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  • 1
    Keywords: evaluation ; Germany ; THERAPY ; CLASSIFICATION ; DIAGNOSIS ; SUPPORT ; COHORT ; DISEASE ; DRUG ; PATIENT ; HEALTH ; STRATEGIES ; ORGANIZATION ; COMPLICATIONS ; MANAGEMENT ; FEATURES ; ADULTS ; THERAPIES ; prospective studies ; methods ; ENGLAND ; MEDICINE ; WORLD ; ACUTE-RENAL-FAILURE ; COMPLICATED MALARIA ; TRAVELERS
    Abstract: Introduction Imported falciparum malaria is characterized by a broad spectrum of potentially life- threatening complications that may arise even after initiation of appropriate antimalarial drug therapy. Hence, at Heidelberg University Hospital, all patients with newly diagnosed falciparum malaria are initially treated in the intermediate care unit ( IMC) or intensive care unit ( ICU). The present study was undertaken to evaluate critically the benefit of this strategy, which includes daily consultation with senior specialists in tropical medicine. Methods We conducted a retrospective cohort study at the 14-bed combined IMC/ ICU of a 1,685- bed university hospital. A cohort of 122 patients with imported falciparum malaria admitted from 1 January 1996 to 31 December 2003 was included. Results Thirty- four patients ( 27.9%) developed complications, defined according to the current World Health Organization classification. Most patients ( 80.3%) studied did not take the recommended chemoprophylaxis against malaria. The majority of patients ( 89.3% [ n = 109]) could be adequately treated in the IMC. Life- threatening complications requiring ICU support occurred in 13 patients ( 10.7%). All complications were successfully managed. Fifty- five patients ( 45.1%) fulfilling recently published criteria for outpatient treatment had an excellent therapeutic response and did not require ICU support. Conclusion This retrospective evaluation demonstrated favourable therapeutic results in hospitalized patients with imported falciparum malaria. Both initial treatment in the medical IMC/ ICU and close collaboration between intensivists and specialists in tropical medicine may improve disease outcome among affected patients. Prospective studies are needed to confirm these preliminary findings
    Type of Publication: Journal article published
    PubMed ID: 18294371
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  • 2
    Keywords: RECEPTOR ; EXPRESSION ; GROWTH ; CELL ; Germany ; liver ; GENE ; GENE-EXPRESSION ; microarray ; transcription ; DIFFERENTIATION ; MOLECULES ; DNA ; TRANSCRIPTION FACTOR ; DOMAIN ; hepatocytes ; BINDING ; BIOLOGY ; MOLECULE ; MATURATION ; MOUSE ; TRANSCRIPTION FACTORS ; gene expression ; MUTATION ; genetics ; DNA-BINDING ; MUTATIONS ; glucocorticoid receptor ; BODY ; GLUCOCORTICOID-RECEPTOR ; REPRESSION ; heredity ; CROSS-TALK ; BODIES ; RE ; BODY-SIZE ; interaction ; ACTIVATOR ; SIGNAL TRANSDUCER ; GROWTH-FACTOR-I ; SIZE ; USA ; STAT5 ; SET ; BONE-GROWTH ; Cre-loxP ; growth hormone ; LYMPHOID DEVELOPMENT ; somatomedin
    Abstract: The glucocorticoid receptor regulates transcription through DNA binding as well as through cross-talk with other transcription factors. In hepatocytes, the glucocorticoid receptor is critical for normal postnatal growth. Using hepatocyte- specific and domain-selective mutations in the mouse we show that Stat5 in hepatocytes is essential for normal postnatal growth and that it mediates the growth- promoting effect of the glucocorticoid receptor through a direct interaction involving the N-terminal tetramerization domain of Stat5b. This interaction mediates a selective and unexpectedly extensive part of the transcriptional actions of these molecules since it controls the expression of gene sets involved in growth and sexual maturation
    Type of Publication: Journal article published
    PubMed ID: 17504935
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  • 3
    Keywords: RECEPTOR ; GROWTH ; CELL ; Germany ; IN-VIVO ; MODEL ; VIVO ; SUPPORT ; liver ; GENE ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; transcription ; MICE ; ACTIVATION ; TRANSCRIPTION FACTOR ; REDUCTION ; hepatocytes ; TRANSCRIPTION FACTORS ; hormone ; inactivation ; DNA-BINDING ; REGION ; REGIONS ; TARGETED DISRUPTION ; BINDING PROTEIN-3 ; I IGF-I ; postnatal body growth,glucocorticoid receptor,growth hormone signaling,Stat5 ; STAT5B
    Abstract: Mice carrying a hepatocyte-specific inactivation of the glucorticoid receptor (GR) gene show a dramatic reduction in body size. Growth hormone signaling mediated by the Stat5 transcription factors is impaired. We show that Stat5 proteins physically interact with GR and GR is present in vivo on Stat5-dependent IGF-I and ALS regulatory regions. Interestingly, mice with a DNA-binding-deficient GR but an unaltered ability to interact with STAT5(GR(dim/dim)) have a normal body size and normal levels of Stat5-dependent mRNAs. These findings strongly support the model in which GR acts as a coactivator for Stat5-dependent transcription upon GH stimulation and reveal an essential role of hepatic GR in the control of body growth
    Type of Publication: Journal article published
    PubMed ID: 15037546
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