Osculating orbits in Schwarzschild spacetime, with an application to extreme mass-ratio inspirals

We present a method to integrate the equations of motion that govern bound, accelerated orbits in Schwarzschild spacetime. At each instant the true worldline is assumed to lie tangent to a reference geodesic, called an osculating orbit, such that the worldline evolves smoothly from one such geodesic to the next. Because a geodesic is uniquely identified by a set of constant orbital elements, the transition between osculating orbits corresponds to an evolution of the elements. In this paper we derive the evolution equations for a convenient set of orbital elements, assuming that the force acts only within the orbital plane; this is the only restriction that we impose on the formalism, and we do not assume that the force must be small. As an application of our method, we analyze the relative motion of two massive bodies, assuming that one body is much smaller than the other. Using the hybrid Schwarzschild/post-Newtonian equations of motion formulated by Kidder, Will, and Wiseman, we treat the unperturbed motion as geodesic in a Schwarzschild spacetime whose mass parameter is equal to the system's total mass. The force then consists of terms that depend on the system's reduced mass. We highlight the importance of conservative terms in this force, which cause significant long-term changes in the time-dependence and phase of the relative orbit. From our results we infer some general limitations of the radiative approximation to the gravitational self-force, which uses only the dissipative terms in the force.Comment: 18 pages, 6 figures, final version to be published in Physical Review

Evaluation of HCMM data for assessing soil moisture and water table depth

Soil moisture in the 0-cm to 4-cm layer could be estimated with 1-mm soil temperatures throughout the growing season of a rainfed barley crop in eastern South Dakota. Empirical equations were developed to reduce the effect of canopy cover when radiometrically estimating the soil temperature. Corrective equations were applied to an aircraft simulation of HCMM data for a diversity of crop types and land cover conditions to estimate the soil moisture. The average difference between observed and measured soil moisture was 1.6% of field capacity. Shallow alluvial aquifers were located with HCMM predawn data. After correcting the data for vegetation differences, equations were developed for predicting water table depths within the aquifer. A finite difference code simulating soil moisture and soil temperature shows that soils with different moisture profiles differed in soil temperatures in a well defined functional manner. A significant surface thermal anomaly was found to be associated with shallow water tables

Evaluation of HCMM data for assessing soil moisture and water table depth

Data were analyzed for variations in eastern South Dakota. Soil moisture in the 0-4 cm layer could be estimated with 1-mm soil temperatures throughout the growing season of a rainfed barley crop (% cover ranging from 30% to 90%) with an r squared = 0.81. Empirical equations were developed to reduce the effect of canopy cover when radiometrically estimating the 1-mm soil temperature, r squared = 0.88. The corrective equations were applied to an aircraft simulation of HCMM data for a diversity of crop types and land cover conditions to estimate the 0-4 cm soil moisture. The average difference between observed and measured soil moisture was 1.6% of field capacity. HCMM data were used to estimate the soil moisture for four dates with an r squared = 0.55 after correction for crop conditions. Location of shallow alluvial aquifers could be accomplished with HCMM predawn data. After correction of HCMM day data for vegetation differences, equations were developed for predicting water table depths within the aquifer (r=0.8)

Molecular characterization of glucose-6-phosphate dehydrogenase deficiency in Jeddah, Kingdom of Saudi Arabia

International audienceABSTRACT: BACKGROUND: The development of polymerase chain reaction (PCR)-based methods for the detection of known mutations has facilitated detecting specific red blood cell (RBC) enzyme deficiencies. We carried out a study on glucose-6-phosphate dehydrogenase (G6PD) deficient subjects in Jeddah to evaluate the molecular characteristics of this enzyme deficiency and the frequency of nucleotide1311 and IVS-XI-93 polymorphisms in the glucose-6-phosphate dehydrogenase gene. RESULTS: A total of 1584 unrelated Saudis (984 neonates and 600 adults) were screened for glucose-6-phosphate dehydrogenase deficiency. The prevalence of glucose-6-phosphate dehydrogenase deficiency was 6.9% (n=110). G6PD Mediterranean mutation was observed in 98 (89.1%) cases, G6PD Aures in 11 (10.0%) cases, and G6PD Chatham in 1 (0.9%) case. None of the samples showed G6PD A mutation. Samples from 29 deficient subjects (25 males and 4 females) were examined for polymorphism. The association of two polymorphisms of exon/intron 11 (c.1311T/IVS XI 93C) was observed in 14 (42.4%) of 33 chromosomes studied. This association was found in 9 (31.0%) carriers of G6PD Mediterranean and in 4 (13.8%) carriers of G6PD Aures. CONCLUSIONS: The majority of mutations were G6PD Mediterranean, followed by G6PD Aures and <1% G6PD Chatham. We conclude that 1311T is a frequent polymorphism in subjects with G6PD Mediterranean and Aures variants in Jeddah

Identification of a novel mechanism of blood-brain communication during peripheral inflammation via choroid plexus-derived extracellular vesicles

Here, we identified release of extracellular vesicles (EVs) by the choroid plexus epithelium (CPE) as a new mechanism of blood-brain communication. Systemic inflammation induced an increase in EVs and associated pro-inflammatory miRNAs, including miR-146a and miR-155, in the CSF. Interestingly, this was associated with an increase in amount of multivesicular bodies (MVBs) and exosomes per MVB in the CPE cells. Additionally, we could mimic this using LPS-stimulated primary CPE cells and choroid plexus explants. These choroid plexus-derived EVs can enter the brain parenchyma and are taken up by astrocytes and microglia, inducing miRNA target repression and inflammatory gene up-regulation. Interestingly, this could be blocked in vivo by intracerebroventricular (icv) injection of an inhibitor of exosome production. Our data show that CPE cells sense and transmit information about the peripheral inflammatory status to the central nervous system (CNS) via the release of EVs into the CSF, which transfer this pro-inflammatory message to recipient brain cells. Additionally, we revealed that blockage of EV secretion decreases brain inflammation, which opens up new avenues to treat systemic inflammatory diseases such as sepsis

On the construction of model Hamiltonians for adiabatic quantum computation and its application to finding low energy conformations of lattice protein models

In this report, we explore the use of a quantum optimization algorithm for obtaining low energy conformations of protein models. We discuss mappings between protein models and optimization variables, which are in turn mapped to a system of coupled quantum bits. General strategies are given for constructing Hamiltonians to be used to solve optimization problems of physical/chemical/biological interest via quantum computation by adiabatic evolution. As an example, we implement the Hamiltonian corresponding to the Hydrophobic-Polar (HP) model for protein folding. Furthermore, we present an approach to reduce the resulting Hamiltonian to two-body terms gearing towards an experimental realization.Comment: 35 pages, 8 figure

Kernicterus by glucose-6-phosphate dehydrogenase deficiency: a case report and review of the literature

<p>Abstract</p> <p>Introduction</p> <p>Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive disease that causes acute or chronic hemolytic anemia and potentially leads to severe jaundice in response to oxidative agents. This deficiency is the most common human innate error of metabolism, affecting more than 400 million people worldwide.</p> <p>Case presentation</p> <p>Here, we present the first documented case of kernicterus in Panama, in a glucose-6-phosphate dehydrogenase-deficient newborn clothed in naphthalene-impregnated garments, resulting in reduced psychomotor development, neurosensory hypoacousia, absence of speech and poor reflex of the pupil to light.</p> <p>Conclusion</p> <p>Mutational analysis revealed the glucose-6-phosphate dehydrogenase Mediterranean polymorphic variant, which explained the development of kernicterus after exposition of naphthalene. As the use of naphthalene in stored clothes is a common practice, glucose-6-phosphate dehydrogenase testing in neonatal screening could prevent severe clinical consequences.</p

Impact of the Method of G6PD Deficiency Assessment on Genetic Association Studies of Malaria Susceptibility

BACKGROUND:Clinical association studies have yielded varied results regarding the impact of glucose-6-phosphate dehydrogenase (G6PD) deficiency upon susceptibility to malaria. Analyses have been complicated by varied methods used to diagnose G6PD deficiency. METHODOLOGY/PRINCIPAL FINDINGS:We compared the association between uncomplicated malaria incidence and G6PD deficiency in a cohort of 601 Ugandan children using two different diagnostic methods, enzyme activity and G6PD genotype (G202A, the predominant East African allele). Although roughly the same percentage of males were identified as deficient using enzyme activity (12%) and genotype (14%), nearly 30% of males who were enzymatically deficient were wild-type at G202A. The number of deficient females was three-fold higher with assessment by genotype (21%) compared to enzyme activity (7%). Heterozygous females accounted for the majority (46/54) of children with a mutant genotype but normal enzyme activity. G6PD deficiency, as determined by G6PD enzyme activity, conferred a 52% (relative risk [RR] 0.48, 95% CI 0.31-0.75) reduced risk of uncomplicated malaria in females. In contrast, when G6PD deficiency was defined based on genotype, the protective association for females was no longer seen (RR = 0.99, 95% CI 0.70-1.39). Notably, restricting the analysis to those females who were both genotypically and enzymatically deficient, the association of deficiency and protection from uncomplicated malaria was again demonstrated in females, but not in males (RR = 0.57, 95% CI 0.37-0.88 for females). CONCLUSIONS/SIGNIFICANCE:This study underscores the impact that the method of identifying G6PD deficient individuals has upon association studies of G6PD deficiency and uncomplicated malaria. We found that G6PD-deficient females were significantly protected against uncomplicated malaria, but this protection was only seen when G6PD deficiency is described using enzyme activity. These observations may help to explain the discrepancy in some published association studies involving G6PD deficiency and uncomplicated malaria