Population-Based Study of Sleep Apnea in Pregnancy and Maternal and Infant Outcomes

Study Objectives: To examine the association between sleep apnea and pregnancy outcomes in a large population-based cohort. Methods: Population-based cohort study using linked birth and hospital records was conducted in New South Wales, Australia. Participants were all women who gave birth in hospital from 2002 to 2012 (N=636,227). Sleep apnea in the year before pregnancy or during pregnancy was identified from hospital records. Outcomes of interest were gestational diabetes, pregnancy hypertension, planned delivery, caesarean section, preterm birth, perinatal death, 5-minute Apgar score, admission to neonatal intensive care or special care nursery, and infant size for gestational age. Maternal outcomes were identified using a combination of hospital and birth records. Infant outcomes came from the birth record. Modified Poisson regression models were used to examine associations between sleep apnea and each outcome taking into account maternal age, country of birth, socioeconomic disadvantage, smoking, obesity, parity, pre-existing diabetes and hypertension. Results: Sleep apnea was significantly associated with pregnancy hypertension (adjusted RR 1.68; 95% CI 1.40 – 2.07), planned delivery (1.15; 1.07 – 1.23), preterm birth (1.50; 1.21 – 1.84), 5-minute Apgar <7 (1.60; 1.07 – 2.38), admission to neonatal intensive care/special care nursery (1.26; 1.11 – 1.44), large-for-gestational-age infants (1.27; 1.04 – 1.55) but not with gestational diabetes (1.09; 0.82 – 1.46), caesarean section (1.06; 0.96 – 1.17), perinatal death (1.73; 0.92 – 3.25), or small-for-gestational-age infants (0.81; 0.61 – 1.08). Conclusions: Sleep apnea is associated with higher rates of obstetric complications and intervention, as well as preterm delivery. Future research should examine if these are independent of obstetric history.NHMRC, AR

Detecting Inspiring Content on Social Media

Inspiration moves a person to see new possibilities and transforms the way they perceive their own potential. Inspiration has received little attention in psychology, and has not been researched before in the NLP community. To the best of our knowledge, this work is the first to study inspiration through machine learning methods. We aim to automatically detect inspiring content from social media data. To this end, we analyze social media posts to tease out what makes a post inspiring and what topics are inspiring. We release a dataset of 5,800 inspiring and 5,800 non-inspiring English-language public post unique ids collected from a dump of Reddit public posts made available by a third party and use linguistic heuristics to automatically detect which social media English-language posts are inspiring.Comment: accepted at ACII 202

Diverse hepatitis C virus glycoproteins mediate viral infection in a CD81-dependent manner

We recently reported that retroviral pseudotypes bearing the hepatitis C virus (HCV) strain H and Con1 glycoproteins, genotype 1a and 1b, respectively, require CD81 as a coreceptor for virus-cell entry and infection. Soluble truncated E2 cloned from a number of diverse HCV genotypes fail to interact with CD81, suggesting that viruses of diverse origin may utilize different receptors and display altered cell tropism. We have used the pseudotyping system to study the tropism of viruses bearing diverse HCV glycoproteins. Viruses bearing these glycoproteins showed a 150-fold range in infectivity for hepatoma cells and failed to infect lymphoid cells. The level of glycoprotein incorporation into particles varied considerably between strains, generally reflecting the E2 expression level within transfected cells. However, differences in glycoprotein incorporation were not associated with virus infectivity, suggesting that infectivity is not limited by the absolute level of glycoprotein. All HCV pseudotypes failed to infect HepG2 cells and yet infected the same cells after transduction to express human CD81, confirming the critical role of CD81 in HCV infection. Interestingly, these HCV pseudotypes differed in their ability to infect HepG2 cells expressing a panel of CD81 variants, suggesting subtle differences in the interaction of CD81 residues with diverse viral glycoproteins. Our current model of HCV infection suggests that CD81, together with additional unknown liver specific receptor(s), mediate the virus-cell entry process

Effects of Noise, Correlations and errors in the preparation of initial states in Quantum Simulations

In principle a quantum system could be used to simulate another quantum system. The purpose of such a simulation would be to obtain information about problems which cannot be simulated with a classical computer due to the exponential increase of the Hilbert space with the size of the system and which cannot be measured or controlled in an actual experiment. The system will interact with the surrounding environment, with the other particles in the system and be implemented using imperfect controls making it subject to noise. It has been suggested that noise does not need to be controlled to the same extent as it must be for general quantum computing. However the effects of noise in quantum simulations and how to treat them are not completely understood. In this paper we study an existing quantum algorithm for the one-dimensional Fano-Anderson model to be simulated using a liquid-state NMR device. We calculate the evolution of different initial states in the original model, and then we add interacting spins to simulate a more realistic situation. We find that states which are entangled with their environment, and sometimes correlated but not necessarily entangled have an evolution which is described by maps which are not completely positive. We discuss the conditions for this to occur and also the implications.Comment: Revtex 4-1, 14 pages, 21 figures, version 2 has typos corrected and acknowledgement adde

MicroRNA-21 is Induced by Rapamycin in a Model of Tuberous Sclerosis (TSC) and Lymphangioleiomyomatosis (LAM)

Lymphangioleiomyomatosis (LAM), a multisystem disease of women, is manifest by the proliferation of smooth muscle-like cells in the lung resulting in cystic lung destruction. Women with LAM can also develop renal angiomyolipomas. LAM is caused by mutations in the tuberous sclerosis complex genes (TSC1 or TSC2), resulting in hyperactive mammalian Target of Rapamycin (mTOR) signaling. The mTOR inhibitor, Rapamycin, stabilizes lung function in LAM and decreases the volume of renal angiomyolipomas, but lung function declines and angiomyolipomas regrow when treatment is discontinued, suggesting that factors induced by mTORC1 inhibition may promote the survival of TSC2-deficient cells. Whether microRNA (miRNA, miR) signaling is involved in the response of LAM to mTORC1 inhibition is unknown. We identified Rapamycin-dependent miRNA in LAM patient angiomyolipoma-derived cells using two separate screens. First, we assayed 132 miRNA of known significance to tumor biology. Using a cut-off of >1.5-fold change, 48 microRNA were Rapamycin-induced, while 4 miRs were downregulated. In a second screen encompassing 946 miRNA, 18 miRs were upregulated by Rapamycin, while eight were downregulated. Dysregulation of miRs 29b, 21, 24, 221, 106a and 199a were common to both platforms and were classified as candidate “RapamiRs.” Validation by qRT-PCR confirmed that these microRNA were increased. miR-21, a pro-survival miR, was the most significantly increased by mTOR-inhibition (p<0.01). The regulation of miR-21 by Rapamycin is cell type independent. mTOR inhibition promotes the processing of the miR-21 transcript (pri-miR-21) to a premature form (pre-miR-21). In conclusion, our findings demonstrate that Rapamycin upregulates multiple miRs, including pro-survival miRs, in TSC2-deficient patient-derived cells. The induction of miRs may contribute to the response of LAM and TSC patients to Rapamycin therapy

Probing Lyman-alpha Absorbers in Cosmological Simulations with Double Lines of Sight

We perform a double line of sight (DLOS) analysis of the Lyman-alpha forest structures that form and evolve in cosmological N-body/hydrodynamic simulations. Pairs of simulated spectra, extracted from lines of sight separated by distances from D=12.5kpc up to 800kpc, and a ``control sample'' of unrelated lines of sight, are analyzed at redshifts 3, 2, and 1. Coincident line samples are defined for HI column density thresholds of Nco = 10^{12.5}, 10^{13}, and 10^{14} per square cm. We find that: 1) Under the assumption of a single structure size, a Bayesian analysis yields sizes that are larger for smaller Nco, and at fixed Nco the size decreases with decreasing redshift. However, these derived sizes are found to increase with increasing D indicating that the assumption of a single structure size is invalid. 2) The column densities of coincident pairs are highly correlated for small D, with increasing scatter as D is increased, consistent with structures that have a centrally peaked N(HI) that decreases gradually with radius. 3) The velocity difference distribution for coincident lines is very narrow for small D, and widens as D is increased to meet the expectation for chance coincidences in unrelated lines of sight. This behavior is indicative of organized motion within the structures. 4) For small D, the distribution of anticoincident line column densities, Nac, falls steeply as Nac increases from the cutoff value, but has a significant tail at large values which is inconsistent with a population of spherical absorbers with sharp edges, and consistent with a flattened geometry. The conclusions reached on the basis of the DLOS analysis are validated by an examination of the three-dimensional structures and velocity flows in the simulation data.Comment: 17 pages, Latex file, and 8 PostScript figures; Submitted to the Astrophysical Journal; Available as a single compressed Postscript file at http://www.astro.psu.edu/users/charlto

Passive scalars, random flux, and chiral phase fluids

We study the two-dimensional localization problem for (i) a classical diffusing particle advected by a quenched random mean-zero vorticity field, and (ii) a quantum particle in a quenched random mean-zero magnetic field. Through a combination of numerical and analytic techniques we argue that both systems have extended eigenstates at a special point in the spectrum, $E_c$, where a sublattice decomposition obtains. In a neighborhood of this point, the Lyapunov exponents of the transfer-matrices acquire ratios characteristic of conformal invariance allowing an indirect determination of $1/r$ for the typical spatial decay of eigenstates.Comment: use revtex, two-column, 4 pages, 5 postscript figures, submitted to PR

A Dominant Mutation in mediator of paramutation2, One of Three Second-Largest Subunits of a Plant-Specific RNA Polymerase, Disrupts Multiple siRNA Silencing Processes

Paramutation involves homologous sequence communication that leads to meiotically heritable transcriptional silencing. We demonstrate that mop2 (mediator of paramutation2), which alters paramutation at multiple loci, encodes a gene similar to Arabidopsis NRPD2/E2, the second-largest subunit of plant-specific RNA polymerases IV and V. In Arabidopsis, Pol-IV and Pol-V play major roles in RNA–mediated silencing and a single second-largest subunit is shared between Pol-IV and Pol-V. Maize encodes three second-largest subunit genes: all three genes potentially encode full length proteins with highly conserved polymerase domains, and each are expressed in multiple overlapping tissues. The isolation of a recessive paramutation mutation in mop2 from a forward genetic screen suggests limited or no functional redundancy of these three genes. Potential alternative Pol-IV/Pol-V–like complexes could provide maize with a greater diversification of RNA–mediated transcriptional silencing machinery relative to Arabidopsis. Mop2-1 disrupts paramutation at multiple loci when heterozygous, whereas previously silenced alleles are only up-regulated when Mop2-1 is homozygous. The dramatic reduction in b1 tandem repeat siRNAs, but no disruption of silencing in Mop2-1 heterozygotes, suggests the major role for tandem repeat siRNAs is not to maintain silencing. Instead, we hypothesize the tandem repeat siRNAs mediate the establishment of the heritable silent state—a process fully disrupted in Mop2-1 heterozygotes. The dominant Mop2-1 mutation, which has a single nucleotide change in a domain highly conserved among all polymerases (E. coli to eukaryotes), disrupts both siRNA biogenesis (Pol-IV–like) and potentially processes downstream (Pol-V–like). These results suggest either the wild-type protein is a subunit in both complexes or the dominant mutant protein disrupts both complexes. Dominant mutations in the same domain in E. coli RNA polymerase suggest a model for Mop2-1 dominance: complexes containing Mop2-1 subunits are non-functional and compete with wild-type complexes

Genetically Determined Plasma Lipid Levels and Risk of Diabetic Retinopathy: A Mendelian Randomization Study.

Results from observational studies examining dyslipidemia as a risk factor for diabetic retinopathy (DR) have been inconsistent. We evaluated the causal relationship between plasma lipids and DR using a Mendelian randomization approach. We pooled genome-wide association studies summary statistics from 18 studies for two DR phenotypes: any DR (N = 2,969 case and 4,096 control subjects) and severe DR (N = 1,277 case and 3,980 control subjects). Previously identified lipid-associated single nucleotide polymorphisms served as instrumental variables. Meta-analysis to combine the Mendelian randomization estimates from different cohorts was conducted. There was no statistically significant change in odds ratios of having any DR or severe DR for any of the lipid fractions in the primary analysis that used single nucleotide polymorphisms that did not have a pleiotropic effect on another lipid fraction. Similarly, there was no significant association in the Caucasian and Chinese subgroup analyses. This study did not show evidence of a causal role of the four lipid fractions on DR. However, the study had limited power to detect odds ratios less than 1.23 per SD in genetically induced increase in plasma lipid levels, thus we cannot exclude that causal relationships with more modest effect sizes exist