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Faculty Spolight On:
Dr. Helen Bramlett

 

 

 


Dr. Bramlett


 
Research Interests 

 

Affiliations 

  

 

Publications


Contact Information:


 

The Miami Project
to Cure Paralysis

 

1095 NW 14th Terrace

 

Locator Code R-48

 

Miami, Florida 33136

 

 

Tel:  (305) 243-8926
Fax: (305) 243-3914

 

 

hbramlett@med.miami.edu

 

Home Our Research Faculty > Helen Bramlett, Ph.D.

 

HELEN M. BRAMLETT, PH.D.

Professor, Department of Neurological Surgery

 

The Pathophysiology and Treatment of CNS Injury

 

Research Interests

 

 

The main focus of my laboratory is investigating the pathophysiology of traumatic injury leading to the use of therapeutic strategies targeting specific mechanisms of damage. My laboratory focuses on three areas of traumatic research: 1) hormonal influences on traumatic injury, 2) progressive damage after trauma and 3) secondary injury mechanisms after traumatic brain injury (TBI).

 

Several recent studies have reported on the efficacy of hormones in treating stroke and traumatic brain injury. The mechanisms of action that hormones are working through are now being elucidated. We have demonstrated endogenous neuroprotection from hormones in intact females compared to males and ovariectomized animals on histopathological outcome measures. We are now focusing on the influence of the inflammatory response on outcome following TBI and the effect that hormones play in this response. In addition to studies in TBI, we are also studying the effects of hormones in attenuating damage and improving behavioral outcome after spinal cord injury (SCI). Based on the findings from these studies, it may be advantageous to use estrogen in combination with other growth factors to facilitate regeneration after SCI. Estrogen has been shown to produce proliferation of Schwann cells as well as neurite growth.

 

Our laboratory and others have documented in a clinically relevant model of TBI that there is progressive atrophy of brain structures following injury. However, it is unknown what is causing this continued gray and white matter tissue loss. Is it due to the initial injury or are there active processes ongoing that continue to degrade the tissue? Current studies in the laboratory are designed to determine what mechanisms may be contributing to this progressive damage in order to design appropriate treatment strategies to halt this loss.

 

One problem that arises in studying TBI is using a model that is clinically relevant. There is an ongoing debate on whether simple models or complicated models of TBI should be utilized in the laboratory. Secondary hypoxia and hypotension frequently occur clinically after TBI. Several laboratories are employing this paradigm to study the pathophysiology of this complicated model. We have also documented an exacerbation of histopathological damage as well as behavioral deficits following TBI and secondary hypoxia. Another factor that may play a critical role in traumatic outcome is the presence of a systemic inflammatory response secondary to multi-organ injury. This systemic inflammatory response syndrome is characterized by local and systemic production and release of different inflammatory mediators. TBI patients including soldiers with blast injuries commonly have injuries to other organs thus using an injury model that mimics polytrauma can be advantageous.   We are currently concentrating on obtaining evidence for aggravated vascular dysfunction leading to an enhanced inflammatory response in our own polytrauma injury paradigm and testing novel therapeutic strategies to enhance recovery.


 

 
 
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