Media and the making of migrants

[BOOK REVIEW]Hegde, Radha Sarma (2016) Mediating migration. Cambridge: Polity Press. ISBN 978-0-7456-4632-9 hbk. Pages x + 161 This book is about how the migration experience is mediated by new technologies. This mediation is clearly articulated in the introductory chapter which outlines the mediating role that media, technology and other forms of communication plays in the migration experience. As Hegde argues: “New technologies enable both the disciplining and self-expression of migrant communities worldwide. Devices, technologies and various types of changing media platforms are being widely used by migrants to reinvent and redefine identity” (p 11). &nbsp

Ramanujan Hegde: The prion puzzle and protein translocation

Hegde uses prion protein as a model to explore how cells handle protein translocation and trafficking

The Truncated Cauchy Distribution: Estimation of Parameters and Application to Stock Returns

The problem addressed in this dissertation is the existence and estimation of the parameters of a truncated Cauchy distribution. It is known that when a number of distributions with infinite support are truncated to a finite interval that the maximum likelihood estimator of the scale parameter fails to exist with positive probability. In particular, necessary and sufficient conditions which give rise to instances of non-existence have been found for the exponential (Deemer and Votaw (1955)), gamma (Broeder (1955), Hegde and Dahiya (1989)), Weibull (Mittal and Dahiya (1989)) and normal distribution (Barndorff-Nielsen (1978), Mittal and Dahiya (1987), Hegde and Dahiya (1989)). Alternative estimators have been proposed to deal with the problems of non-existence and blowing up of the estimates. Mittal and Dahiya (1987, 1989) employ the Bayes model estimator of Blumenthal and Marcus (1975) for the normal and Weibull cases and Hegde and Dahiya (1989) apply it to the gamma. Hegde (1986) also studies the harmonic mean estimator of Joe and Reid (1984). Here we prove a sufficient and asymptotically necessary condition for the existence of the ML estimator of the scale parameter of the truncated Cauchy distribution. A modified ML estimator and an estimator based on equating population and sample quantiles are presented as alternatives. These estimators exist with probability one. The performance of these estimators is examined by making use of simulations. Asymptotic variances of the ML estimators are also given. Finally, an application of truncated distributions is presented. The fit of returns on common stocks to the normal, Cauchy, truncated normal, and truncated Cauchy distributions is compared via the Kolmogorov-Smirnov statistic. The results show that a truncated distribution is a better fitting model in virtually all cases

Crisis-ready responsible selves: how national governments demanded self-sufficiency during the pandemic

‘Save yourself to save others’: Shani Orgad (LSE) and Radha Sarma Hegde (New York University) discuss how national governments used their COVID-19 campaigns to stress the importance of self-sufficiency, playing down the responsibilities of the state

Development and Validation of Clinical Whole-Exome and Whole-Genome Sequencing for Detection of Germline Variants in Inherited Disease

Context.-With the decrease in the cost of sequencing, the clinical testing paradigm has shifted from single gene to gene panel and now whole-exome and whole-genome sequencing. Clinical laboratories are rapidly implementing next-generation sequencing-based whole-exome and whole-genome sequencing. Because a large number of targets are covered by whole-exome and whole-genome sequencing, it is critical that a laboratory perform appropriate validation studies, develop a quality assurance and quality control program, and participate in proficiency testing. Objective.-To provide recommendations for wholeexome and whole-genome sequencing assay design, validation, and implementation for the detection of germline variants associated in inherited disorders. Data Sources.-An example of trio sequencing, filtration and annotation of variants, and phenotypic consideration to arrive at clinical diagnosis is discussed. Conclusions.-It is critical that clinical laboratories planning to implement whole-exome and whole-genome sequencing design and validate the assay to specifications and ensure adequate performance prior to implementation. Test design specifications, including variant filtering and annotation, phenotypic consideration, guidance on consenting options, and reporting of incidental findings, are provided. These are important steps a laboratory must take to validate and implement whole-exome and whole-genome sequencing in a clinical setting for germline variants in inherited disorders

Information Theoretic Limits for Standard and One-Bit Compressed Sensing with Graph-Structured Sparsity

In this paper, we analyze the information theoretic lower bound on the necessary number of samples needed for recovering a sparse signal under different compressed sensing settings. We focus on the weighted graph model, a model-based framework proposed by Hegde et al. (2015), for standard compressed sensing as well as for one-bit compressed sensing. We study both the noisy and noiseless regimes. Our analysis is general in the sense that it applies to any algorithm used to recover the signal. We carefully construct restricted ensembles for different settings and then apply Fano's inequality to establish the lower bound on the necessary number of samples. Furthermore, we show that our bound is tight for one-bit compressed sensing, while for standard compressed sensing, our bound is tight up to a logarithmic factor of the number of non-zero entries in the signal

Targeting of the prion protein to the cytosol: mechanisms and consequences

Prion diseases are characterized by the conformational transition of the cellular prion protein (PrPC) into an aberrant protein conformer, designated scrapie-prion protein (PrPSc). A causal link between protein misfolding and neurodegeneration has been established for a variety of neurodegenerative disease, such as Alzheimer's disease, Parkinson's disease and polyglutamine diseases, but there is an ongoing debate about the nature of the neurotoxic species and how non-native conformers can damage neuronal populations. PrP is normally imported into the endoplasmic reticulum (ER) and targeted to the outer leaflet of the plasma membrane via a glycosylphosphatidylinositol (GPI) anchor. However, several conditions, such as ER stress or some pathogenic mutations in the PrP gene, can induce the mislocalization of PrP in the cytosol, where it has a neurotoxic potential as demonstrated in cell culture and transgenic mouse models. In this review we focus on intrinsic factors and cellular pathways implicated in the import of PrP into the ER and its mistargeting to the cytosol. The findings summarized here not only reveal a complex regulation of the biogenesis of PrP, but also provide interesting new insight into toxic activities of pathogenic protein conformers and quality control pathways of ER-targeted proteins