The Midpoint Rule as a Variational--Symplectic Integrator. I. Hamiltonian Systems

Numerical algorithms based on variational and symplectic integrators exhibit special features that make them promising candidates for application to general relativity and other constrained Hamiltonian systems. This paper lays part of the foundation for such applications. The midpoint rule for Hamilton's equations is examined from the perspectives of variational and symplectic integrators. It is shown that the midpoint rule preserves the symplectic form, conserves Noether charges, and exhibits excellent long--term energy behavior. The energy behavior is explained by the result, shown here, that the midpoint rule exactly conserves a phase space function that is close to the Hamiltonian. The presentation includes several examples.Comment: 11 pages, 8 figures, REVTe

An Integrated Assessment of Archaeobotanical Recovery Methods in the Neotropical Rainforest of Northern Belize: Flotation and Dry Screening

This report presents results of a study examining the ancient use of plants at four Late Classic (CE 600-900) Maya rural farmsteads in northwestern Belize. Our research specifically targeted residential middens for macrobotanical recovery. Samples yielded the remains of more than a dozen plant families, representing some genera that do not currently grow in the area. These plants were used in the Late Classic, countering the idea that ancient botanical remains do not survive in Neotropical archaeological contexts. We also evaluated two macrobotanical sample processing methods vis-à-vis one another: flotation and dry screening. Our results indicate that flotation recovered 58% more seeds than dry screening, while dry screening yielded almost twice as much charcoal and other wood as flotation. The divergent quantities in the types of material recovered suggest a comprehensive macrobotanical recovery program should include the use of both processing methods

Shubnikov-de Haas Effect and Magnetic Breakdown in Be

Magnetic breakdown in the basal plane of Be was investigated in fields up to 150 kG. Geometrical aspects of the open orbits caused by breakdown are discussed. An estimate of 30 kG for the characteristic breakdown field is obtained by applying the theory of Falicov et al. Shubnikov-de Haas frequency measurements are reported for the central-cigar cross section. These measurements are relevant to a recent conjecture that the Onsager-Lifshitz quantization scheme may be violated in the presence of magnetic breakdown

The NAD(P)H oxidase homolog Nox4 modulates insulin-stimulated generation of H\u3csub\u3e2\u3c/sub\u3e0\u3csub\u3e2\u3c/sub\u3e and plays an integral role in insulin signal transduction

Insulin stimulation of target cells elicits a burst of H2O2 that enhances tyrosine phosphorylation of the insulin receptor and its cellular substrate proteins as well as distal signaling events in the insulin action cascade. The molecular mechanism coupling the insulin receptor with the cellular oxidant-generating apparatus has not been elucidated. Using reverse transcription-PCR and Northern blot analyses, we found that Nox4, a homolog of gp91phox, the phagocytic NAD(P)H oxidase catalytic subunit, is prominently expressed in insulin-sensitive adipose cells. Adenovirus-mediated expression of Nox4 deletion constructs lacking NAD(P)H or FAD/NAD(P)H cofactor binding domains acted in a dominant-negative fashion in differentiated 3T3-L1 adipocytes and attenuated insulin-stimulated H2O2 generation, insulin receptor (IR) and IRS-1 tyrosine phosphorylation, activation of downstream serine kinases, and glucose uptake. Transfection of specific small interfering RNA oligonucleotides reduced Nox4 protein abundance and also inhibited the insulin signaling cascade. Overexpression of Nox4 also significantly reversed the inhibition of insulin-stimulated IR tyrosine phosphorylation induced by coexpression of PTP1B by inhibiting PTP1B catalytic activity. These data suggest that Nox4 provides a novel link between the IR and the generation of cellular reactive oxygen species that enhance insulin signal transduction, at least in part via the oxidative inhibition of cellular protein-tyrosine phosphatases (PTPases), including PTP1B, a PTPase that has been previously implicated in the regulation of insulin action

Acute kidney injury in critically ill newborns: What do we know? What do we need to learn?

Outcomes in critically ill neonates have improved over the past three decades, yet high residual mortality and morbidity rates exist. Acute kidney injury (AKI) is not just an innocent by-stander in the critically ill patient. Research on incidence and outcomes of AKI in the critically ill neonatal population is scarce. The objective of this publication is to (a) review original articles on the short- and long-term outcomes after neonatal AKI, (b) highlight key articles on adults and children with AKI in order to demonstrate how such insights might be applied to neonates, and (c) suggest clinical research studies to fill the gaps in our understanding of neonatal AKI. To date, observational studies suggest high rates of AKI and poor outcomes in critically ill neonates. Neonates with AKI are at risk of developing chronic kidney disease and hypertension. Large prospective studies are needed to test definitions and to better understand risk factors, incidence, independent outcomes, and mechanisms that lead to poor short- and long-term outcomes. Early biomarkers of AKI need to be explored in critically ill neonates. Infants with AKI need to be followed for sequelae after AKI