scholarly journals Hepatic Expression of Serum Amyloid A1 Is Induced by Traumatic Brain Injury and Modulated by Telmisartan

2015 ◽  
Vol 185 (10) ◽  
pp. 2641-2652 ◽  
Author(s):  
Sonia Villapol ◽  
Dmitry Kryndushkin ◽  
Maria G. Balarezo ◽  
Ashley M. Campbell ◽  
Juan M. Saavedra ◽  
...  
2019 ◽  
Vol 35 (11) ◽  
pp. 1180-1195 ◽  
Author(s):  
Cristina Sánchez Carabias ◽  
Ana María Castaño-León ◽  
B Blanca Navarro ◽  
Irene Panero ◽  
Carla Eiriz ◽  
...  

Extracranial injury is frequently present in patients with traumatic brain injury (TBI). However, no reliable biomarker exists nowadays to evaluate the magnitude and extension of extracranial injury as well as the identification of patients who are at risk of developing secondary injuries. The purpose of this study was to identify new possible peptide biomarkers by mass spectrometry analysis in patients with TBI and ascertain whether the novel biomarker discovered by peptide mass fingerprinting, serum amyloid A1 (SAA1), is capable of reflecting the condition of the patient and both intracranial and extracranial injury extension. Demographic characteristics, clinical data, and serum samples were prospectively collected from 120 patients with TBI (Glasgow Coma Scale [GCS] score 3-15) on admission. Biomarkers were quantified by enzyme-linked immunosorbent assay. Intracranial lesion volume was measured from the semiautomatic segmentation of hematoma on computed tomography (CT) using Analyze software. Functional outcome was evaluated using the Glasgow Outcome Scale (GOS) at hospital discharge and GOS extended scores at 6 months. The SAA1 levels were significantly associated with intracranial (GCS score at admission, lesion load measured with cranial CT, and pupil responsiveness) and extracranial clinical severity (all Abbreviated Injury Scale regions, Injury Severity Score, major extracranial injury, polytrauma, and orthopedic fractures presence), along with systemic secondary insults and functional outcome. SAA1 was is associated with the volume of traumatic intracranial lesions. The SAA1 levels were correlated with astroglial S100β and glial fibrillary acidic protein (GFAP), neuronal neuron-specific enolase (NSE), and axonal total tau (T-tau) and phosphorylated neurofilament heavy chain (pNF-H) injury markers. SAA1 predicts unfavorable outcome and mortality at hospital discharge (area under the curve [AUC] = 0.90, 0.82) and 6 months (AUC = 0.89). SAA1 can be established as a marker for the overall patient condition due to its involvement in the neuroendocrine axis of the systemic response to craniocerebral trauma.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Evan Wicker ◽  
Leah Benton ◽  
Kershina George ◽  
William Furlow ◽  
Sonia Villapol

Traumatic brain injury (TBI) causes a wide variety of neuroinflammatory events. These neuroinflammatory events depend, to a greater extent, on the severity of the damage. Our previous studies have shown that the liver produces serum amyloid A (SAA) at high levels in the initial hours after controlled cortical impact (CCI) injury in mice. Clinical studies have reported detectable SAA in the plasma of brain injury patients, but it is not clear if SAA levels depend on TBI severity. To evaluate this question, we performed a mild to severe CCI injury in wild-type mice. We collected blood samples and brains at 1, 3, and 7 days after injury for protein detection by western blotting, enzyme-linked immunosorbent assay, or immunohistochemical analysis. Our results showed that severe CCI injury compared to mild CCI injury or sham mice caused an increased neuronal death, larger lesion volume, increased microglia/macrophage density, and augmented neutrophil infiltration. Furthermore, we found that the serum levels of SAA protein ascended in the blood in correlation with high neuroinflammatory and neurodegenerative responses. Altogether, these results suggest that serum SAA may be a novel neuroinflammation-based, and severity-dependent, biomarker for acute TBI.


2020 ◽  
Vol 40 (7) ◽  
pp. 1199-1211 ◽  
Author(s):  
Sirena Soriano ◽  
Bridget Moffet ◽  
Evan Wicker ◽  
Sonia Villapol

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.


2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.


2019 ◽  
Vol 28 (3) ◽  
pp. 1363-1370 ◽  
Author(s):  
Jessica Brown ◽  
Katy O'Brien ◽  
Kelly Knollman-Porter ◽  
Tracey Wallace

Purpose The Centers for Disease Control and Prevention (CDC) recently released guidelines for rehabilitation professionals regarding the care of children with mild traumatic brain injury (mTBI). Given that mTBI impacts millions of children each year and can be particularly detrimental to children in middle and high school age groups, access to universal recommendations for management of postinjury symptoms is ideal. Method This viewpoint article examines the CDC guidelines and applies these recommendations directly to speech-language pathology practices. In particular, education, assessment, treatment, team management, and ongoing monitoring are discussed. In addition, suggested timelines regarding implementation of services by speech-language pathologists (SLPs) are provided. Specific focus is placed on adolescents (i.e., middle and high school–age children). Results SLPs are critical members of the rehabilitation team working with children with mTBI and should be involved in education, symptom monitoring, and assessment early in the recovery process. SLPs can also provide unique insight into the cognitive and linguistic challenges of these students and can serve to bridge the gap among rehabilitation and school-based professionals, the adolescent with brain injury, and their parents. Conclusion The guidelines provided by the CDC, along with evidence from the field of speech pathology, can guide SLPs to advocate for involvement in the care of adolescents with mTBI. More research is needed to enhance the evidence base for direct assessment and treatment with this population; however, SLPs can use their extensive knowledge and experience working with individuals with traumatic brain injury as a starting point for post-mTBI care.


ASHA Leader ◽  
2010 ◽  
Vol 15 (13) ◽  
pp. 38-38
Author(s):  
G. Gayle Kelley

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