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Type 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.
Burns Trauma
January 2025
Department of Critical Care Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No. 321 Zhongshan Road, Gulou District, Nanjing, Jiangsu 210008, China.
Background: Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.
View Article and Find Full Text PDFGrowth Hormone Increase Induced by Oral Administration of Melatonin in a Young Woman With Sleep Disturbances.
JCEM Case Rep
February 2025
Clinica Medica 3, Department of Medicine-DIMED, University Hospital of Padova, Padova 35128, Italy.
Growth hormone (GH) secretion by the pituitary is regulated by stimulatory and inhibitory pathways such as growth hormone releasing hormone (GHRH) and somatostatin, respectively, being also modulated by different neurotransmitters acting at the hypothalamic/pituitary level. The pineal gland hormone melatonin regulates GH secretion in many mammals, including humans, although its role in modulating GH secretion has been debated. We describe the case of a young woman chronically taking melatonin for sleep disturbances, referring to her general practitioner for flushing that appeared just after starting melatonin intake.
View Article and Find Full Text PDFPractical management of adverse events in patients receiving tarlatamab, a delta-like ligand 3-targeted bispecific T-cell engager immunotherapy, for previously treated small cell lung cancer.
Cancer
February 2025
University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland Medical Center, Baltimore, Maryland, USA.
Tarlatamab is a bispecific T-cell engager immunotherapy targeting delta-like ligand 3 (DLL3) and the cluster of differentiation 3 (CD3) molecule. In the phase 2 DeLLphi-301 trial of tarlatamab for patients with previously treated small cell lung cancer, tarlatamab 10 mg every 2 weeks achieved durable responses and encouraging survival outcomes. Analyses of updated safety data from the DeLLphi-301 trial demonstrated that the most common treatment-emergent adverse events were cytokine release syndrome (53%), pyrexia (38%), decreased appetite (36%), dysgeusia (32%), and an emia (30%).
View Article and Find Full Text PDFZNF169 promotes thyroid cancer progression via upregulating FBXW10.
Cell Div
January 2025
Department of Nuclear Medicine, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South university/Hunan Cancer Hospital, No. 283 Tongzipo Road, Yuelu District, Changsha, 410013, Hunan, P.R. China.
Background: Zinc finger protein 169 (ZNF169) plays a key role in cancer development. However, the specific role of ZNF169 in the tumorigenesis of thyroid carcinoma (THCA) remains poorly understood.
Methods: The expression of ZNF169 was measured using immunohistochemistry, RT-qPCR, and western blot.
Roxadustat-Induced Central Hypothyroidism Masked by Uremia at the Initiation of Hemodialysis: A Case Report.
Cureus
December 2024
Nephrology, Yokohama Municipal Citizen's Hospital, Yokohama, JPN.
Hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) is a novel class of orally administered medications for renal anemia in patients with end-stage renal disease (ESRD). Roxadustat, a HIF-PHI, has a structure similar to that of triiodothyronine and may work as an agonist for thyroid hormone receptor-beta in the pituitary gland and/or hypothalamus. Therefore, roxadustat may cause central hypothyroidism due to suppressing thyroid-stimulating hormone (TSH) release in the pituitary gland and/or thyrotropin-releasing hormone release in the hypothalamus.
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