Publications by authors named "K J Heering"

Advanced prostate cancers are treated with therapies targeting the androgen receptor (AR) signaling pathway. While many tumors initially respond to AR inhibition, nearly all develop resistance. It is critical to understand how prostate tumor cells respond to AR inhibition in order to exploit therapy-induced phenotypes prior to the outgrowth of treatment-resistant disease.

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Objectives: Graves' hyperthyroidism (GH) interferes with iron metabolism and elevates ferritin. The precise mechanisms remain unclear. The influence of thyroid hormones on the synthesis/regulation of hepcidin, an important regulator of iron metabolism, remains uncharacterized.

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Background: The Copenhagen Child Cohort, CCC 2000, was established to investigate developmental psychopathology prospectively from birth in a general population.

Methods: A random sample of 211 children from the CCC 2000 was investigated when the children were 1(1/2) years of age. The prevalence and associates of mental health problems and psychopathology were studied by clinical and standardised strategies, including videotape recordings, parent interviews and the following instruments: The Child Behavior Check List 1(1/2)-5 (CBCL 1(1/2)-5), The Infant Toddler Symptom Check List (ITSCL), Checklist for Autism in Toddlers (CHAT), Bayley Scales of Infant Development II (BSID II), The Parent Child Early Relationship Assessment (PC ERA) and Parent Infant Relationship Global Assessment Scale (PIR-GAS).

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We present a case of acquired von Willebrand syndrome (AVWS) due to a monoclonal gammopathy of undetermined significance. Initially this case was diagnosed as congenital von Willebrand disease (VWD); however, re-examination of the medical history rendered a congenital bleeding disorder unlikely. A normal plasma von Willebrand factor (VWF) propeptide level and a very short half-life of VWF after a test infusion with factor VIII/VWF concentrate confirmed the diagnosis AVWS.

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With the use of DNA-fiber fluorescent in situ hybridization, a BCL2 protein positive follicular lymphoma with a novel BCL2 breakpoint involving the immunoglobulin heavy chain (IGH) switch mu (S(mu)) region instead of the J(H) or D(H) gene segments was identified. Sequence analysis showed that the genomic breakpoint is localized between the S(mu) region of the IGH complex and the first intron of BCL2. Reverse-transcriptase polymerase chain reaction showed expression of a unique hybrid IGH-BCL2 transcript involving the transcription initiation site I(mu).

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