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Significant correlations were observed between GH concentration and impairments on several EDI-2 subscales (drive for thinness, body dissatisfaction, interoceptive awareness, sense of ineffectiveness, interpersonal distrust, maturity fear) and on SCL-90 subitems (depression, hostility, obsessivity compulsivity, anxiety), suggesting a possible hormonal modulatory effect on specific aspects of eating disorders.
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Patients examined at 1 year or several years from complicated mild traumatic brain injury had a similarly high occurrence of isolated GH deficiency
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Single nucleotide variant in GH1 gene is associated with isolated growth hormone deficiency.
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In newborns, serum PRL and hGH levels show a positive correlation that can be explained by common regulatory factors or a drift phenomenon. A higher gestational week is associated with a higher PRL/hGH ratio.
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This review describes the endocrine profile of centenarians concerning the GH/IGF-I/insulin system, focusing on the relevance of this pathway on the modulation of ageing and longevity.
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Data suggest that patients with NICTH (non-islet cell tumor hypoglycemia) exhibit low serum growth hormone levels during hypoglycemic episodes. [Retrospective Study & REVIEW of Case Reports]
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Homozygous GH1 deletion is associated with growth hormone deficiency.
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Human Growth Hormone Inhibits CLAUDIN-1 Expression Through Activation of Signal Transducer and Activator of Transcription 3 (STAT3).
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Serum GH was unrelated to type 2 diabetes, fasting blood glucose, or HbA1c level.
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GH1 and GHRHR screening revealed eleven variations in 24 (21%) patients with isolated growth hormone deficiency of which, four were novel deleterious, one novel non-pathogenic and six reported changes.
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The results suggest that GH regulates energy metabolism directly in myocytes and that UCP2 participates in the signal transduction pathway that functions downstream of the GHR/JAK/STAT.
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These results implicate TIMP3 as a modulator of cell surface GHR abundance and the ability of GH to promote cellular signaling.
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Children with GH excess underwent medical treatment with lanreotide and a minimum clinical/biochemical follow up of 2 years is reported. The present study demonstrates that GH excess should be considered as a relative frequent endocrine manifestation in NF1 patients, similarly to central precocious puberty
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Thus, GHRH analogs of the Miami series powerfully suppress tumor growth, but have only a weak endocrine GH inhibitory activity. The suppression of tumor growth could be induced in part by the downregulation of GHRH receptors levels.
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the levels and kinetics of phosphorylation mediated by the main signalling proteins triggered by 22K-GH or 20K-GH were not exactly the same.
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A negative regulation of locally produced GH by androgens/AR in Prostate cancer cells following treatment with AR agonists (R1881) and antagonists (enzalutamide, bicalutamide).
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The intrinsic amyloidogenicity of growth hormone, in the presence of contaminating prion protein (and perhaps prolactin as well) and amyloid-beta contained in some cadavers' pituitaries, may have led to the observed co-occurring of Creutzfeldt-Jakob disease and Alzheimer's disease.
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GH potentially negatively modulates the maturation and accumulation of lipid in adipocytes.
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To our knowledge, c.-223C>T is the first homozygous point mutation in the GH1 promoter that leads to short stature due to idiopathic growth hormone deficiency.
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Data show that the recombinant protein produced by the plasmid-free E coli strain was purified and characterized to be human growth hormone (hGH).