scholarly journals Vancomycin Is Protective in a Neonatal Mouse Model of Staphylococcus epidermidis-Potentiated Hypoxic-Ischemic Brain Injury

2019 ◽  
Vol 64 (3) ◽  
Author(s):  
Jacqueline C. Y. Lai ◽  
Pernilla Svedin ◽  
C. Joakim Ek ◽  
Amin Mottahedin ◽  
Xiaoyang Wang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Mouse Model ◽  
Preterm Infants ◽  
Staphylococcus Epidermidis ◽  
Neonatal Mouse ◽  
Neurodevelopmental Outcomes ◽  
Ischemic Brain ◽  
Content Type ◽  
Increased Risk ◽  
The Brain

ABSTRACT Infection is correlated with increased risk of neurodevelopmental sequelae in preterm infants. In modeling neonatal brain injury, Toll-like receptor agonists have often been used to mimic infections and induce inflammation. Using the most common cause of bacteremia in preterm infants, Staphylococcus epidermidis, we present a more clinically relevant neonatal mouse model that addresses the combined effects of bacterial infection together with subsequent hypoxic-ischemic brain insult. Currently, there is no neuroprotective treatment for the preterm population. Hence, we tested the neuroprotective effects of vancomycin with and without adjunct therapy using the anti-inflammatory agent pentoxifylline. We characterized the effects of S. epidermidis infection on the inflammatory response in the periphery and the brain, as well as the physiological changes in the central nervous system that might affect neurodevelopmental outcomes. Intraperitoneal injection of postnatal day 4 mice with a live clinical isolate of S. epidermidis led to bacteremia and induction of proinflammatory cytokines in the blood, as well as transient elevations of neutrophil and monocyte chemotactic cytokines and caspase 3 activity in the brain. When hypoxia-ischemia was induced postinfection, more severe brain damage was observed in infected animals than in saline-injected controls. This infection-induced inflammation and potentiated brain injury was inoculum dose dependent and was alleviated by the antibiotic vancomycin. Pentoxifylline did not provide any additional neuroprotective effect. Thus, we show for the first time that live S. epidermidis potentiates hypoxic-ischemic preterm brain injury and that peripheral inhibition of inflammation with antibiotics, such as vancomycin, reduces the extent of brain injury.

Minocycline worsens hypoxic-ischemic brain injury in a neonatal mouse model

2004 ◽  
Vol 189 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Masahiro Tsuji ◽  
Mary Ann Wilson ◽  
Mary S. Lange ◽  
Michael V. Johnston
Keyword(s):  
Brain Injury ◽  
Mouse Model ◽  
Neonatal Mouse ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Sport-related concussions

2014 ◽  
Vol 8 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Jéssica Natuline Ianof ◽  
Fabio Rios Freire ◽  
Vanessa Tomé Gonçalves Calado ◽  
Juliana Rhein Lacerda ◽  
Fernanda Coelho ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Behavioral Changes ◽  
American Football ◽  
Health Concern ◽  
Public Health Concern ◽  
Increased Risk ◽  
High Prevalence ◽  
Biomechanical Forces ◽  
The Brain

ABSTRACT Traumatic brain injury (TBI) is a major cause of lifelong disability and death worldwide. Sport-related traumatic brain injury is an important public health concern. The purpose of this review was to highlight the importance of sport-related concussions. Concussion refers to a transient alteration in consciousness induced by external biomechanical forces transmitted directly or indirectly to the brain. It is a common, although most likely underreported, condition. Contact sports such as American football, rugby, soccer, boxing, basketball and hockey are associated with a relatively high prevalence of concussion. Various factors may be associated with a greater risk of sport-related concussion, such as age, sex, sport played, level of sport played and equipment used. Physical complaints (headache, fatigue, dizziness), behavioral changes (depression, anxiety, irritability) and cognitive impairment are very common after a concussion. The risk of premature return to activities includes the prolongation of post-concussive symptoms and increased risk of concussion recurrence.

scholarly journals Predictive Value of Cranial Ultrasound for Neurodevelopmental Outcomes of Very Preterm Infants with Brain Injury

2018 ◽  
Vol 131 (8) ◽  
pp. 920-926 ◽  
Author(s):  
Xue-Hua Zhang ◽  
Shi-Jun Qiu ◽  
Wen-Juan Chen ◽  
Xi-Rong Gao ◽  
Ya Li ◽  
...  
Keyword(s):  
Brain Injury ◽  
Preterm Infants ◽  
Predictive Value ◽  
Cranial Ultrasound ◽  
Neurodevelopmental Outcomes ◽  
Very Preterm Infants ◽  
Very Preterm

scholarly journals Importance of T Lymphocytes in Brain Injury, Immunodeficiency, and Recovery after Cerebral Ischemia

2012 ◽  
Vol 32 (4) ◽  
pp. 598-611 ◽  
Author(s):  
Vanessa H Brait ◽  
Thiruma V Arumugam ◽  
Grant R Drummond ◽  
Christopher G Sobey
Keyword(s):  
Brain Injury ◽  
T Lymphocytes ◽  
T Lymphocyte ◽  
Lymphocyte Activation ◽  
Infectious Complications ◽  
Increased Risk ◽  
The Hours ◽  
Immunodeficiency Syndrome ◽  
Subsets Of T Lymphocytes ◽  
The Brain

Following an ischemic stroke, T lymphocytes become activated, infiltrate the brain, and appear to release cytokines and reactive oxygen species to contribute to early inflammation and brain injury. However, some subsets of T lymphocytes may be beneficial even in the early stages after a stroke, and recent evidence suggests that T lymphocytes can also contribute to the repair and regeneration of the brain at later stages. In the hours to days after stroke, T-lymphocyte numbers are then reduced in the blood and in secondary lymphoid organs as part of a ‘stroke-induced immunodeficiency syndrome,’ which is mediated by hyperactivity of the sympathetic nervous system and the hypothalamic—pituitary—adrenal axis, resulting in increased risk of infectious complications. Whether or not poststroke T-lymphocyte activation occurs via an antigen-independent process, as opposed to a classical antigen-dependent process, is still controversial. Although considerable recent progress has been made, a better understanding of the roles of the different T-lymphocyte subpopulations and their temporal profile of damage versus repair will help to clarify whether T-lymphocyte targeting may be a viable poststroke therapy for clinical use.

scholarly journals Temporal Characterization of Microglia/Macrophage Phenotypes in a Mouse Model of Neonatal Hypoxic-Ischemic Brain Injury

2016 ◽  
Vol 10 ◽  
Author(s):  
Nina Hellström Erkenstam ◽  
Peter L. P. Smith ◽  
Bobbi Fleiss ◽  
Syam Nair ◽  
Pernilla Svedin ◽  
...  
Keyword(s):  
Brain Injury ◽  
Mouse Model ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Macrophage Phenotypes ◽  
Hypoxic Ischemic Brain Injury

Attenuation of brain injury and reduction of neuron-specific enolase by nicardipine in systemic circulation following focal ischemia and reperfusion in a rat model

1997 ◽  
Vol 87 (5) ◽  
pp. 731-737 ◽  
Author(s):  
Mamoru Kittaka ◽  
Steven L. Giannotta ◽  
Vladimir Zelman ◽  
Jorge D. Correale ◽  
Christopher M. DeGiorgio ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuron Specific Enolase ◽  
Neuronal Injury ◽  
Systemic Circulation ◽  
Specific Marker ◽  
Neuroprotective Effects ◽  
Doppler Flowmetry ◽  
Ischemic Brain ◽  
Content Type ◽  
Edema Volume

✓ reversible middle cerebral artery occlusion was performed in rats to determine whether nicardipine, a dihydropyridine voltage-sensitive Ca++ channel (VSCC) antagonist, exerts neuroprotective effects when administered 10 minutes following an ischemic insult, and if it does, whether this is due to its vasodilatory action and effect on cerebral blood flow (CBF) or to direct blockade of Ca++ entry into ischemic brain cells. An increase in the intracellular calcium, [Ca++]i, plays a major role in neuronal injury during cerebral ischemia. Although a large amount of Ca++ enters neurons through the VSCC during ischemia, inconsistent neuroprotective effects have been reported with the antagonists of the VSCC. An intraperitoneal injection of nicardipine (1.2 mg/kg) was administered to rats 10 minutes after the onset of ischemia, and 8, 16, and 24 hours after occlusion. Cortical CBF was determined by laser-Doppler flowmetry. Neurological and neuropathological examinations were performed after 72 hours. Neuron-specific enolase, a specific marker for the incidence of neuronal injury, was measured in plasma. The CBF and other physiological parameters were not affected by nicardipine during occlusion or reperfusion. However, nicardipine treatment significantly improved motor neurological outcome by 29%, and the infarction and edema volume in the pallium as well as the edema volume in the striatum were significantly reduced by 27%, 37%, and 52%, respectively. Nicardipine also reduced the neuron-specific enolase plasma levels by 50%, 42%, and 59% at 24, 48, and 72 hours after the occlusion, respectively. It is concluded that nicardipine may attenuate focal ischemic brain injury by exerting direct neuroprotective and antiedematous effects that do not depend on CBF.

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