5–3.0 Wm^(−2), for a layer 2.5 bar deep. The time constant for resupply of zonal mean kinetic energy by eddies is in the range 2–4 months, less than the interval between Voyager encounters. The rate of energy conversion is more than 10% of the total infrared heat flux for Jupiter, in contrast with earth where it is only 0.1% of the infrared heat flux. This hundred-fold difference suggests that the thermomechanical energy cycles are very different on the two planets

Flow fields within Jupiter's great red spot and white oval BC

Using sequences of Voyager 1 high-resolution images of Jupiter's Great Red Spot (GRS) and White Oval BC we map the flow fields within the GRS and Oval BC. We compute relative vorticity within these features as a function of semi-major axis length and position angle in a coordinate system consisting of concentric ellipses of equal eccentricity. Both the velocity and the relative vorticity profiles are nearly identical for Oval BC and the outer portion of the GRS. Wind speeds of 110–120 m/s are observed near the outer edges of both features. Along their minor axes relative vorticity profiles reach a maximum of ∼6 × 10^(−5) s^(−1). This is several times greater than the ambient 1.5 × 10^(−5) s^(−1) meridional shear of zonal winds at the latitudes of the GRS and Oval BC. Maximum Rossby numbers of 0.36 are computed for flows within both the GRS and the Oval BC. Generally, the Rossby numbers within these features are much lower, indicating strongly geostrophic constraints on the flow. The difference in streamline curvature within the GRS and the Oval BC is found to compensate for the difference in planetary vorticity at the respective latitudes of the features. Motions within the central region of the GRS are much slower and more random than around the spot’s outer portion

The initiator methionine tRNA drives secretion of type II collagen from stromal fibroblasts to promote tumor growth and angiogenesis

Summary: Expression of the initiator methionine tRNA (tRNAi Met) is deregulated in cancer. Despite this fact, it is not currently known how tRNAi Met expression levels influence tumor progression. We have found that tRNAi Met expression is increased in carcinoma-associated fibroblasts, implicating deregulated expression of tRNAi Met in the tumor stroma as a possible contributor to tumor progression. To investigate how elevated stromal tRNAi Met contributes to tumor progression, we generated a mouse expressing additional copies of the tRNAi Met gene (2+tRNAi Met mouse). Growth and vascularization of subcutaneous tumor allografts was enhanced in 2+tRNAi Met mice compared with wild-type littermate controls. Extracellular matrix (ECM) deposited by fibroblasts from 2+tRNAi Met mice supported enhanced endothelial cell and fibroblast migration. SILAC mass spectrometry indicated that elevated expression of tRNAi Met significantly increased synthesis and secretion of certain types of collagen, in particular type II collagen. Suppression of type II collagen opposed the ability of tRNAi Metoverexpressing fibroblasts to deposit pro-migratory ECM. We used the prolyl hydroxylase inhibitor ethyl- 3,4-dihydroxybenzoate (DHB) to determine whether collagen synthesis contributes to the tRNAi Met-driven pro-tumorigenic stroma in vivo. DHB had no effect on the growth of syngeneic allografts in wild-type mice but opposed the ability of 2+tRNAi Met mice to support increased angiogenesis and tumor growth. Finally, collagen II expression predicts poor prognosis in high-grade serous ovarian carcinoma. Taken together, these data indicate that increased tRNAi Met levels contribute to tumor progression by enhancing the ability of stromal fibroblasts to synthesize and secrete a type II collagen-rich ECM that supports endothelial cell migration and angiogenesis

The Lantern Vol. 16, No. 1, Fall 1947

• A Little Light • Social Solidarity • The Struggle • 1949 Report • Blues • Angel\u27s Wings • Street Death • The Giant • Not Alone • B or Something • After Argument • Friendship • Built That Way • The Passing • Freshman • Asleep • John J. Heilemannhttps://digitalcommons.ursinus.edu/lantern/1043/thumbnail.jp

Mercury's Surface Magnetic Field Determined from Proton-Reflection Magnetometry

Solar wind protons observed by the MESSENGER spacecraft in orbit about Mercury exhibit signatures of precipitation loss to Mercury's surface. We apply proton-reflection magnetometry to sense Mercury's surface magnetic field intensity in the planet's northern and southern hemispheres. The results are consistent with a dipole field offset to the north and show that the technique may be used to resolve regional-scale fields at the surface. The proton loss cones indicate persistent ion precipitation to the surface in the northern magnetospheric cusp region and in the southern hemisphere at low nightside latitudes. The latter observation implies that most of the surface in Mercury's southern hemisphere is continuously bombarded by plasma, in contrast with the premise that the global magnetic field largely protects the planetary surface from the solar wind

Multicentric Carpotarsal Osteolysis Is Caused by Mutations Clustering in the Amino-Terminal Transcriptional Activation Domain of MAFB

(The American Journal of Human Genetics, 90, 494–501; March 9, 2012)\ud In the published version of this article, the amino acid alteration caused by c.161C>T should have been notated as\ud p.Ser54Leu and not p.Pro54Leu. The wild-type amino acid is incorrectly notated in the main text, in Table 2, and in\ud Figure 4. The authors regret this error. Additionally, The Journal regrets that this erratum, originally requested in 2012,\ud was not published in a timely fashion

Impact of registration on clinical trials on infection risk in pediatric acute myeloid leukemia

Little is known about the impact of enrollment on therapeutic clinical trials on adverse event rates. Primary objective was to describe the impact of clinical trial registration on sterile site microbiologically documented infection for children with newly diagnosed acute myeloid leukemia (AML). We conducted a multicenter cohort study that included children aged ≤18 years with de novo AML. Primary outcome was microbiologically documented sterile site infection. Infection rates were compared between those registered and not registered on clinical trials. Five hundred seventy-four children with AML were included of which 198 (34.5%) were registered on a therapeutic clinical trial. Overall, 400 (69.7%) had at least one sterile site microbiologically documented infection. In multiple regression, registration on clinical trials was independently associated with a higher risk of microbiologically documented sterile site infection [adjusted odds ratio (OR) 1.24, 95% confidence interval (CI) 1.01-1.53; p = 0.040] and viridans group streptococcal infection (OR 1.46, 95% CI 1.08-1.98; p = 0.015). Registration on trials was not associated with Gram-negative or invasive fungal infections. Children with newly diagnosed AML enrolled on clinical trials have a higher risk of microbiologically documented sterile site infection. This information may impact on supportive care practices in pediatric AML

Current State of the Science: Health Effects and Indoor Environmental Quality

Our understanding of the relationship between human health and the indoor environment continues to evolve. Previous research on health and indoor environments has tended to concentrate on discrete pollutant sources and exposures and on specific disease processes. Recently, efforts have been made to characterize more fully the complex interactions between the health of occupants and the interior spaces they inhabit. In this article we review recent advances in source characterization, exposure assessment, health effects associated with indoor exposures, and intervention research related to indoor environments. Advances in source characterization include a better understanding of how chemicals are transported and processed within spaces and the role that other factors such as lighting and building design may play in determining health. Efforts are under way to improve our ability to measure exposures, but this remains a challenge, particularly for biological agents. Researchers are also examining the effects of multiple exposures as well as the effects of exposures on vulnerable populations such as children and the elderly. In addition, a number of investigators are also studying the effects of modifying building design, materials, and operations on occupant health. Identification of research priorities should include input from building designers, operators, and the public health community