2021
DOI: 10.1016/j.bbi.2021.01.026
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Treelet transform analysis to identify clusters of systemic inflammatory variance in a population with moderate-to-severe traumatic brain injury

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Cited by 13 publications
(10 citation statements)
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“…Yet, it remains unknown how acute cortisol profiles correspond to cortisol measurements in subsequent months post-injury, 55 particularly in the setting of ongoing inflammation post-TBI. 56 Unmeasured health and environmental post-acute factors may also influence stress and cortisol levels, including socioeconomic challenges, caregiver support, or other adverse life or health events occurring between initial hospitalization due to TBI and 6-month outcomes. As an observational study, we also cannot determine if cortisol profiles directly influence cognition or are indicators of other processes affecting cognition.…”
Section: Discussionmentioning
confidence: 99%
“…Yet, it remains unknown how acute cortisol profiles correspond to cortisol measurements in subsequent months post-injury, 55 particularly in the setting of ongoing inflammation post-TBI. 56 Unmeasured health and environmental post-acute factors may also influence stress and cortisol levels, including socioeconomic challenges, caregiver support, or other adverse life or health events occurring between initial hospitalization due to TBI and 6-month outcomes. As an observational study, we also cannot determine if cortisol profiles directly influence cognition or are indicators of other processes affecting cognition.…”
Section: Discussionmentioning
confidence: 99%
“…In addition to the increased release of corticoids and catecholamines, TBI induces a systemic immune response, which can progress to systemic immune response syndrome (SIRS), releasing immune mediators of inflammation (cytokines, chemokines) into the circulation (59)(60)(61)(62)(63). Systemic inflammation can persist for months in patients suffering mild (59) and severe TBI (63)(64)(65).…”
Section: Mechanisms Of Tbi-induced Alterations In Brain-gut Communicationmentioning
confidence: 99%
“…In addition to the increased release of corticoids and catecholamines, TBI induces a systemic immune response, which can progress to systemic immune response syndrome (SIRS), releasing immune mediators of inflammation (cytokines, chemokines) into the circulation (59)(60)(61)(62)(63). Systemic inflammation can persist for months in patients suffering mild (59) and severe TBI (63)(64)(65). In prospective cohort studies, TBI patients had elevated serum IL-1β, IL-6, IL-8, IL-10, and TNF-α levels over the first year after injury when compared with age-matched healthy controls (64).…”
Section: Mechanisms Of Tbi-induced Alterations In Brain-gut Communicationmentioning
confidence: 99%
“…sTN-FRII is considered to produce anti-inflammatory responses, whereas sTNFRI produces a TNF-α mediated inflammatory response. Vijapur et al (2021) found that sTNFRII, when coupled with sIL-2Ra, was a significant predictor of GCS at 6-months in multiple models.…”
Section: Il-1β Interleukin 1 Beta (Il-1βmentioning
confidence: 92%
“…TNF-α is implicated in apoptosis, inflammation, immunity, and infectious disease, and sTNFRI has been studied as a prognostic factor in a variety of illnesses (Galvani et al, 2000;Sedger & McDermott, 2014). Vijapur et al (2021) found that levels of sTNFRI, especially when coupled with sTNFRII, sIL-2Ra, and sVCAM-1, predicted 6-month GCS score (e.g., high sTNFRI predicted lower GCS at 6 months). sTNFRII.…”
Section: Il-1β Interleukin 1 Beta (Il-1βmentioning
confidence: 99%