Differential association of baseline body weight and body-weight loss with neurological deficits, histology, and death after repetitive closed head traumatic brain injury

2021 ◽  
pp. 136430
Author(s):  
Aydan Kahriman ◽  
James Bouley ◽  
Daryl A. Bosco ◽  
Mohammed Salman Shazeeb ◽  
Nils Henninger
Keyword(s):  
Traumatic Brain Injury ◽  
Weight Loss ◽  
Body Weight ◽  
Brain Injury ◽  
Body Weight Loss ◽  
Differential Association ◽  
Neurological Deficits ◽  
Baseline Body Weight ◽  
Closed Head

Possible protective effect of endogenous opioids in traumatic brain injury

1990 ◽  
Vol 72 (2) ◽  
pp. 252-261 ◽  
Author(s):  
Ronald L. Hayes ◽  
Bruce G. Lyeth ◽  
Larry W. Jenkins ◽  
Richard Zimmerman ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Body Weight ◽  
Brain Injury ◽  
Endogenous Opioids ◽  
Neurological Deficits ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Drug Treatments

✓ Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

Abstract T P223: Post-stroke Body Weight Loss Predicts Acute Stroke Outcome In Mice

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jiwon Yang ◽  
Sunghee Cho
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Brain Injury ◽  
Infarct Volume ◽  
Body Weight Loss ◽  
Stroke Recovery ◽  
Physiological Parameter ◽  
Ischemic Time ◽  
Post Stroke ◽  
Longitudinal Imaging

Background and Purpose: Longitudinal imaging studies in stroke demonstrated that infarct development is a dynamic process and it matures over several days, even weeks depending on the severity of stroke. However, due to high cost and multiple exposure of anesthesia associated with repeated imaging, infarct volume has been typically measured at a fixed time point in preclinical studies, which prevent further assessment of behaviors during stroke recovery. In identifying a non-invasive physiological parameter that predicts the extent of stroke-induced brain injury, the study investigated whether acute body weight loss predicts the extent of brain injury and swelling. Methods: C57 male mice (10-12 wk old, 25-30 gr) were subjected to the proximal middle cerebral artery (MCA) occlusion for 30 min. Body weight was recorded daily. Infarct volume corrected with swelling (IVInd) and percent hemispheric swelling (%SW) were determined at 1, 3 and 7d after MCAO. In a retrospective study, we analyzed correlations between 3d %body weight reduction (%BWred) and stroke outcomes (IVInd & %SW) in C57 male animals that were subjected to MCAO by 3 different individuals over 8 years (n=91-96). Results: Stroke induced acute BW loss (%BWred; 1d, 88.9±3.3; 3d, 84.5±8.6; 5d, 86.8±10.6; 7d, 88.9±8.9). Correlation analyses in the post-ischemic time points showed IVind and %SW were significantly correlated with only at 3d BW reduction, but not 1d and 7d (Fig.1). A retrospective analysis in C57 mice also showed a significant correlation between 3d %BWred and IVInd & %SW (Fig.2). Conclusions: The study showed that acute post-stroke BWred is a simple and suitable index to predict the extent of stroke injury in C57 mice. Whether the prediction can be generalized across different strains and in comorbid conditions warrant further investigation.

scholarly journals Marked Protection by Moderate Hypothermia after Experimental Traumatic Brain Injury

1991 ◽  
Vol 11 (1) ◽  
pp. 114-121 ◽  
Author(s):  
Guy L. Clifton ◽  
Ji Y. Jiang ◽  
Bruce G. Lyeth ◽  
Larry W. Jenkins ◽  
Robert J. Hamm ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Temperature ◽  
Body Weight Loss ◽  
Neurological Deficits ◽  
Moderate Hypothermia ◽  
Surface Cooling ◽  
Clinical Value ◽  
Hypothermia Group ◽  
Experimental Traumatic Brain Injury

These experiments examined the effects of moderate hypothermia on mortality and neurological deficits observed after experimental traumatic brain injury (TBI) in the rat. Brain temperature was measured continuously in all experiments by intraparenchymal probes. Brain cooling was induced by partial immersion (skin protected by a plastic barrier) in a water bath (0°C) under general anesthesia (1.5% halothane/70% nitrous oxide/30% oxygen). In experiment I, we examined the effects of moderate hypothermia induced prior to injury on mortality following fluid percussion TBI. Rats were cooled to 36°C ( n = 16), 33°C ( n = 17), or 30°C ( n = 11) prior to injury and maintained at their target temperature for 1 h after injury. There was a significant (p < 0.04) reduction in mortality by a brain temperature of 30°C. The mortality rate at 36°C was 37.5%, at 33°C was 41%, and at 30°C was 9.1%. In experiment II, we examined the effects of mod erate hypothermia or hyperthermia initiated after TBI or long-term behavioral deficits. Rats were cooled to 36°C ( n = 10), 33°C ( n = 10), or 30°C ( n = 10) or warmed to 38°C ( n = 10) or 40°C ( n = 12) starting at 5 min after injury and maintained at their target temperatures for 1 h. Hypothermia-treated rats had significantly less beam-walking beam-balance, and body weight loss deficits compared to normothermic (38°C) rats. The greatest protection was observed in the 30°C hypothermia group. Since a temperature of 30°C can be induced in humans by surface cooling without coagulopathy or ventricular fibrillation, hypothermia to 30°C may have potential clinical value for treatment of human brain injury.

1965-P: Glucagon Receptor Agonism Stimulates Body Weight Loss in Antibiotic Treatment in Obese Mice

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1965-P
Author(s):  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
SHELLY NASON ◽  
NATALIE PRESEDO ◽  
WILLIAM J. VAN DER POL ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Antibiotic Treatment ◽  
Body Weight Loss ◽  
Obese Mice ◽  
Glucagon Receptor

Relation between change in treatment for central diabetes insipidus and body weight loss

2018 ◽  
Vol 44 (1) ◽  
Author(s):  
Ayako Ito ◽  
Aya Nozaki ◽  
Ichiro Horie ◽  
Takao Ando ◽  
Atsushi Kawakami
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Diabetes Insipidus ◽  
Body Weight Loss ◽  
Central Diabetes Insipidus
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