Lepidoptera of New York and Neighboring States, Part 1 (1923). William T. M. Forbes. Los Angeles: Entomological Reprint Specialists, 1969. 729 pp. $17.50.

Excerpt: Entomological Reprint Specialists have done a fine service to the field of entomology and the study of Lepidoptera in particular by making the first volume of Forbes\u27 work on the Lepidoptera of the northeastern states generally available. This volume remains the only comprehensive work on the numerous families included in the primitive moths, Microlepidoptera, Pyraloidea, and Bombycoidea for a major portion of North America

Analyst Coverage And The Diversification Discount

We use financial analyst coverage as a measure of information asymmetry to examine excess firm values associated with single- and multi-segment firms.  We explicitly examine whether differences in analyst coverage can explain the diversification discount.  We find that information asymmetry plays a major role in the valuation of companies and explains a large portion of the diversification discount.  However, a significant diversification discount remains after controlling for the effects of analyst coverage

Managerial Incentives And Changes In Corporate Focus

We examine how Chief Executive Officer (CEO) equity ownership, CEO tenure, and the percentage of options in CEO annual compensation are related to decisions regarding changes in corporate focus.  We document that the CEOs whose companies change their level of corporate focus have significant differences from CEOs whose firms do not change focus.  However, we find no differences in the characteristics of CEOs who increase their firm’s level of diversification and the CEOs who decrease their firm’s level of diversification.  Firm characteristics, such as size or whether the firm sells at a premium or discount to its peers, are better predictors of changes in corporate focus than CEO characteristics. Overall, we find no evidence that changes in diversification are related to self-serving managers attempting to maximize their own wealth

Catalog of the type specimens of Gelechioidea (Lepidoptera) in the collection of the National Museum of Natural History, Smithsonian Institution, Washington, DC

The collection of the National Museum of Natural History, Smithsonian Institution, Washington, D.C., is second only to that of The Natural History Museum (formerly British Museum of Natural History), London, in the number of type specimens of the superfamily Gelechioidea (Lepidoptera). The Smithsonian houses 1,375 gelechioid types: 1,249 holotypes, 48 lectotypes, 1 neotype, 69 species represented by one or more syntypes, and 8 species represented by one or more pseudotypes (Le., specimens identified as type by an accompanying label that are unlikely to be the type). Three former curators are responsible for the vast majority of the type specimens: August Busck, ]. F. Gates Clarke, and Ronald W. Hodges. We present a list of the species for which a type is deposited in the USNM, organized alphabetically. For each species we provide an abbreviated reference to the original description and label data. This list represents the second contribution to a larger effort to make available information on the Lepidoptera type holdings of the USNM

Far-Field Optical Imaging and Manipulation of Individual Spins with Nanoscale Resolution

A fundamental limit to existing optical techniques for measurementand manipulation of spin degrees of freedom is set by diffraction, which does not allow spins separated by less than about a quarter of a micrometre to be resolved using conventional far-field optics. Here, we report an efficient far-field optical technique that overcomes the limiting role of diffraction, allowing individual electronic spins to be detected, imaged and manipulated coherently with nanoscale resolution. The technique involves selective flipping of the orientation of individual spins, associated with nitrogen-vacancy centres in room-temperature diamond, using a focused beam of light with intensity vanishing at a controllable location, which enables simultaneous single-spin imaging and magnetometry at the nanoscale with considerably less power than conventional techniques. Furthermore, by inhibiting spin transitions away from the laser intensity null, selective coherent rotation of individual spins is realized. This technique can be extended to subnanometre dimensions, thus enabling applications in diverse areas ranging from quantum information science to bioimaging.Physic

Deweyan tools for inquiry and the epistemological context of critical pedagogy

This article develops the notion of resistance as articulated in the literature of critical pedagogy as being both culturally sponsored and cognitively manifested. To do so, the authors draw upon John Dewey\u27s conception of tools for inquiry. Dewey provides a way to conceptualize student resistance not as a form of willful disputation, but instead as a function of socialization into cultural models of thought that actively truncate inquiry. In other words, resistance can be construed as the cognitive and emotive dimensions of the ongoing failure of institutions to provide ideas that help individuals both recognize social problems and imagine possible solutions. Focusing on Dewey\u27s epistemological framework, specifically tools for inquiry, provides a way to grasp this problem. It also affords some innovative solutions; for instance, it helps conceive of possible links between the regular curriculum and the study of specific social justice issues, a relationship that is often under-examined. The aims of critical pedagogy depend upon students developing dexterity with the conceptual tools they use to make meaning of the evidence they confront; these are background skills that the regular curriculum can be made to serve even outside social justice-focused curricula. Furthermore, the article concludes that because such inquiry involves the exploration and potential revision of students\u27 world-ordering beliefs, developing flexibility in how one thinks may be better achieved within academic subjects and topics that are not so intimately connected to students\u27 current social lives, especially where students may be directly implicated

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1,131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (pvalue=4.82e-08, OR=2.12), and two known loci: UNC13A, led by rs1297319 (pvalue=1.27e-08, OR=1.50) and HLA-DQA2 led by rs17219281 (pvalue=3.22e-08, OR=1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n≥3) as compared to controls (n=0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g. DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis

Frontotemporal dementia and its subtypes: a genome-wide association study

SummaryBackground Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes—MAPT, GRN, and C9orf72—have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder. Methods We did a two-stage genome-wide association study on clinical FTD, analysing samples from 3526 patients with {FTD} and 9402 healthy controls. To reduce genetic heterogeneity, all participants were of European ancestry. In the discovery phase (samples from 2154 patients with {FTD} and 4308 controls), we did separate association analyses for each {FTD} subtype (behavioural variant FTD, semantic dementia, progressive non-fluent aphasia, and {FTD} overlapping with motor neuron disease FTD-MND), followed by a meta-analysis of the entire dataset. We carried forward replication of the novel suggestive loci in an independent sample series (samples from 1372 patients and 5094 controls) and then did joint phase and brain expression and methylation quantitative trait loci analyses for the associated (p<5 × 10−8) single-nucleotide polymorphisms. Findings We identified novel associations exceeding the genome-wide significance threshold (p<5 × 10−8). Combined (joint) analyses of discovery and replication phases showed genome-wide significant association at 6p21.3, \{HLA\} locus (immune system), for rs9268877 (p=1·05 × 10−8; odds ratio=1·204 95% \{CI\} 1·11–1·30), rs9268856 (p=5·51 × 10−9; 0·809 0·76–0·86) and rs1980493 (p value=1·57 × 10−8, 0·775 0·69–0·86) in the entire cohort. We also identified a potential novel locus at 11q14, encompassing RAB38/CTSC (the transcripts of which are related to lysosomal biology), for the behavioural \{FTD\} subtype for which joint analyses showed suggestive association for rs302668 (p=2·44 × 10−7; 0·814 0·71–0·92). Analysis of expression and methylation quantitative trait loci data suggested that these loci might affect expression and methylation in cis. Interpretation Our findings suggest that immune system processes (link to 6p21.3) and possibly lysosomal and autophagy pathways (link to 11q14) are potentially involved in FTD. Our findings need to be replicated to better define the association of the newly identified loci with disease and to shed light on the pathomechanisms contributing to FTD. Funding The National Institute of Neurological Disorders and Stroke and National Institute on Aging, the Wellcome/MRC Centre on Parkinson's disease, Alzheimer's Research UK, and Texas Tech University Health Sciences Center

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development