Unequal rapidity correlators in the dilute limit of JIMWLK

We study unequal rapidity correlators in the stochastic Langevin picture of Jalilian-Marian– Iancu–McLerran–Weigert–Leonidov–Kovner (JIMWLK) evolution in the Color Glass Conden- sate effective field theory. By separately evolving the Wilson lines in the direct and complex conjugate amplitudes, we use the formalism to study two-particle production at large rapidity separations. We show that the evolution between the rapidities of the two produced particles can be expressed as a linear equa- tion, even in the full nonlinear limit. We also show how the Langevin formalism for two-particle correlations reduces to a BFKL picture in the dilute limit and in momentum space, providing an interpretation of BFKL evolution as a stochastic process for color charges.Peer reviewe

Unequal rapidity correlators in the dilute limit of JIMWLK

We study unequal rapidity correlators in the stochastic Langevin picture of Jalilian-Marian– Iancu–McLerran–Weigert–Leonidov–Kovner (JIMWLK) evolution in the Color Glass Conden- sate effective field theory. By separately evolving the Wilson lines in the direct and complex conjugate amplitudes, we use the formalism to study two-particle production at large rapidity separations. We show that the evolution between the rapidities of the two produced particles can be expressed as a linear equa- tion, even in the full nonlinear limit. We also show how the Langevin formalism for two-particle correlations reduces to a BFKL picture in the dilute limit and in momentum space, providing an interpretation of BFKL evolution as a stochastic process for color charges.Peer reviewe

JIMWLK evolution of the odderon

We study the effects of a parity-odd "odderon" correlation in Jalilian-Marian-Iancu-McLerran-Weigert-Leonidov-Kovner renormalization group evolution at high energy. Firstly we show that in the eikonal picture where the scattering is described by Wilson lines, one obtains a strict mathematical upper limit for the magnitude of the odderon amplitude compared to the parity-even Pomeron one. This limit increases with N-c, approaching infinity in the infinite N-c limit. We use a systematic extension of the Gaussian approximation including both two-and three-point correlations which enables us to close the system of equations even at finite N-c. In the large-N-c limit we recover an evolution equation derived earlier. By solving this equation numerically we confirm that the odderon amplitude decreases faster in the nonlinear case than in the linear Balitsky-Fadin-Kuraev-Lipatov limit. We also point out that, in the three-point truncation at finite N-c, the presence of an odderon component introduces azimuthal angular correlations similar to cos(n phi) at all n in the target color field. These correlations could potentially have an effect on future studies of multiparticle angular correlations.Peer reviewe

Short-period line profile and light variations in the Beta Cephei star 19 Monocerotis

We present an analysis of 555 high-dispersion echelle spectra of 19 Mon obtained from two sites as well as 115 Strömgren uvby observations. We show that three periodicities are present at 5.229 94, 0.170 19 and 4.889 56 cycle d−1. The first periodicity has by far the largest amplitude. Photometric amplitude ratios and phase differences indicate an ℓ=2 mode, while the line profile variations unequivocally point to ℓ=2,m=-2. Because of the low amplitudes of the other two modes, very little can be said concerning them. Although 19 Mon was originally selected on the basis of its classification as a marginal Be star, the Be nature of the star is not supported by our observation

Reactive Oxygen Species Modulate the Barrier Function of the Human Glomerular Endothelial Glycocalyx

Reactive oxygen species (ROS) play a key role in the pathogenesis of proteinuria in glomerular diseases like diabetic nephropathy. Glomerular endothelial cell (GEnC) glycocalyx covers the luminal aspect of the glomerular capillary wall and makes an important contribution to the glomerular barrier. ROS are known to depolymerise glycosaminoglycan (GAG) chains of proteoglycans, which are crucial for the barrier function of GEnC glycocalyx. The aim of this study is to investigate the direct effects of ROS on the structure and function of GEnC glycocalyx using conditionally immortalised human GEnC. ROS were generated by exogenous hydrogen peroxide. Biosynthesis and cleavage of GAG chains was analyzed by radiolabelling (S35 and 3H-glucosamine). GAG chains were quantified on GEnC surface and in the cell supernatant using liquid chromatography and immunofluorescence techniques. Barrier properties were estimated by measuring trans-endothelial passage of albumin. ROS caused a significant loss of WGA lectin and heparan sulphate staining from the surface of GEnC. This lead to an increase in trans-endothelial albumin passage. The latter could be inhibited by catalase and superoxide dismutase. The effect of ROS on GEnC was not mediated via the GAG biosynthetic pathway. Quantification of radiolabelled GAG fractions in the supernatant confirmed that ROS directly caused shedding of HS GAG. This finding is clinically relevant and suggests a mechanism by which ROS may cause proteinuria in clinical conditions associated with high oxidative stress. © 2013 Singh et al.published_or_final_versio

Cutaneous vasculitis and recurrent infection caused by deficiency in complement factor I

Cutaneous leukocytoclastic vasculitis arises from immune complex deposition and dysregulated complement activation in small blood vessels. There are many causes, including dysregulated host response to infection, drug reactions, and various autoimmune conditions. It is increasingly recognised that some monogenic autoinflammatory diseases cause vasculitis, although genetic causes of vasculitis are extremely rare. We describe a child of consanguineous parents who presented with chronic cutaneous leukocytoclastic vasculitis, recurrent upper respiratory tract infection, and hypocomplementaemia. A homozygous p.His380Arg mutation in the complement factor I (CFI) gene CFI was identified as the cause, resulting in complete absence of alternative complement pathway activity, decreased classical complement activity, and low levels of serum factor I, C3, and factor H. C4 and C2 levels were normal. The same homozygous mutation and immunological defects were also identified in an asymptomatic sibling. CFI deficiency is thus now added to the growing list of monogenic causes of vasculitis and should always be considered in vasculitis patients found to have persistently low levels of C3 with normal C4

Popular Culture, Radical Egalitarianism, and Formations of Muslim Selfhood in South Asia

In early twentieth century leftist politics on the geographical fringes of South Asia, Islam played a major role. Were activists in these movements leftist despite their understandings of Islam, or because of them? This essay introduces the project represented in the essays of this special section of South Asian History and Culture, as well as the essays that will appear in a complementary section in a subsequent issue this year. The editors of this project reconstruct a conversation on surprising resonances in subaltern sources in Pashto and Bengali of early twentieth-century grassroots indigenous traditions of radical Muslim egalitarianism. What should we make of these resonances? Building on Latin American decolonisation theory in the wake of Subaltern Studies, we introduce a series of articles that together illustrate what Ramon Grosfoguel calls a ‘pluriverse’ of perspectives on the ethical self: some rooted in the local lifeworlds of Bengal and some in the Afghan borderland; all interlinked through a series of ‘middle actors’. In so doing, we excavate some dense but hidden two-way traffic between subaltern worlds of Muslim piety and devotion on two distant ends of South Asia, and all-India, international or cosmopolitan politics. These together helped constitute a surprising amount of what we know as the South Asian left, from what are usually seen as its geographical, social, and especially intellectual peripheries

Rapid, ultra low coverage copy number profiling of cell-free DNA as a precision oncology screening strategy.

Current cell-free DNA (cfDNA) next generation sequencing (NGS) precision oncology workflows are typically limited to targeted and/or disease-specific applications. In advanced cancer, disease burden and cfDNA tumor content are often elevated, yielding unique precision oncology opportunities. We sought to demonstrate the utility of a pan-cancer, rapid, inexpensive, whole genome NGS of cfDNA approach (PRINCe) as a precision oncology screening strategy via ultra-low coverage (~0.01x) tumor content determination through genome-wide copy number alteration (CNA) profiling. We applied PRINCe to a retrospective cohort of 124 cfDNA samples from 100 patients with advanced cancers, including 76 men with metastatic castration-resistant prostate cancer (mCRPC), enabling cfDNA tumor content approximation and actionable focal CNA detection, while facilitating concordance analyses between cfDNA and tissue-based NGS profiles and assessment of cfDNA alteration associations with mCRPC treatment outcomes. Therapeutically relevant focal CNAs were present in 42 (34%) cfDNA samples, including 36 of 93 (39%) mCRPC patient samples harboring AR amplification. PRINCe identified pre-treatment cfDNA CNA profiles facilitating disease monitoring. Combining PRINCe with routine targeted NGS of cfDNA enabled mutation and CNA assessment with coverages tuned to cfDNA tumor content. In mCRPC, genome-wide PRINCe cfDNA and matched tissue CNA profiles showed high concordance (median Pearson correlation = 0.87), and PRINCe detectable AR amplifications predicted reduced time on therapy, independent of therapy type (Kaplan-Meier log-rank test, chi-square = 24.9, p < 0.0001). Our screening approach enables robust, broadly applicable cfDNA-based precision oncology for patients with advanced cancer through scalable identification of therapeutically relevant CNAs and pre-/post-treatment genomic profiles, enabling cfDNA- or tissue-based precision oncology workflow optimization