886 research outputs found

    Miller v. Commissioner: Deductibility of Casualty Losses After Voluntary Election Not to File an Insurance Claim

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    Taxpayers who suffer casualty losses may decide, for a variety of reasons, not to file an insurance claim for recovery of those losses. Section 165 of the Internal Revenue Code of 1954 allows a deduction for “any loss sustained during the taxable year and not compensated for by insurance or otherwise.”\u27 Consequently, the question arises whether a taxpayer may claim a casualty loss deduction even though the taxpayer did not seek insurance reimbursement for the loss. In Miller v. Commissioner, the United States Court of Appeals for the Sixth Circuit, in a 6-5 en banc decision, expressly overruled its previous decision in Kentucky Utilities Co. v. Glenn and held that a taxpayer who voluntarily chooses not to file an insurance claim for recovery of a loss could still claim a section 165 deduction. Part I of this comment examines the Miller holding and its underlying rationale. Part II addresses the impact of Miller on federal income tax law and suggests that by overruling Kentucky Utilities, Miller changes the law regarding the deductibility of losses under section 165 after a voluntary election not to file an insurance claim. Part III concludes that the Sixth Circuit\u27s literal interpretation of section 165(a)\u27s language “not compensated for by insurance or otherwise”\u27 is a significant defeat for the Internal Revenue Service

    Radiation effects on silicon solar cells Final report, Dec. 1, 1961 - Dec. 31, 1962

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    Displacement defects in silicon solar cells by high energy electron irradiation using electron spin resonance, galvanometric, excess carrier lifetime, and infrared absorption measurement

    Heat Shock Protein-90 Inhibitors Enhance Antigen Expression on Melanomas and Increase T Cell Recognition of Tumor Cells

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    In an effort to enhance antigen-specific T cell recognition of cancer cells, we have examined numerous modulators of antigen-expression. In this report we demonstrate that twelve different Hsp90 inhibitors (iHsp90) share the ability to increase the expression of differentiation antigens and MHC Class I antigens. These iHsp90 are active in several molecular and cellular assays on a series of tumor cell lines, including eleven human melanomas, a murine B16 melanoma, and two human glioma-derived cell lines. Intra-cytoplasmic antibody staining showed that all of the tested iHsp90 increased expression of the melanocyte differentiation antigens Melan-A/MART-1, gp100, and TRP-2, as well as MHC Class I. The gliomas showed enhanced gp100 and MHC staining. Quantitative analysis of mRNA levels showed a parallel increase in message transcription, and a reporter assay shows induction of promoter activity for Melan-A/MART-1 gene. In addition, iHsp90 increased recognition of tumor cells by T cells specific for Melan-A/MART-1. In contrast to direct Hsp90 client proteins, the increased levels of full-length differentiation antigens that result from iHsp90 treatment are most likely the result of transcriptional activation of their encoding genes. In combination, these results suggest that iHsp90 improve recognition of tumor cells by T cells specific for a melanoma-associated antigen as a result of increasing the expressed intracellular antigen pool available for processing and presentation by MHC Class I, along with increased levels of MHC Class I itself. As these Hsp90 inhibitors do not interfere with T cell function, they could have potential for use in immunotherapy of cancer
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