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Yi Guo,
Joseph Jankovic,
Zhi Song,
Huarong Yang,
Wen Zheng,
Weidong Le, Xiangqi Tang,
Xiong Deng,
Yan Yang,
Sheng Deng,
Ziqiang Luo,
Hao Deng
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ABSTRACT: Essential tremor (ET) has been hypothesized to be a risk factor for the development of Parkinson disease (PD). Recently, rs9652490 variant in the leucine-rich repeat and Ig domain containing 1 gene (LINGO1) was found to be associated with ET susceptibility. To evaluate whether the same variant is associated also with PD susceptibility, we investigated the association between the LINGO1 rs9652490 variant and PD phenotype in Caucasian and Chinese PD subjects. We found no significant differences in genotypic and allele distribution between patients and control subjects (χ(2)=1.931, p=0.381 for genotypic distribution; χ(2)=0.001, p=0.973 for allele distribution), suggesting this variant is not associated with PD.
Neuroscience Letters 10/2010; 487(2):174-6. · 2.11 Impact Factor
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ABSTRACT: Oxygen therapy is a promising treatment strategy for ischemic stroke. One potential safety concern with oxygen therapy, however, is the possibility of increased generation of reactive oxygen species (ROS), which could exacerbate ischemic brain injury. Our previous study indicated that normobaric hyperoxia (NBO, 95% O(2) with 5% CO(2)) treatment during ischemia salvaged ischemic brain tissue and significantly reduced ROS generation in transient experimental stroke. In this follow-up study, we tested the hypothesis that suppression of NADPH oxidase is an important mechanism for NBO-induced reduction of ROS generation in focal cerebral ischemia. Male Sprague-Dawley rats were given NBO (95% O(2)) or normoxia (21% O(2)) during 90-min filament occlusion of the middle cerebral artery, followed by 22.5-hour reperfusion. NBO treatment increased the tissue oxygen partial pressure (pO(2)) level in the ischemic penumbra close to the pre-ischemic value, as measured by electronic paramagnetic resonance (EPR), and led to a 30.2% reduction in magnetic resonance imaging (MRI) apparent diffusion coefficients (ADC) lesion volume. Real time PCR and western blot analyses showed that the mRNA and protein expression of NADPH oxidase catalytic subunit gp91(phox) were upregulated in the ischemic brain, which was significantly inhibited by NBO. As a consequence of gp91(phox) inhibition, NBO treatment reduced NADPH oxidase activity in the ischemic brain. Our results suggest that NBO treatment given during ischemia reduces ROS generation via inhibiting NADPH oxidase, which may serve as an important mechanism underlying NBO's neuroprotection in acute ischemic stroke.
Brain research 08/2010; 1348:174-80. · 2.46 Impact Factor
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ABSTRACT: Small heat shock proteins(sHSPs), with a small molecular mass of 12-43 kDa, are molecular chaperones that protect cells against stress by assisting them in the correct folding of denatured proteins and thus prevent aggregation of misfolded proteins. During the past several years, there has been an increasing interest in the relationship between sHSPs and neuropathy. sHSPs have emerged as a particularly potent neuroprotectant in diverse neurological disorders. Therefor, in this review, we will focus on the expression of sHSPs in different neurological disorders, and discuss the recent findings of the biological implications of sHSPs in physiological and pathological processes in these diseases. Novel therapeutic strategies aiming at restoring sHSPs in neuropathy will also be presented.
Current neurovascular research 05/2010; 7(2):155-66. · 3.23 Impact Factor
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ABSTRACT: The Golgi apparatus (GA) is a cytoplasmic organelle that is of great interest to all scientists for its key role in the biosynthesis, transporting and sorting of both lipids and proteins located at the intersection of the secretory and endocytic pathways. Recently, more and more evidence shows that changes in the Golgi apparatus play an important role in the clinical progression and pathological development of many diseases. In this review, we will summarize the alteration of the Golgi apparatus in blood cells and anti-Golgi complex antibodies in blood serum under different conditions and further clarify the contribution of the Golgi apparatus dysfunction to the course of these diseases and its pathophysiological basis, which will significantly improve our understanding and impact our ability to develop more effective therapies for these diseases.
Clinical laboratory 01/2010; 56(5-6):231-43. · 0.90 Impact Factor
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Journal of clinical rheumatology: practical reports on rheumatic & musculoskeletal diseases 03/2009; 15(1):48. · 1.19 Impact Factor
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ABSTRACT: Neurodegenerative disorders are typically characterized by progressive and extensive neuronal loss in specific populations of neurons and brain areas which lead to the observed clinical manifestations. Despite the recent advances in molecular neuroscience, the subcellular bases such as Golgi apparatus (GA) for most neurodegenerative diseases are poorly understood. This review gives a brief overview of the contribution of the neuronal GA in the pathogeneses of neurodegeneration, summarizes what is known of the GA machinery in these diseases, and present the relationship between GA fragmentation and the aggregation and accumulation of misfolded or aberrant proteins including mutant SOD1, a-synuclein, tau, which is considered to be a key event in the pathogenic process, and perturbating in calcium homeostasis, regulation of hormones, lipid metabolism are also linkage to the function of the GA thought to underlie neurodegeneration. Although these precise diseases mechanisms remain to be clarified, more research is needed to better understand how GA function for it and to enable physicians to use this knowledge for the benefit of the patients.
International Journal of Developmental Neuroscience 11/2008; 26(6):523-34. · 2.42 Impact Factor
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ABSTRACT: Transforming growth factor2 (TGFbeta2) is a prototypic member of a large superfamily of multifunctional cytokines, and its potential mechanisms of the neuroprotective activity in ischemic stroke and subcellular compartmentalization are largely unknown. The present study investigated TGF-beta2 protein expression in hippocampal neuronal cells after transient forebrain ischemia (TFI). TFI was induced in male adult gerbils with bilateral occlusion of both common carotid arteries for 10 minutes. With immunohistochemical methods we observe the expression of TGF-beta2 and morphological alternation in Golgi appratus (GA) in different postischemic periods and sham-operation (6 hours, 1, 3 and 7 days). In addition, the subcellular localization of TGF-beta2 is determined in trans-Golgi network (TGN) by double-labeling confocal immunofluorographs with TGN38.The results showed that TGF-beta2 persistent express in the ischemic animals and it peaks at 3 days, then decreased 7 days postocclusion. No significant alterations to the GA were noted at the point of 6 hours,1 and 3 days following TFI, but there are a few neurons in which the GA lost the normal network-like configuration and its elements decreased in cortical cells from gerbils survived 7 days postocclusion. In addition, TGF-beta2 was colocalized with TGN38 in the TGN after TFI .Taken together, this result suggested that TGF-beta2 protein expression increased in neurons after ischemia, which may represent an endogenous adaptative response of the brain damage and its secretion via GA after ischemia is supposed to be beneficial for GA . Furthermore, fragmentation of GA is not common phenomenon in the ischemia, but intact GA structural of neurons is beneficial for cell survival.
Current neurovascular research 09/2008; 5(3):178-84. · 3.23 Impact Factor
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ABSTRACT: Flow metabolism coupling ensures adequate cerebral oxygenation. When subarachnoid hemorrhage (SAH) occurs, the flow metabolism coupling lost its balance and results in cerebral ischemia and infarction second to cortical magnesium and energy metabolism alternation. During chronic vasospasm, change in cortical energy metabolism is coupled with change in cerebral blood flow after SAH.
What kind of noninvasive technique can be used to directly investigate the biochemical environment in the SAH brain? Studies showed that (31)P magnetic resonance spectroscopy ((31)P MRS) is ideally suited to evaluate the pathophysiology of SAH, especially for cortical magnesium and energy metabolism.
The results showed that cortical magnesium and energy metabolism were significantly decreased in both animal models and human beings after SAH by using (31)P MRS, which is associated with the severity and outcome of SAH, especially after aneurysmal SAH.
(31)P MRS data, combined with other MRI sequences, provide a comprehensive assessment of both structural and functional deficits and a guidance on clinical therapy for SAH.
Cerebrovascular Diseases 01/2008; 26(3):223-30. · 2.72 Impact Factor
