Person: Wu, Limin
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Wu
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Limin
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Wu, Limin
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Publication Are Onconeural Antibodies a Clinical Phenomenology in Paraneoplastic Limbic Encephalitis?(Hindawi Publishing Corporation, 2013) Zhang, Hongliang; Zhou, Chunkui; Wu, Limin; Ni, Fengming; Zhu, Jie; Jin, TaoParaneoplastic neurological syndromes (PNSs) occur in patients with cancer and can cause clinical symptoms and signs of dysfunction of the nervous system that are not due to a local effect of the tumor or its metastases. Most of these clinical syndromes in adults are associated with lung cancer, especially small cell lung cancer (SCLC), lymphoma, and gynecological tumors. The finding of highly specific antibodies directed against onconeural antigens has revolutionized the diagnosis and promoted the understanding of these syndromes and led to the current hypothesis of an autoimmune pathophysiology. Accumulating data strongly suggested direct pathogenicity of these antibodies. The field of PNS has expanded rapidly in the past few years with the discovery of limbic encephalitis associated with glutamic acid decarboxylase (GAD) 65, the voltage (VGKC-gated potassium channel) complex, the methyl (N-NMDA-D-aspartate), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and gamma aminobutyric acid (GABA) (B) receptors, and so forth. Despite this, the clinical spectrum of these diseases has not yet been fully investigated. The clinical importance of these conditions lies in their frequent response to immunotherapies and, less commonly, their association with distinctive tumors. This review provides an overview on the pathogenesis and diagnosis of PNS, with emphasis on the role of antibodies in limbic encephalitis.Publication More Severe Manifestations and Poorer Short-Term Prognosis of Ganglioside-Associated Guillain-Barré Syndrome in Northeast China(Public Library of Science, 2014) Wu, Xiujuan; Wu, Wei; Wang, Zhengzheng; Shen, Donghui; Pan, Wei; Wang, Ying; Wu, Limin; Wu, Xiaokun; Feng, Jiachun; Liu, Kangding; Zhu, Jie; Zhang, Hong-LiangGanglioside as a neurotrophic drug has been hitherto widely used in China, although Guillain-Barré syndrome (GBS) following intravenous ganglioside treatment was reported in Europe several decades ago. We identified 7 patients who developed GBS after intravenous use of gangliosides (ganglioside+ group) and compared their clinical data with those of 77 non-ganglioside-associated GBS patients (ganglioside− group) in 2013, aiming at gaining the distinct features of ganglioside-associated GBS. Although the mean age, protein levels in cerebrospinal fluid (CSF) and frequency of cranial nerve involvement were similar between the two groups, the Hughes Functional Grading Scale (HFGS) score and the Medical Research Council (MRC) sum score at nadir significantly differed (4.9±0.4 vs 3.6±1.0; 7.7±5.5 vs 36.9±14.5, both p<0.001), indicating a higher disease severity of ganglioside-associated GBS. A higher ratio of patients with ganglioside-associated GBS required mechanical ventilation (85.7% vs 15.6%, p<0.01). The short-term prognosis of ganglioside-associated GBS, as measured by the HFGS score and the MRC sum score at discharge, was poorer (4.3±0.5 vs 2.8±1.1; 17.3±12.9 vs 46.0±13.9, both p<0.001). All the patients in the ganglioside+ group presented an axonal form of GBS, namely acute motor axonal neuropathy (AMAN). When compared with the AMAN patients in the ganglioside− group, more severe functional deficits at nadir and poorer recovery after standard treatment were still prominent in ganglioside-associated GBS. Anti-GM1 and anti-GT1a antibodies were detectable in patients with AMAN while not in patients with the demyelinating subtype of GBS. The concentrations of these antibodies in patients with AMAN were insignificantly different between the ganglioside+ and ganglioside− groups. In sum, ganglioside-associated GBS may be a devastating side effect of intravenous use of gangliosides, which usually manifests a more severe clinical course and poorer outcome.Publication Neuregulin1-β Decreases IL-1β -Induced Neutrophil Adhesion to Human Brain Microvascular Endothelial Cells(Springer Nature, 2014) Wu, Limin; Walas, Samantha; Leung, Wendy; Sykes, David; Wu, Jiang; Lo, Eng; Lok, Josephine M.Neuroinflammation contributes to the pathophysiology of diverse diseases including stroke, traumatic brain injury, Alzheimer's Disease, Parkinson's Disease, and multiple sclerosis, resulting in neurodegeneration and loss of neurological function. The response of the microvascular endothelium often contributes to neuroinflammation. One such response is the up-regulation of endothelial adhesion molecules which facilitate neutrophil adhesion to the endothelium and their migration from blood to tissue. Neuregulin-1 (NRG1) is an endogenous growth factor which has been reported to have anti-inflammatory effects in experimental stroke models. We hypothesized that NRG1 would decrease the endothelial response to inflammation, and result in a decrease in neutrophil adhesion to endothelial cells. We tested this hypothesis in an in-vitro model of cytokine-induced endothelial injury, in which human brain microvascular endothelial cells (BMECs) were treated with IL-1β, along with co-incubation with vehicle or NRG1-β. Outcome measures included protein levels of endothelial ICAM-1, VCAM-1, and E-selectin; as well as the number of neutrophils that adhere to the endothelial monolayer. Our data show that NRG1-β decreased the levels of VCAM-1, E-selectin, and neutrophil adhesion to brain microvascular endothelial cells activated by IL1-β. These findings open new possibilities for investigating NRG1 in neuroprotective strategies in brain injury.Publication Acute Necrotizing Encephalopathy: An Underrecognized Clinicoradiologic Disorder(Hindawi Publishing Corporation, 2015) Wu, Xiujuan; Wu, Wei; Pan, Wei; Wu, Limin; Liu, Kangding; Zhang, Hong-LiangAcute necrotizing encephalopathy (ANE) is a rare but distinctive type of acute encephalopathy with global distribution. Occurrence of ANE is usually preceded by a virus-associated febrile illness and ensued by rapid deterioration. However, the causal relationship between viral infections and ANE and the exact pathogenesis of ANE remain unclear; both environmental and host factors might be involved. Most cases of ANE are sporadic and nonrecurrent, namely, isolated or sporadic ANE; however, few cases are recurrent and with familial episodes. The recurrent and familial forms of ANE were found to be incompletely autosomal-dominant. Further the missense mutations in the gene encoding the nuclear pore protein Ran Binding Protein 2 (RANBP2) were identified. Although the clinical course and the prognosis of ANE are diverse, the hallmark of neuroradiologic manifestation of ANE is multifocal symmetric brain lesions which are demonstrated by computed tomography (CT) or magnetic resonance imaging (MRI). The treatment of ANE is still under investigation. We summarize the up-to-date knowledge on ANE, with emphasis on prompt diagnosis and better treatment of this rare but fatal disease.