Long-term endocrine consequences of traumatic brain injury in children

Rogol, Alan D.

doi:10.1530/eje-19-0186

Cited by 3 publications

(1 citation statement)

References 8 publications

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“…Despite growing evidence showing a clear relationship between TBI and hypopituitarism in children, little research specifically address recovery and development. Few studies have long term quality of life (QoL) scores, neuropsychologic testing and development, but in the studies available, all contain pediatric TBI patients that have acute and chronic hormone deficiencies, abnormal development and increased poor QoL (141)(142)(143)(144)(145)(146). One study specifically observed changes in sexual health, an underrepresented area of study following TBI, and found teenagers with a TBI had a higher incidence of poor sexual health compared to age-matched peers (147).…”

Section: Hormonalmentioning

confidence: 99%

Pathophysiology of Pediatric Traumatic Brain Injury

et al. 2021

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The national incidence of traumatic brain injury (TBI) exceeds that of any other disease in the pediatric population. In the United States the Centers for Disease Control and Prevention (CDC) reports 697,347 annual TBIs in children ages 0–19 that result in emergency room visits, hospitalization or deaths. There is a bimodal distribution within the pediatric TBI population, with peaks in both toddlers and adolescents. Preclinical TBI research provides evidence for age differences in acute pathophysiology that likely contribute to long-term outcome differences between age groups. This review will examine the timecourse of acute pathophysiological processes during cerebral maturation, including calcium accumulation, glucose metabolism and cerebral blood flow. Consequences of pediatric TBI are complicated by the ongoing maturational changes allowing for substantial plasticity and windows of vulnerabilities. This review will also examine the timecourse of later outcomes after mild, repeat mild and more severe TBI to establish developmental windows of susceptibility and altered maturational trajectories. Research progress for pediatric TBI is critically important to reveal age-associated mechanisms and to determine knowledge gaps for future studies.

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Section: Hormonalmentioning

confidence: 99%

Pathophysiology of Pediatric Traumatic Brain Injury

et al. 2021

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The rate of empty sella (ES) in traumatic brain injury: Links with endocrine profiles

Famà

Sindoni

Feldt‐Rasmussen

et al. 2022

Cellular, Molecular, Physiological, and Behavioral Aspects of Traumatic Brain Injury

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Yes-associated protein regulates the differentiation and osteoporosis of bone marrow mesenchymal stem cells

Wang,

Jiang,

Ying

et al. 2024

mat express

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Mammalian Yes-associated protein (YAP) is involved in the regulation of various biological behaviors. Osteoporosis (OP) is a common orthopedic disease. However, the role of YAP in the differentiation and osteoporosis of Bone marrow mesenchymal stem cells (BMSCs) is unclear. Ovariectomy (OVX)-induced OP rat model was constructed and YAP plasmid was transfected to detect bone density and alkaline phosphatase (ALP) activity. Rat BMSCs were assigned into 3 groups: sham group, OP group, and YAP group, in which YAP plasmid was transfected followed by analysis of YAP expression by real-time PCR. After 14 days of induction culture, type I collagen, Osterix and FABP4 mRNA expression was detected by real-time PCR along with Wnt5 protein expression by western blot and TGF-β secretion by ELISA. In OP rats, YAP expression was significantly down-regulated and the bone density and ALP activity decreased (P <0.05). YAP transfection in OP rats reversed the changes in OP rats. In OP group, YAP expression was decreased, and type I collagen and Osterix expression decreased, FABP4 expression increased, β-catenin expression and TGF-β secretion decreased (P <0.05). Transfection of YAP plasmid in BMSCs of OP group significantly reversed the above changes (P <0.05). In conclusion, YAP level decreases in OP and up-regulating its expression in BMSCs can promote osteogenic differentiation and inhibit adipogenic differentiation by regulating Tnt5/TGF-β signaling.

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Long-term endocrine consequences of traumatic brain injury in children

Cited by 3 publications

References 8 publications

Pathophysiology of Pediatric Traumatic Brain Injury

Pathophysiology of Pediatric Traumatic Brain Injury

The rate of empty sella (ES) in traumatic brain injury: Links with endocrine profiles

Yes-associated protein regulates the differentiation and osteoporosis of bone marrow mesenchymal stem cells

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