Antenatal and Intrapartum Risk Factors for Use of Emergency and Restorative Medicaid Dental Services for Children

Purpose: To investigate the relationship between antenatal/intrapartum factors and Medicaid use. Methods: Three databases were used: (1) birth records; (2) Medicaid files; and (3) Medicaid dental claims. Results: Children of Caucasian mothers were 34 percent more likely to have more than one restorative claim versus children of African American mothers (odds ratio [OR] equals 1.34, 95 percent confidence interval [95% CI] equals 1.10 to 1.65, P<.005). Children born with low birth weight were 37 percent more likely to have emergency claims (OR equals 1.37, 95% CI equals 1.02 to 1.83, P=.03). The adjusted analysis found that Caucasian mothers had higher odds ratio of having a dental claim than African American mothers (P<.001): 33 percent for a restorative claim and 56 percent for an emergency claim. When race was analyzed, the odds of a restorative claim among African American mothers were 2.5 times higher in children delivered by C-section versus those vaginally delivered (OR equals 2.52, 95% CI equals 1.02-6.2, P<.001). Conclusions: This study found: an association between children of Caucasian mothers and the likelihood of experiencing claims; and a relationship between children born with low birth weight and C-section and the likelihood of use of Medicaid services

Energy hole mitigation through cooperative transmission in wireless sensor networks

The energy balancing capability of cooperative communication is utilized to solve the energy hole problem in wireless sensor networks. We first propose a cooperative transmission strategy, where intermediate nodes participate in two cooperative multi-input single-output (MISO) transmissions with the node at the previous hop and a selected node at the next hop, respectively. Then, we study the optimization problems for power allocation of the cooperative transmission strategy by examining two different approaches: network lifetime maximization (NLM) and energy consumption minimization (ECM). For NLM, the numerical optimal solution is derived and a searching algorithm for suboptimal solution is provided when the optimal solution does not exist. For ECM, a closed-form solution is obtained. Numerical and simulation results show that both the approaches have much longer network lifetime than SISO transmission strategies and other cooperative communication schemes. Moreover, NLM which features energy balancing outperforms ECM which focuses on energy efficiency, in the network lifetime sense

Scalar-Torsion Mode in a Cosmological Model of the Poincar\'{e} Gauge Theory of Gravity

We investigate the equation of state (EoS) of the scalar-torsion mode in Poincar\'{e} gauge theory of gravity. We concentrate on two cases with the constant curvature solution and positive kinetic energy, respectively. In the former, we find that the torsion EoS has different values in the various stages of the universe. In particular, it behaves like the radiation (matter) EoS of $w_r=1/3$ ($w_m=0$) in the radiation (matter) dominant epoch, while in the late time the torsion density is supportive for the accelerating universe. In the latter, our numerical analysis shows that in general the EoS has an asymptotic behavior in the high redshift regime, while it could cross the phantom divide line in the low redshift regime.Comment: 12 pages, 2 figures, title changed, revised version accepted for publication in JCA

Why Does Steady-State Magnetic Reconnection Have A Maximum Local Rate Of Order 0.1?

Simulations suggest collisionless steady-state magnetic reconnection of Harris-type current sheets proceeds with a rate of order 0.1, independent of dissipation mechanism. We argue this long-standing puzzle is a result of constraints at the magnetohydrodynamic (MHD) scale. We perform a scaling analysis of the reconnection rate as a function of the opening angle made by the upstream magnetic fields, finding a maximum reconnection rate close to 0.2. The predictions compare favorably to particle-in-cell simulations of relativistic electron-positron and non-relativistic electron-proton reconnection. The fact that simulated reconnection rates are close to the predicted maximum suggests reconnection proceeds near the most efficient state allowed at the MHD-scale. The rate near the maximum is relatively insensitive to the opening angle, potentially explaining why reconnection has a similar fast rate in differing models

The Discovery of A Luminous Broad Absorption Line Quasar at A Redshift of 7.02

Despite extensive efforts, only two quasars have been found at $z>7$ to date due to a combination of low spatial density and high contamination from more ubiquitous Galactic cool dwarfs in quasar selection. This limits our current knowledge of the super-massive black hole (SMBH) growth mechanism and reionization history. In this letter, we report the discovery of a luminous quasar at $z=7.021$, DELS J003836.10$-$152723.6 (hereafter J0038$-$1527), selected using photometric data from DESI Legacy imaging Survey (DELS), Pan-STARRS1 (PS1) imaging Survey, as well as Wide-field Infrared Survey Explore ($WISE$) mid-infrared all-sky survey. With an absolute magnitude of $M_{1450}$=$-$27.1 and bolometric luminosity of $L_{\rm Bol}$=5.6$\times$10$^{13}$ $L_\odot$, J0038$-$1527 is the most luminous quasar known at $z>7$. Deep optical to near infrared spectroscopic observations suggest that J0038-1527 hosts a 1.3 billion solar mass BH accreting at the Eddington limit, with an Eddington ratio of 1.25$\pm$0.19. The CIV broad emission line of J0038$-$1527 is blue-shifted by more than 3000 km s$^{-1}$ to the systemic redshift. More detailed investigations of the high quality spectra reveal three extremely high velocity CIV broad absorption lines (BALs) with velocity from 0.08 to 0.14 times the speed of light and total balnicity index of more than 5000 km s$^{-1}$, suggesting the presence of relativistic outflows. J0038$-$1527 is the first quasar found at the epoch of reionization (EoR) with such strong outflows and provides a unique laboratory to investigate AGN feedback on the formation and growth of the most massive galaxies in the early universe.Comment: ApJL in pres

FLJ10540 is associated with tumor progression in nasopharyngeal carcinomas and contributes to nasopharyngeal cell proliferation, and metastasis via osteopontin/CD44 pathway

BACKGROUND: Nasopharyngeal carcinoma (NPC) is well-known for its highly metastatic characteristics, but little is known of its molecular mechanisms. New biomarkers that predict clinical outcome, in particular the ability of the primary tumor to develop metastatic tumors are urgently needed. The aim of this study is to investigate the role of FLJ10540 in human NPC development. METHODS: A bioinformatics approach was used to explore the potentially important regulatory genes involved in the growth/metastasis control of NPC. FLJ10540 was chosen for this study. Two co-expression strategies from NPC microarray were employed to identify the relationship between FLJ10540 and osteopontin. Quantitative-RT-PCR, immunoblotting, and immunohistochemistry analysis were used to investigate the mRNA and protein expression profiles of FLJ10540 and osteopontin in the normal and NPC tissues to confirm microarray results. TW01 and Hone1 NPC cells with overexpression FLJ10540 or siRNA to repress endogenous FLJ10540 were generated by stable transfection to further elucidate the molecular mechanisms of FLJ10540-elicited cell growth and metastasis under osteopontin stimulation. RESULTS: We found that osteopontin expression exhibited a positive correlation with FLJ10540 in NPC microarray. We also demonstrated comprehensively that FLJ10540 and osteopontin were not only overexpressed in NPC specimens, but also significantly correlated with advanced tumor and lymph node-metastasis stages, and had a poor 5-year survival rate, respectively. Stimulation of NPC parental cells with osteopontin results in an increase in FLJ10540 mRNA and protein expressions. Functionally, FLJ10540 transfectant alone, or stimulated with osteopontin, exhibited fast growth and increased metastasis as compared to vehicle control with or without osteopontin stimulation. Conversely, knockdown of FLJ10540 by siRNA results in the suppression of NPC cell growth and motility. Treatment with anti-CD44 antibodies in NPC parental cells not only resulted in a decrease of FLJ10540 protein, but also affected the abilities of FLJ10540-elicited cell growth and motility in osteopontin stimulated-NPC cells. CONCLUSIONS: These findings suggest that FLJ10540 may be critical regulator of disease progression in NPC, and the underlying mechanism may involve in the osteopontin/CD44 pathway

Selection of DDX5 as a novel internal control for Q-RT-PCR from microarray data using a block bootstrap re-sampling scheme

<p>Abstract</p> <p>Background</p> <p>The development of microarrays permits us to monitor transcriptomes on a genome-wide scale. To validate microarray measurements, quantitative-real time-reverse transcription PCR (Q-RT-PCR) is one of the most robust and commonly used approaches. The new challenge in gene quantification analysis is how to explicitly incorporate statistical estimation in such studies. In the realm of statistical analysis, the various available methods of the probe level normalization for microarray analysis may result in distinctly different target selections and variation in the scores for the correlation between microarray and Q-RT-PCR. Moreover, it remains a major challenge to identify a proper internal control for Q-RT-PCR when confirming microarray measurements.</p> <p>Results</p> <p>Sixty-six Affymetrix microarray slides using lung adenocarcinoma tissue RNAs were analyzed by a statistical re-sampling method in order to detect genes with minimal variation in gene expression. By this approach, we identified <it>DDX5 </it>as a novel internal control for Q-RT-PCR. Twenty-three genes, which were differentially expressed between adjacent normal and tumor samples, were selected and analyzed using 24 paired lung adenocarcinoma samples by Q-RT-PCR using two internal controls, <it>DDX5 </it>and <it>GAPDH</it>. The percentage correlation between Q-RT-PCR and microarray were 70% and 48% by using <it>DDX5 </it>and <it>GAPDH </it>as internal controls, respectively.</p> <p>Conclusion</p> <p>Together, these quantification strategies for Q-RT-PCR data processing procedure, which focused on minimal variation, ought to significantly facilitate internal control evaluation and selection for Q-RT-PCR when corroborating microarray data.</p

A novel tumor suppressor gene ECRG4 interacts directly with TMPRSS11A (ECRG1) to inhibit cancer cell growth in esophageal carcinoma

<p>Abstract</p> <p>Background</p> <p>The esophageal carcinoma related gene 4 (ECRG4) was initially identified and cloned from human normal esophageal epithelium in our laboratory (GenBank accession no.<ext-link ext-link-id="AF325503" ext-link-type="gen">AF325503</ext-link>). ECRG4 has been described as a novel tumor suppressor gene associated with prognosis in esophageal squamous cell carcinoma (ESCC).</p> <p>Methods</p> <p>In this study, binding affinity assay in vitro and co-immunoprecipitation experiment in vivo were utilized to verify the physical interaction between ECRG4 and transmembrane protease, serine 11A (TMPRSS11A, also known as ECRG1, GenBank accession no. <ext-link ext-link-id="AF 071882" ext-link-type="gen">AF 071882</ext-link>). Then, p21 protein expression, cell cycle and cell proliferation regulations were examined after ECRG4 and ECRG1 co-transfection in ESCC cells.</p> <p>Results</p> <p>We revealed for the first time that ECRG4 interacted directly with ECRG1 to inhibit cancer cell proliferation and induce cell cycle G1 phase block in ESCC. Binding affinity and co-immunoprecipitation assays demonstrated that ECRG4 interacted directly with ECRG1 in ESCC cells. Furthermore, the ECRG4 and ECRG1 co-expression remarkably upregulatd p21 protein level by Western blot (P < 0.001), induced cell cycle G1 phase block by flow cytometric analysis (P < 0.001) and suppressed cell proliferation by MTT and BrdU assay (both P < 0.01) in ESCC cells.</p> <p>Conclusions</p> <p>ECRG4 interacts directly with ECRG1 to upregulate p21 protein expression, induce cell cycle G1 phase block and inhibit cancer cells proliferation in ESCC.</p