The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Guoming Luan - One of the best experts on this subject based on the ideXlab platform.
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hmgb1 tlr signaling in Rasmussens Encephalitis
Journal of neuroinfectious diseases, 2016Co-Authors: Tianfu Li, Guoming LuanAbstract:Rasmussen’s Encephalitis is neurological disorder of childhood characterized by uni-hemispheric inflammation, intractable focal epilepsy and progressive cognitive and neurological deficits. Currently, the pathogenesis of Rasmussen’s Encephalitis is still enigmatic and hemispherectomy is the only effective method to control the seizures associated with Rasmussen’s Encephalitis. Recently data indicated that intrinsic activation of endogenous proinflammation high-mobility group box-1 (HMGB1) and Toll-like receptor (TLR) is involved in the development of Rasmussen’s Encephalitis. Activation of HMGB1-TLR signaling plays a critical role in brain inflammation, development of epilepsy and cognitive dysfunction. Targeted therapy on HMGB1-TLR signaling might be a novel strategy with anti-inflammation, anti-epilepsy as well as improving cognitive dysfunction associated with epilepsy in Rasmussen’s Encephalitis.
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adenosine dysfunction in Rasmussens Encephalitis
Neuropsychiatry, 2016Co-Authors: Tianfu Li, Guoming LuanAbstract:Rasmussen’s Encephalitis (RE) is neurological disorder of childhood characterized by uni-hemispheric inflammation, intractable focal epilepsy and progressive cognitive and neurological deficits. Currently, hemispherectomy is the only effective method to control the seizures associated with RE. Although this disease has been heavily investigated, the pathogenesis of RE with unilateral cortex atrophy and focal seizure is still enigmatic. Overexpression of the ADK, the major adenosine removing enzyme, was observed in the lesions of RE. As the upper neuromodulator of the brain, adenosine is well known with anti-inflammtion, aniti-epilepsy as well as improving cognitive dysfunction associated with epilepsy. Overexpression of ADK and resulting adenosine deficiency is involved in the development of RE- pharmacoresistant seizures, inflammation, and deficits in cognitive function. Dysregulation of adenosine signaling is a common pathologic hallmark of RE, which suggest the specific targets in the treatment of epilepsy, inflammation and cognitive deterioration associated with epilepsy in RE patients.
Tianfu Li - One of the best experts on this subject based on the ideXlab platform.
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hmgb1 tlr signaling in Rasmussens Encephalitis
Journal of neuroinfectious diseases, 2016Co-Authors: Tianfu Li, Guoming LuanAbstract:Rasmussen’s Encephalitis is neurological disorder of childhood characterized by uni-hemispheric inflammation, intractable focal epilepsy and progressive cognitive and neurological deficits. Currently, the pathogenesis of Rasmussen’s Encephalitis is still enigmatic and hemispherectomy is the only effective method to control the seizures associated with Rasmussen’s Encephalitis. Recently data indicated that intrinsic activation of endogenous proinflammation high-mobility group box-1 (HMGB1) and Toll-like receptor (TLR) is involved in the development of Rasmussen’s Encephalitis. Activation of HMGB1-TLR signaling plays a critical role in brain inflammation, development of epilepsy and cognitive dysfunction. Targeted therapy on HMGB1-TLR signaling might be a novel strategy with anti-inflammation, anti-epilepsy as well as improving cognitive dysfunction associated with epilepsy in Rasmussen’s Encephalitis.
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adenosine dysfunction in Rasmussens Encephalitis
Neuropsychiatry, 2016Co-Authors: Tianfu Li, Guoming LuanAbstract:Rasmussen’s Encephalitis (RE) is neurological disorder of childhood characterized by uni-hemispheric inflammation, intractable focal epilepsy and progressive cognitive and neurological deficits. Currently, hemispherectomy is the only effective method to control the seizures associated with RE. Although this disease has been heavily investigated, the pathogenesis of RE with unilateral cortex atrophy and focal seizure is still enigmatic. Overexpression of the ADK, the major adenosine removing enzyme, was observed in the lesions of RE. As the upper neuromodulator of the brain, adenosine is well known with anti-inflammtion, aniti-epilepsy as well as improving cognitive dysfunction associated with epilepsy. Overexpression of ADK and resulting adenosine deficiency is involved in the development of RE- pharmacoresistant seizures, inflammation, and deficits in cognitive function. Dysregulation of adenosine signaling is a common pathologic hallmark of RE, which suggest the specific targets in the treatment of epilepsy, inflammation and cognitive deterioration associated with epilepsy in RE patients.
