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Published in Michael B O’Neill, Michelle Mary Mcevoy, Alf J Nicholson, Terence Stephenson, Stephanie Ryan, Diagnosing and Treating Common Problems in Paediatrics, 2017
Michael B O’Neill, Michelle Mary Mcevoy, Alf J Nicholson, Terence Stephenson, Stephanie Ryan
Isolated growth hormone deficiency is a clinical diagnosis, supported by auxological, biochemical and radiological findings. Growth hormone deficiency can be divided into three categories; congenital, acquired and idiopathic. Congenital causes can be the result of genetic mutations or structural defects. Known genes include those that code for growth hormone (GH1), growth-hormone-releasing hormone receptor (GHRHR) and transcription factor SOX3. Acquired causes of growth hormone deficiency include space occupying lesions, head trauma, infection, radiation therapy, infiltrative disease such as histiocytocis and autoimmune conditions such as lymphocytic hypophysitis. Idiopathic growth hormone deficiency is where no known cause is found. The phenotype of children with growth hormone deficiency is highly variable. However, they have a characteristically immature facies with a prominent forehead and depressed midline development. When other pituitary hormone deficiencies are present, there may be a history of neonatal jaundice, hypoglycaemia, micropenis with undescended testes and hypothyroidism.
Alveolar epithelial cell growth hormone releasing hormone receptor in alveolar epithelial inflammation
Published in Experimental Lung Research, 2023
Tengjiao Cui, Medhi Wangpaichitr, Andrew V. Schally, Anthony J. Griswold, Irving Vidaurre, Wei Sha, Robert M. Jackson
Growth hormone releasing hormone receptor (GHRH-R) is present in lung tissue and is expressed in AT2 cells. Several lines of evidence mechanistically link the GHRH-R with inflammation. Inhibition of the GHRH-R using an antagonistic peptide (e.g., MIA-602) reduced inflammation and fibrosis in lungs of mice treated with bleomycin.4 GHRH-R antagonist inhibits JAK/STAT signaling and Th17 cell differentiation reducing ocular and neural inflammation.5 GHRH-R antagonists also protect the lung vasculature from unfolded protein response, maintain endothelial barrier integrity and have anti-inflammatory effects in sarcoid granulomas.6–8 Pro-inflammatory JAK/STAT and NF-kB pathways are linked to GHRH-R activation (e.g., by GHRH-R agonist MR-409) and are downregulated by GHRH-R antagonists (e.g., by MIA-602).9–11
Atrazine neural and reproductive toxicity
Published in Toxin Reviews, 2022
Hamidreza Sadeghnia, Sara Shahba, Alireza Ebrahimzadeh-Bideskan, Shabnam Mohammadi, Amir Mohammad Malvandi, Abbas Mohammadipour
Owing to its high affinity to the growth hormone-releasing hormone receptor (GHRHR), atrazine has also been shown to have pituitary toxicity effects (Fakhouri et al. 2010). After treating rat pituitary cells with atrazine, at environmentally relevant concentrations (1 ppb and 1 ppm), atrazine binds to the GHRHR of the pituitary cells. This binding results in the inhibition of growth hormone and gene transcription, ultimately leading to a reduced growth hormone expression (Fakhouri et al. 2010). Thus, this herbicide can affect children's growth and their average height.