On Exchange of Orbital Angular Momentum Between Twisted Photons and Atomic Electrons

We obtain an expression for the matrix element for a twisted (Laguerre-Gaussian profile) photon scattering from a hydrogen atom. We consider photons incoming with an orbital angular momentum (OAM) of $\ell \hbar$, carried by a factor of $e^{i \ell \phi}$ not present in a plane-wave or pure Gaussian profile beam. The nature of the transfer of $+2\ell$ units of OAM from the photon to the azimuthal atomic quantum number of the atom is investigated. We obtain simple formulae for these OAM flip transitions for elastic forward scattering of twisted photons when the photon wavelength $\lambda$ is large compared with the atomic target size $a$, and small compared the Rayleigh range $z_R$, which characterizes the collimation length of the twisted photon beam.Comment: 16 page

THE PATIENT-SPECIFIC INJURY SCORE: PRECISION MEDICINE IN TRAUMA PATIENTS PREDICTS ORGAN DYSFUNCTION AND OUTCOMES

poster abstractIntroduction: Current injury scoring systems in polytraumatized patients are limited at predicting patient outcomes. We present a novel method that quantifies mechanical tissue damage and cumulative hypoperfusion using a precision medicine approach. We hypothesized that a Patient-Specific Injury score formulated from individualized injury indices would stratify patient risk for developing organ dysfunction after injury. We compared correspondence between PSI and the Injury Severity Score with outcomes of organ dysfunction and MOF. Methods: Fifty Multiply-injured-patients (MIPs) were studied. Tissue Damage Volume scores were measured from admission pan-axial CT scans using purpose-designed post-processing software to quantify volumetric magnitude and distribution of injuries. Ischemic injury was quantified using Shock Volumes. SV is a time-magnitude integration of shock index. Values above 0.9 were measured in the 24-hours after injury. Metabolic response was quantified by subtracting the lowest first 24 hr pH from 7.40. PSI combines these indices into the formula: PSI=[0.2TDV+SV]*MR. Correspondence coefficients from regression modeling between PSI and organ dysfunction, measured by the Marshall Multiple Organ Dysfunction score averaged from days 2-5 post-injury, were compared to similar regression models of ISS vs. day 2-5 MOD-scores. We compared PSI and ISS in patients that did or did not develop MOF. Results: PSI demonstrated better correlation to organ dysfunction (r2=0.576) in comparison to ISS (r2=0.393) using the MOD-score on days 2-5. Mean PSI increased 3.4x(58.5vs.17.0;p<0.02) and ISS scores increased 1.4x(39.0vs.28.0;p=0.10) in patients that developed MOF versus those that did not. Conclusions: This study shows that a precision medicine approach that integrates patient-specific indices of mechanical tissue damage, ischemic tissue injury, and metabolic response better corresponds to phenotypic changes including organ dysfunction and MOF compared to ISS in MIPs. The PSI-score can be calculated within 24 hours of injury, making it useful for stratifying risk and predicting the magnitude of organ dysfunction to anticipate

Gene therapy with Angiotensin-(1-9) preserves left ventricular systolic function after myocardial infarction

BACKGROUND: Angiotensin-(1-9) [Ang-(1-9)] is a novel peptide of the counter-regulatory axis of the renin angiotensin system previously demonstrated to have therapeutic potential in hypertensive cardiomyopathy when administered via osmotic minipump in mice. Here, we investigate whether gene transfer of Ang-(1-9) is cardioprotective in a murine model of myocardial infarction (MI). OBJECTIVES: To evaluate effects of Ang-(1-9) gene therapy on myocardial structural and functional remodeling post infarction. METHODS: C57BL/6 mice underwent permanent left anterior descending coronary artery ligation and cardiac function was assessed using echocardiography for 8 weeks followed by a terminal measurement of left ventricular (LV) pressure-volume loops. Ang-(1-9) was delivered by adeno-associated viral vector via single tail vein injection immediately following induction of MI. Direct effects of Ang-(1-9) on cardiomyocyte excitation–contraction coupling and cardiac contraction were evaluated in isolated mouse and human cardiomyocytes and in an ex vivo Langendorff perfused whole heart model. RESULTS: Gene delivery of Ang-(1-9) significantly reduced sudden cardiac death post-MI. Pressure–volume measurements revealed complete restoration of end systolic pressure, ejection fraction, end systolic volume and the end diastolic pressure–volume relationship by Ang-(1-9) treatment. Stroke volume and cardiac output were significantly increased versus sham. Histological analysis revealed only mild effects on cardiac hypertrophy and fibrosis, but a significant increase in scar thickness. Direct assessment of Ang-(1-9) on isolated cardiomyocytes demonstrated a positive inotropic effect via increasing calcium transient amplitude and increasing contractility. Ang-(1-9) increased contraction in the Langendorff model through a protein kinase A-dependent mechanism. CONCLUSIONS: Our novel findings show that Ang-(1-9) gene therapy preserves LV systolic function post-MI, restoring cardiac function. Furthermore, Ang-(1-9) has a direct effect on cardiomyocyte 3 calcium handling through a protein kinase A-dependent mechanism. These data highlight Ang-(1-9) gene therapy as a potential new strategy in the context of MI

Electronic structure of sodium tungsten bronzes Na<SUB>x</SUB>WO<SUB>3</SUB> by high-resolution angle-resolved photoemission spectroscopy

The electronic structure of sodium tungsten bronzes, NaxWO3, for full range of x is investigated by high-resolution angle-resolved photoemission spectroscopy (HR-ARPES). The experimentally determined valence-band structure has been compared with the results of ab initio band-structure calculation. The HR-ARPES spectra taken in both the insulating and metallic phase of NaxWO3 reveal the origin of metal-insulator transition (MIT) in the sodium tungsten bronze system. In the insulating NaxWO3, the near-EF states are localized due to the strong disorder caused by the random distribution of Na+ ions in WO3 lattice. While the presence of an impurity band (level) induced by Na doping is often invoked to explain the insulating state found at low concentrations, there is no signature of impurity band (level) found from our results. Due to disorder and Anderson localization effect, there is a long-range Coulomb interaction of conduction electrons; as a result, the system is insulating. In the metallic regime, the states near EF are populated and the Fermi level shifts upward rigidly with increasing electron doping (x). The volume of electronlike Fermi surface (FS) at the &#915;(X) point gradually increases with increasing Na concentration due to W 5dt2g band filling. A rigid shift of EF is found to give a qualitatively good description of the FS evolution

Polymorphic Allele of Human IRGM1 Is Associated with Susceptibility to Tuberculosis in African Americans

An ancestral polymorphic allele of the human autophagy-related gene IRGM1 is associated with altered gene expression and a genetic risk for Crohn's Disease (CD). We used the single nucleotide polymorphism rs10065172C/T as a marker of this polymorphic allele and genotyped 370 African American and 177 Caucasian tuberculosis (TB) cases and 180 African American and 110 Caucasian controls. Among African Americans, the TB cases were more likely to carry the CD-related T allele of rs10065172 (odds ratio of 1.54; 95% confidence interval, 1.17–2.02; P<0.01) compared to controls. Our finding suggests that this CD-related IRGM1 polymorphic allele is also associated with human susceptibility to TB disease among African Americans

cn.FARMS: a latent variable model to detect copy number variations in microarray data with a low false discovery rate

Cost-effective oligonucleotide genotyping arrays like the Affymetrix SNP 6.0 are still the predominant technique to measure DNA copy number variations (CNVs). However, CNV detection methods for microarrays overestimate both the number and the size of CNV regions and, consequently, suffer from a high false discovery rate (FDR). A high FDR means that many CNVs are wrongly detected and therefore not associated with a disease in a clinical study, though correction for multiple testing takes them into account and thereby decreases the study's discovery power. For controlling the FDR, we propose a probabilistic latent variable model, ‘cn.FARMS’, which is optimized by a Bayesian maximum a posteriori approach. cn.FARMS controls the FDR through the information gain of the posterior over the prior. The prior represents the null hypothesis of copy number 2 for all samples from which the posterior can only deviate by strong and consistent signals in the data. On HapMap data, cn.FARMS clearly outperformed the two most prevalent methods with respect to sensitivity and FDR. The software cn.FARMS is publicly available as a R package at http://www.bioinf.jku.at/software/cnfarms/cnfarms.html

Publisher Correction: Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

The original version of this article contained an error in the name of the author Ramachandran S. Vasan, which was incorrectly given as Vasan S. Ramachandran. This has now been corrected in both the PDF and HTML versions of the article

Deep coverage whole genome sequences and plasma lipoprotein(a) in individuals of European and African ancestries.

Lipoprotein(a), Lp(a), is a modified low-density lipoprotein particle that contains apolipoprotein(a), encoded by LPA, and is a highly heritable, causal risk factor for cardiovascular diseases that varies in concentrations across ancestries. Here, we use deep-coverage whole genome sequencing in 8392 individuals of European and African ancestry to discover and interpret both single-nucleotide variants and copy number (CN) variation associated with Lp(a). We observe that genetic determinants between Europeans and Africans have several unique determinants. The common variant rs12740374 associated with Lp(a) cholesterol is an eQTL for SORT1 and independent of LDL cholesterol. Observed associations of aggregates of rare non-coding variants are largely explained by LPA structural variation, namely the LPA kringle IV 2 (KIV2)-CN. Finally, we find that LPA risk genotypes confer greater relative risk for incident atherosclerotic cardiovascular diseases compared to directly measured Lp(a), and are significantly associated with measures of subclinical atherosclerosis in African Americans