Publications by authors named "W F Heidenreich"

The long non-coding RNA PARTICLE (Gene PARTICL- 'Promoter of MAT2A-Antisense RadiaTion Induced Circulating LncRNA) partakes in triple helix (triplex) formation, is transiently elevated following low dose irradiation and regulates transcription of its neighbouring gene - Methionine adenosyltransferase 2A. It now emerges that PARTICLE triplex sites are predicted in many different genes across all human chromosomes. In silico analysis identified additional regions for PARTICLE triplexes at >1600 genomic locations.

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This case report describes a 52-year-old, female applicant for long term-care insurance with a history of an autoimmune connective tissue disease initially diagnosed as systemic lupus erythematosus (SLE). Over several years, the signs and symptoms evolved into a clear diagnosis of primary Sjögren's syndrome (PSS). The specific criteria for this diagnosis are reviewed including the symptoms, antinuclear antibodies (ANA), extractable nuclear antigen antibodies (ENA), abnormal salivary scintigraphy and positive Schirmer test.

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A 25-year-old male with "MODY2" (maturity onset diabetes of the young type 2) applied for life and disability insurance. MODY2 is also identified by the glucokinase gene that is mutated in this disorder. The etiology, clinical characteristics, and long-term risks of this disorder are reviewed.

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A 42-year-old female applied for life insurance. She was diagnosed with dopa-responsive dystonia as a child. Just prior to applying for insurance, she attempted to go off her carbidopa-levodopa resulting in increased symptoms of stiffness with some imbalance.

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Medulloblastomas in Patched heterozygous mice (Ptc1(+/-) mice) are induced with high probability by ionizing radiation applied in the immediate post-natal period. A mathematical model is described here that accommodates the dependence of the medulloblastoma incidence on dose, age at exposure and age. The model assumes that the first step in the development of the cancer is already present in all cells of the patched mouse due to germ-line inactivation of one allele of the patched tumor suppressor gene.

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