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Meiyuan Xincun, China

Chen T.-Z.,Shandong University | Chen T.-Z.,Taishan Medical University | Xu G.-J.,Taishan Medical University | Zhou G.-A.,Central Hospital of Taian | And 3 more authors.
Brain Research | Year: 2014

There is compelling evidence that postural instability occurs at very early clinical stages of Parkinsons disease (PD), making it tempting to speculate that changes in postural sway may even occur at a prodromal phase. Studies estimate that approximately half of patients with idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) will eventually develop PD, so RBD may be an indicator of prodromal PD. This study was undertaken to investigate postural sway and its relation to stereopsis function in patients with RBD. We examined 24 patients with polysomnography-confirmed RBD and 23 healthy, sex-and age-matched control subjects. Postural sway was measured with an accelerometer at the center of mass at the lower spine. Subjects were asked to stand quietly for 30 s under two usual conditions (eyes open and eyes closed) and three challenging conditions (eyes open with dual task, eyes closed with dual task, and tandem standing). Stereopsis was assessed using the Titmus fly test. RBD patients showed an increased variability of trunk acceleration and a decrease of smoothness of sway, compared to control subjects. These differences reached significance in the challenging conditions. RBD patients demonstrated significant impairment in stereopsis. There were statistically significant correlations between log seconds of arc of the Titmus test and some sway parameters within the RBD group. RBD patients with abnormal stereopsis showed a significant increase of JERK values compared to patients with normal stereopsis in the challenging conditions. Our results indicate that idiopathic RBD patients, especially with abnormal stereopsis, have subtle signs of postural instability under challenging conditions. Postural sway performance may serve as a biological marker for prodromal PD. © 2014 Elsevier B.V. Source


Wu T.,Xuanwu Hospital | Hallett M.,U.S. National Institutes of Health
Current Clinical Neurology | Year: 2013

In the last 20 years, functional MRI (fMRI) has been an exciting development. Since its appearance, it has been extensively used in studies on movement disorders. This chapter will briefly introduce a basic overview of fMRI. We will then focus on the successful application of blood oxygen level-dependent (BOLD) fMRI in idiopathic Parkinson disease (iPD), a common and critical movement disorder. BOLD fMRI has been extensively used to understand the neural correlates of motor deficits in iPD from both a regional brain activity and network basis. This technique has also provided new insight into nonmotor deficits such as cognitive, psychiatric, and olfactory impairments. fMRI studies on asymptomatic gene mutation carriers have found a compensatory reorganization of striatocortical motor loops to maintain motor function in the preclinical stage. More recent resting-state fMRI studies have identified iPD-specific spontaneous neural activity or network connectivity patterns. The role of arterial spin labeling (ASL) perfusion MRI in iPD is discussed. fMRI findings in atypical parkinsonism, including multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and dementia with Lewy bodies (DLB) are also presented. Despite some limitations, future fMRI studies will enhance our understanding of pathophysiological changes in movement disorders. fMRI also has potential to be developed as a neuroimaging biomarker of iPD, with the potential to improve early diagnosis, monitor disease progression, differentiate iPD from other parkinsonisms on an individual basis, and may identify novel targets for future therapies. Source


Lu X.,Peking University | Guo J.,Peking University | Zhou X.,Peking University | Li R.,Peking University | And 10 more authors.
Annals of the Rheumatic Diseases | Year: 2011

Objectives: The deletion of LCE3C-LCE3B confers susceptibility to psoriasis and rheumatoid arthritis (RA) in Caucasians. The aim of this study was to investigate the variant involvement in RA in the Chinese Han population and to further explore its potential role in the susceptibility to systemic lupus erythematosus (SLE). Methods: LCE3C-LCE3B-del was genotyped in 898 patients with RA and 681 healthy controls. Two single nucleotide polymorphisms (SNPs, rs4112788 and rs4085613) in strong linkage disequilibrium with LCE3C-LCE3B-del were then genotyped in patients with RA (n=1222), SLE (n=870) and healthy controls (n=1031). Results: The deletion of LCE3C-LCE3B and SNPs rs4112788 and rs4085613 showed an association with RA (allele analysis: p=7.72×10 -4, OR 1.28, 95% CI 1.11 to 1.47;p=6.39×10-4, OR 1.23, 95% CI 1.09 to 1.38; and p=5.38×10-4, OR 1.23, 95% CI 1.10 to 1.39, respectively). The two SNPs were also significantly associated with SLE (allele analysis: p=7.68×10-3, OR 1.19, 95% CI 1.05 to 1.36 and p=5.30×10-3, OR 1.20, 95% CI 1.06 to 1.37). Conclusions This study provides evidence for an association between LCE3C-LCE3B-del and RA in non-Caucasian populations, and SNPs rs4112788 and rs4085613 tagging LCE3C-LCE3B-del were novel susceptibility factors for SLE. Source


Fernagut P.-O.,University of Bordeaux Segalen | Li Q.,Motac Neuroscience Ltd | Li Q.,China Academy of Medical science | Dovero S.,University of Bordeaux Segalen | And 7 more authors.
PLoS ONE | Year: 2010

Background: Radiotracer imaging of the presynaptic nigrostriatal dopaminergic system is used to assess disease progression in Parkinson's disease (PD) and may provide a useful adjunct to clinical assessment during therapeutic trials of potential neuroprotective agents. Several clinical trials comparing dopamine agonists to L-DOPA or early vs. late L-DOPA have revealed differences between clinical assessment and imaging of the presynaptic dopaminergic system, hence questioning the comparability of these measures as neuroprotection outcome variables. Thus, results of these studies may have been affected by factors other than the primary biological process investigated. Methodology/Principal Findings: We tested the possibility that L-DOPA might interfere with DAT binding. Post-mortem DAT binding was conducted in normal and MPTP-treated macaque monkeys that were administered L-DOPA, acutely or chronically. In parallel, DAT SPECT was conducted in MPTP-treated animals that were administered chronic L-DOPA. [99mTc]TRODAT-1 SPECT binding was similarly reduced in all MPTP monkeys regardless of L-DOPA treatment. L-DOPA had no significant effect on post-mortem DAT binding either in saline or in MPTP-lesioned animals. Conclusions/Significance: These data indicate that L-DOPA does not induce modifications of DAT expression detectable by SPECT of by DAT binding autoradiography, suggesting that differences between clinical assessment and radiotracer imaging in clinical trials may not be specifically related to L-DOPA treatment. © 2010 Fernagut et al. Source


Than M.,Christchurch Hospital | Cullen L.,Royal Brisbane and Womens Hospital | Cullen L.,Queensland University of Technology | Reid C.M.,Monash University | And 24 more authors.
The Lancet | Year: 2011

Background Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome. Methods This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279. Intepretation 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11·8) patients had a major adverse cardiac event. The ADP classified 352 (9·8) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0·9) of these patients, giving the ADP a sensitivity of 99·3 (95 CI 97·9-99·8), a negative predictive value of 99·1 (97·3-99·8), and a specificity of 11·0 (10·0-12·2). This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide. Funding Alere Medical (all countries), Queensland Emergency Medicine Research Foundation and National Health and Medical Research Council (Australia), Christchurch Cardio-Endocrine Research Group (New Zealand), Medquest Jaya Global (Indonesia), Science International (Hong Kong), Bio Laboratories Pte (Singapore), National Heart Foundation of New Zealand, and Progressive Group (Taiwan). © 2011 Elsevier Ltd. Source

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