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The dynamic functional connectivity (dFC) in functional magnetic resonance imaging (fMRI) is beneficial for the analysis and diagnosis of neurological brain diseases. The dFCs between regions of interest (ROIs) are generally delineated by a specific template and clustered into multiple different states. However, these models inevitably fell into the model-driven self-contained system which ignored the diversity at spatial level and the dynamics at time level of the data. In this study, we proposed a spatial and time domain feature extraction approach for Alzheimer's disease (AD) and autism spectrum disorder (ASD)-assisted diagnosis which exploited the dynamic connectivity among independent functional sub networks in brain. Briefly, independent sub networks were obtained by applying spatial independent component analysis (SICA) to the preprocessed fMRI data. Then, a sliding window approach was used to segment the time series of the spatial components. After that, the functional connections within the window were obtained sequentially. Finally, a temporal signal-sensitive long short-term memory (LSTM) network was used for classification. The experimental results on Alzheimer's Disease Neuroimaging Initiative (ADNI) and Autism Brain Imaging Data Exchange (ABIDE) datasets showed that the proposed method effectively predicted the disease at the early stage and outperformed the existing algorithms. The dFCs between the different components of the brain could be used as biomarkers for the diagnosis of diseases such as AD and ASD, providing a reliable basis for the study of brain connectomics.

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BACKGROUND: Brain abscesses, a severe infectious disease of the CNS, are usually caused by a variety of different pathogens, which include Streptococcus intermedius (S. intermedius). Pulmonary arteriovenous fistulas (PAVFs), characterized by abnormal direct communication between pulmonary artery and vein, are a rare underlying cause of brain abscesses. CASE PRESENTATION: The patient was a previous healthy 55-year-old man who presented with 5 days of headache and fever. Cerebral magnetic resonance imaging (MRI) suggested a brain abscess. Thoracic CT scan and angiography demonstrated PAVFs. Aiding by metagenomic next-generation sequencing (mNGS) of the cerebrospinal fluid (CSF) sample which identified S. intermedius as the causative pathogen, the patient was switched to the single therapy of large dose of penicillin G and was cured precisely and economically. CONCLUSIONS: It is an alternative way to perform mNGS to identify causative pathogens in patients with brain abscesses especially when the results of traditional bacterial culture were negative. Further thoracic CT or pulmonary angiography should also be undertaken to rule out PAVFs as the potential cause of brain abscess if the patient without any known premorbid history.

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Spinocerebellar ataxias (SCAs) are a group of autosomal dominant, clinically heterogeneous neurodegenerative disorders. SCA18 is a rare autosomal dominant sensory/motor neuropathy with ataxia (OMIM#607458) associated with a single missense variant c.514 A>G in the interferon related developmental regulator 1 (IFRD1) gene previously reported in a five-generation American family of Irish origin. However, to date, there have been no other reports of the IFRD1 mutation to confirm its role in SCA. Here, we report a Han Chinese family with SCA18; the family members presented with a slowly progressing gait ataxia, pyramidal tract signs, and peripheral neuropathy. We identified a missense variant (c.514 A>G, p.I172V) in IFRD1 gene in the family using targeted next-generation sequencing and Sanger direct sequencing with specific primers. Our results suggest that the IFRD1 gene may be the causative allele for SCA18.

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BACKGROUND: This study estimated the effects of ambient temperature on hospital admissions for hemorrhagic stroke during 2004-2009 in Jinan, China, and the effect modification of hypertension status. METHODS: The exposure-response relationship between temperature and hemorrhagic stroke was firstly examined, and then the association between daily mean temperature and hemorrhagic stroke was investigated using a generalized additive model. Stratified analyses were conducted to examine the potential effect modification of hypertension. RESULTS: A total of 1577 hemorrhagic stroke cases were observed between 2004 and 2009, among which, 1058 were hypertensive and 519 were non-hypertensive. We found an approximately linear relationship between ambient temperature and hemorrhagic stroke. Each 1°C decrease in the current day's temperature was associated with 1.63% (95% CI: 0.33%, 2.95%) increase in daily hemorrhagic stroke. The stratified analyses observed that the association was significant among hypertensive hemorrhagic stroke, each 1°C decrease in the current day's temperature was associated with 2.26% (95% CI: 0.57%, 3.98%) increase in daily hypertensive hemorrhagic stroke. While no significant effect was observed for non-hypertensive hemorrhagic stroke. CONCLUSIONS: Low temperature might be one risk factor for hemorrhagic stroke and hypertension may be one effect modifier of this association in Jinan, China.

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Neural disruptions during emotion regulation are common of generalized anxiety disorder (GAD). Identifying distinct functional and effective connectivity patterns in GAD may provide biomarkers for their diagnoses. This study aims to investigate the differences of features of brain network connectivity between GAD patients and healthy controls (HC), and to assess whether those differences can serve as biomarkers to distinguish GAD from controls. Independent component analysis (ICA) with hierarchical partner matching (HPM-ICA) was conducted on resting-state functional magnetic resonance imaging data collected from 20 GAD patients with medicine-free and 20 matched HC, identifying nine highly reproducible and significantly different functional brain connectivity patterns across diagnostic groups. We then utilized Granger causality (GC) to study the effective connectivity between the regions that identified by HPM-ICA. The linear discriminant analysis was finally used to distinguish GAD from controls with these measures of neural connectivity. The GAD patients showed stronger functional connectivity in amygdala, insula, putamen, thalamus, and posterior cingulate cortex, but weaker in frontal and temporal cortex compared with controls. Besides, the effective connectivity in GAD was decreased from the cortex to amygdala and basal ganglia. Applying the ICA and GC features to the classifier led to a classification accuracy of 87.5%, with a sensitivity of 90.0% and a specificity of 85.0%. These findings suggest that the presence of emotion dysregulation circuits may contribute to the pathophysiology of GAD, and these aberrant brain features may serve as robust brain biomarkers for GAD.

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Approximately 20-30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms that underlie why some patients are responsive and others prove resistant to antiepileptic drugs are poorly understood. Increasing evidence supports a role for altered mitochondrial function in the pathogenesis of epilepsy. To gain greater molecular insight in the pathogenesis of intractable epilepsy, we undertook a global analysis of protein expressions in a pharmacoresistant epileptic model selected by phenytoin in electrical amygdala-kindled rats by using two-dimensional gel electrophoresis coupled with matrix-assisted laser desorption/ionization time of flight (MALDI-TOF-TOF). We identified five increased proteins and 14 decreased proteins including voltage-dependent anion channel 1 (VDAC1) with a 2.82-fold increased level (P < 0.05) and voltage-dependent anion channel 2 (VDAC2) with a 3.97-fold decreased level (P < 0.05) in hippocampus of pharmacoresistant rats. The increased VDAC1 and decreased VDAC2 were confirmed by Western blot analysis and immunohistochemistry. Vascular mitochondria and apoptosis neurons were observed through electron microscopy. Energy contents, the adenine nucleotides, were measured by high-performance liquid chromatography (HPLC). The correlation analyses were carried out between VDAC and the energy charge. These findings indicate that the increase of VDAC1 and the decrease of VDAC2 play an important role during the process and provide new molecular evidence in understanding mechanism of refractory epilepsy.

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Objective To study the protective effect and mechanism of Shuxuetong on gerbil brain tissue from the area of ischemia-reperfusion. Methods Cerebral ischemia-reperfusion animal model has made by transient clipping bilateral common carotid arteries in gerbils. Pathological changes in the hippocampal tissue were observed at different reperfusion time (12h, 3 d, 7 d). The expression levels of GABA and TNF-alpha in the hippocampal CA1 subfield were observed using immunohistochemitry at 12 h, 3 d after reperfusion. The difference of above indices among false operation group, ischemia-reperfusion group and treatment group were compared. Results The injuries of pathology to hippocampal area in ischemia reperfusion group were more serious than treatment group. The expression levels of GABA in treatment group were significantly increased compared with ischemia-reperfusion group, but the expression levels of TNF-alpha between the two groups have no difference. Conclusion Shuxuetong has protective effect on brain tissue of ischemia-reperfusion by enhancing the expression of GABA in the hippocampal tissue.

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OBJECTIVE: To investigate the safety and effect of injecting heparin into hematoma on peri-hematoma edema and hematoma volume in pigs with intracerebral hemorrhage (ICH). METHODS: Thirteen sucking pigs were divided randomly into two groups: hemorrhage group, in which 2.5 ml arterial blood was injected into the right frontal lobe and heparin group, in which 0.2 ml of heparin was injected into the hematoma produced by the injection of 2.3 ml of blood into the similar site. The hematoma volume and peri-hematoma edema were determined by the sequences of T2* weighted image (T2*WI), fluid-attenuated inversion- recovery (FLAIR) image and diffusion weighted image (DWI) by 1.5 T magnetic resonance image (MRI) from 30-60 minutes afterwards to 24 hours. The peri-hematoma apparent diffusion coefficient (ADC) was compared with that of contralateral hemisphere, and the corresponding histologic changes were studied. RESULTS: The average volume, shown by T2*WI at 24 hours, was significantly larger than that at 30-60 minutes after hematoma formation in hemorrhagic group [(5.29+/-0.98) cm3 vs. (3.09+/-0.38) cm3, P<0.01]. But there was no significant change in hematoma volume in hemorrhagic group from 30-60 minutes on to 24 hours [(2.21+/-0.28) cm3 vs. (2.33+/-0.30) cm3, P>0.05]. Both increased and decreased ADC were found around the hematoma in some animals of the heparin group compared with that of the contralateral hemisphere. On the other hand, in hemorrhagic group, only increased ADC could be found around the lesion, and there was no decreased ADC. CONCLUSION: Injection of heparin into an intracerebral hematoma leads to enlargement of the hematoma and more marked peri-lesion edema. On ADC maps, enlargement of hematoma is attributed to the edema around the lesion leading to injury to the brain tissue.

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