Analytic expressions for the constitutive parameters of magnetoelectric metamaterials

Electromagnetic metamaterials are artificially structured media typically composed of arrays of resonant electromagnetic circuits, the dimension and spacing of which are considerably smaller than the free-space wavelengths of operation. The constitutive parameters for metamaterials, which can be obtained using full-wave simulations in conjunction with numerical retrieval algorithms, exhibit artifacts related to the finite size of the metamaterial cell relative to the wavelength. Liu showed that the complicated, frequency-dependent forms of the constitutive parameters can be described by a set of relatively simple analytical expressions. These expressions provide useful insight and can serve as the basis for more intelligent interpolation or optimization schemes. Here, we show that the same analytical expressions can be obtained using a transfer-matrix formalism applied to a one-dimensional periodic array of thin, resonant, dielectric, or magnetic sheets. The transfer-matrix formalism breaks down, however, when both electric and magnetic responses are present in the same unit cell, as it neglects the magnetoelectric coupling between unit cells. We show that an alternative analytical approach based on the same physical model must be applied for such structures. Furthermore, in addition to the intercell coupling, electric and magnetic resonators within a unit cell may also exhibit magnetoelectric coupling. For such cells, we find an analytical expression for the effective index, which displays markedly characteristic dispersion features that depend on the strength of the coupling coefficient. We illustrate the applicability of the derived expressions by comparing to full-wave simulations on magnetoelectric unit cells. We conclude that the design of metamaterials with tailored simultaneous electric and magnetic response-such as negative index materials-will generally be complicated by potentially unwanted magnetoelectric coupling. © 2010 The American Physical Society.

Enhancing imaging systems using transformation optics.

We apply the transformation optical technique to modify or improve conventional refractive and gradient index optical imaging devices. In particular, when it is known that a detector will terminate the paths of rays over some surface, more freedom is available in the transformation approach, since the wave behavior over a large portion of the domain becomes unimportant. For the analyzed configurations, quasi-conformal and conformal coordinate transformations can be used, leading to simplified constitutive parameter distributions that, in some cases, can be realized with isotropic index; index-only media can be low-loss and have broad bandwidth. We apply a coordinate transformation to flatten a Maxwell fish-eye lens, forming a near-perfect relay lens; and also flatten the focal surface associated with a conventional refractive lens, such that the system exhibits an ultra-wide field-of-view with reduced aberration.

Multiple endocytic pathways of G protein-coupled receptors delineated by GIT1 sensitivity.

Recently, we identified a GTPase-activating protein for the ADP ribosylation factor family of small GTP-binding proteins that we call GIT1. This protein initially was identified as an interacting partner for the G protein-coupled receptor kinases, and its overexpression was found to affect signaling and internalization of the prototypical beta(2)-adrenergic receptor. Here, we report that GIT1 overexpression regulates internalization of numerous, but not all, G protein-coupled receptors. The specificity of the GIT1 effect is not related to the type of G protein to which a receptor couples, but rather to the endocytic route it uses. GIT1 only affects the function of G protein-coupled receptors that are internalized through the clathrin-coated pit pathway in a beta-arrestin- and dynamin-sensitive manner. Furthermore, the GIT1 effect is not limited to G protein-coupled receptors because overexpression of this protein also affects internalization of the epidermal growth factor receptor. However, constitutive agonist-independent internalization is not regulated by GIT1, because transferrin uptake is not affected by GIT1 overexpression. Thus, GIT1 is a protein involved in regulating the function of signaling receptors internalized through the clathrin pathway and can be used as a diagnostic tool for defining the endocytic pathway of a receptor.

Minor Moves: Growth, Fugitivity, and Children's Physical Movement

From tendencies to reduce the Underground Railroad to the imperative "follow the north star" to the iconic images of Ruby Bridges' 1960 "step forward" on the stairs of William Frantz Elementary School, America prefers to picture freedom as an upwardly mobile development. This preoccupation with the subtractive and linear force of development makes it hard to hear the palpable steps of so many truant children marching in the Movement and renders illegible the nonlinear movements of minors in the Underground. Yet a black fugitive hugging a tree, a white boy walking alone in a field, or even pieces of a discarded raft floating downstream like remnants of child's play are constitutive gestures of the Underground's networks of care and escape. Responding to 19th-century Americanists and cultural studies scholars' important illumination of the child as central to national narratives of development and freedom, "Minor Moves" reads major literary narratives not for the child and development but for the fugitive trace of minor and growth.

In four chapters, I trace the physical gestures of Nathaniel Hawthorne's Pearl, Harriet Beecher Stowe's Topsy, Harriet Wilson's Frado, and Mark Twain's Huck against the historical backdrop of the Fugitive Slave Act and the passing of the first compulsory education bills that made truancy illegal. I ask how, within a discourse of independence that fails to imagine any serious movements in the minor, we might understand the depictions of moving children as interrupting a U.S. preoccupation with normative development and recognize in them the emergence of an alternative imaginary. To attend to the movement of the minor is to attend to what the discursive order of a development-centered imaginary deems inconsequential and what its grammar can render only as mistakes. Engaging the insights of performance studies, I regard what these narratives depict as childish missteps (Topsy's spins, Frado's climbing the roof) as dances that trouble the narrative's discursive order. At the same time, drawing upon the observations of black studies and literary theory, I take note of the pressure these "minor moves" put on the literal grammar of the text (Stowe's run-on sentences and Hawthorne's shaky subject-verb agreements). I regard these ungrammatical moves as poetic ruptures from which emerges an alternative and prior force of the imaginary at work in these narratives--a force I call "growth."

Reading these "minor moves" holds open the possibility of thinking about a generative association between blackness and childishness, one that neither supports racist ideas of biological inferiority nor mandates in the name of political uplift the subsequent repudiation of childishness. I argue that recognizing the fugitive force of growth indicated in the interplay between the conceptual and grammatical disjunctures of these minor moves opens a deeper understanding of agency and dependency that exceeds notions of arrested development and social death. For once we interrupt the desire to picture development (which is to say the desire to picture), dependency is no longer a state (of social death or arrested development) of what does not belong, but rather it is what Édouard Glissant might have called a "departure" (from "be[ing] a single being"). Topsy's hard-to-see pick-pocketing and Pearl's running amok with brown men in the market are not moves out of dependency but indeed social turns (a dance) by way of dependency. Dependent, moving and ungrammatical, the growth evidenced in these childish ruptures enables different stories about slavery, freedom, and childishness--ones that do not necessitate a repudiation of childishness in the name of freedom, but recognize in such minor moves a fugitive way out.

Core and Shell Song Systems Unique to the Parrot Brain.

The ability to imitate complex sounds is rare, and among birds has been found only in parrots, songbirds, and hummingbirds. Parrots exhibit the most advanced vocal mimicry among non-human animals. A few studies have noted differences in connectivity, brain position and shape in the vocal learning systems of parrots relative to songbirds and hummingbirds. However, only one parrot species, the budgerigar, has been examined and no differences in the presence of song system structures were found with other avian vocal learners. Motivated by questions of whether there are important differences in the vocal systems of parrots relative to other vocal learners, we used specialized constitutive gene expression, singing-driven gene expression, and neural connectivity tracing experiments to further characterize the song system of budgerigars and/or other parrots. We found that the parrot brain uniquely contains a song system within a song system. The parrot "core" song system is similar to the song systems of songbirds and hummingbirds, whereas the "shell" song system is unique to parrots. The core with only rudimentary shell regions were found in the New Zealand kea, representing one of the only living species at a basal divergence with all other parrots, implying that parrots evolved vocal learning systems at least 29 million years ago. Relative size differences in the core and shell regions occur among species, which we suggest could be related to species differences in vocal and cognitive abilities.

A noisy linear map underlies oscillations in cell size and gene expression in bacteria.

During bacterial growth, a cell approximately doubles in size before division, after which it splits into two daughter cells. This process is subjected to the inherent perturbations of cellular noise and thus requires regulation for cell-size homeostasis. The mechanisms underlying the control and dynamics of cell size remain poorly understood owing to the difficulty in sizing individual bacteria over long periods of time in a high-throughput manner. Here we measure and analyse long-term, single-cell growth and division across different Escherichia coli strains and growth conditions. We show that a subset of cells in a population exhibit transient oscillations in cell size with periods that stretch across several (more than ten) generations. Our analysis reveals that a simple law governing cell-size control-a noisy linear map-explains the origins of these cell-size oscillations across all strains. This noisy linear map implements a negative feedback on cell-size control: a cell with a larger initial size tends to divide earlier, whereas one with a smaller initial size tends to divide later. Combining simulations of cell growth and division with experimental data, we demonstrate that this noisy linear map generates transient oscillations, not just in cell size, but also in constitutive gene expression. Our work provides new insights into the dynamics of bacterial cell-size regulation with implications for the physiological processes involved.

Discovery of the Elusive UDP-Diacylglucosamine Hydrolase in the Lipid A Biosynthetic Pathway in Chlamydia trachomatis.

Constitutive biosynthesis of lipid A via the Raetz pathway is essential for the viability and fitness of Gram-negative bacteria, includingChlamydia trachomatis Although nearly all of the enzymes in the lipid A biosynthetic pathway are highly conserved across Gram-negative bacteria, the cleavage of the pyrophosphate group of UDP-2,3-diacyl-GlcN (UDP-DAGn) to form lipid X is carried out by two unrelated enzymes: LpxH in beta- and gammaproteobacteria and LpxI in alphaproteobacteria. The intracellular pathogenC. trachomatislacks an ortholog for either of these two enzymes, and yet, it synthesizes lipid A and exhibits conservation of genes encoding other lipid A enzymes. Employing a complementation screen against aC. trachomatisgenomic library using a conditional-lethallpxHmutantEscherichia colistrain, we have identified an open reading frame (Ct461, renamedlpxG) encoding a previously uncharacterized enzyme that complements the UDP-DAGn hydrolase function inE. coliand catalyzes the conversion of UDP-DAGn to lipid Xin vitro LpxG shows little sequence similarity to either LpxH or LpxI, highlighting LpxG as the founding member of a third class of UDP-DAGn hydrolases. Overexpression of LpxG results in toxic accumulation of lipid X and profoundly reduces the infectivity ofC. trachomatis, validating LpxG as the long-sought-after UDP-DAGn pyrophosphatase in this prominent human pathogen. The complementation approach presented here overcomes the lack of suitable genetic tools forC. trachomatisand should be broadly applicable for the functional characterization of other essentialC. trachomatisgenes.IMPORTANCEChlamydia trachomatisis a leading cause of infectious blindness and sexually transmitted disease. Due to the lack of robust genetic tools, the functions of manyChlamydiagenes remain uncharacterized, including the essential gene encoding the UDP-DAGn pyrophosphatase activity for the biosynthesis of lipid A, the membrane anchor of lipooligosaccharide and the predominant lipid species of the outer leaflet of the bacterial outer membrane. We designed a complementation screen against theC. trachomatisgenomic library using a conditional-lethal mutant ofE. coliand identified the missing essential gene in the lipid A biosynthetic pathway, which we designatedlpxG We show that LpxG is a member of the calcineurin-like phosphatases and displays robust UDP-DAGn pyrophosphatase activityin vitro Overexpression of LpxG inC. trachomatisleads to the accumulation of the predicted lipid intermediate and reduces bacterial infectivity, validating thein vivofunction of LpxG and highlighting the importance of regulated lipid A biosynthesis inC. trachomatis.

Dominant Splice Site Mutations in PIK3R1 Cause Hyper IgM Syndrome, Lymphadenopathy and Short Stature.

The purpose of this research was to use next generation sequencing to identify mutations in patients with primary immunodeficiency diseases whose pathogenic gene mutations had not been identified. Remarkably, four unrelated patients were found by next generation sequencing to have the same heterozygous mutation in an essential donor splice site of PIK3R1 (NM_181523.2:c.1425 + 1G > A) found in three prior reports. All four had the Hyper IgM syndrome, lymphadenopathy and short stature, and one also had SHORT syndrome. They were investigated with in vitro immune studies, RT-PCR, and immunoblotting studies of the mutation's effect on mTOR pathway signaling. All patients had very low percentages of memory B cells and class-switched memory B cells and reduced numbers of naïve CD4+ and CD8+ T cells. RT-PCR confirmed the presence of both an abnormal 273 base-pair (bp) size and a normal 399 bp size band in the patient and only the normal band was present in the parents. Following anti-CD40 stimulation, patient's EBV-B cells displayed higher levels of S6 phosphorylation (mTOR complex 1 dependent event), Akt phosphorylation at serine 473 (mTOR complex 2 dependent event), and Akt phosphorylation at threonine 308 (PI3K/PDK1 dependent event) than controls, suggesting elevated mTOR signaling downstream of CD40. These observations suggest that amino acids 435-474 in PIK3R1 are important for its stability and also its ability to restrain PI3K activity. Deletion of Exon 11 leads to constitutive activation of PI3K signaling. This is the first report of this mutation and immunologic abnormalities in SHORT syndrome.