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Institution

Capital Medical University

EducationBeijing, China
About: Capital Medical University is a education organization based out in Beijing, China. It is known for research contribution in the topics: Population & Medicine. The organization has 56150 authors who have published 47290 publications receiving 811249 citations.


Papers
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Journal ArticleDOI
TL;DR: The findings suggest that early deprivation of a single sensory modality induces alterations of functional connectivity between the deprived functional area and other associated brain areas.
Abstract: In early blindness, the primary visual area (PVA) loses the ability to process visual information, and shifts to working on the processing of somatosensory input, auditory input, and some higher-level cognitive functions. It has not yet been investigated whether such functional changes can lead to alterations of the functional connectivity between the PVA and other brain areas in resting state. The purpose of this study is to investigate the differences in the functional connectivity of the PVA between early blind and sighted subjects using resting functional MRI data. The altered functional connectivity was identified by comparing the correlation coefficients of the PVA with other brain areas between 16 early blind subjects (blindness onset within 1 year of age) and 32 gender- and age-matched healthy sighted volunteers. Compared with the sighted, the early blind subjects showed decreased functional connectivity between the left PVA and the bilateral supplementary motor area (SMA), pre- and postcentral gyri, superior parietal lobule, and the left superior and middle temporal gyri. Early blind subjects also showed decreased functional connectivity between the right PVA and the bilateral SMA, pre- and postcentral gyri. Our findings suggest that early deprivation of a single sensory modality induces alterations of functional connectivity between the deprived functional area and other associated brain areas.

128 citations

Journal Article
TL;DR: The use of dual antiplatelet therapy for a period longer than 12 months in patients who had received zotarolimus-eluting stents was not significantly more effective than aspirin monotherapy in reducing adverse cardiac or cerebrovascular event.
Abstract: Objective:To evaluate the potential benefit of prolonging 12-month dual antiplatelet therapy among patients with coronary artery disease receiving zotarolimus-eluting stents.Methods:From Sep.2006 to Jue.2009,patients with coronary artery disease undergoing PCI with zotarolimus-eluting stents in the cardiology department of Beijing Anzhen Hospital were enrolled.Our clinical endpoint focused on major adverse cardiac or cerebrovascular events(MACCE),death,nonfatal myocardial infarction(MI),stroke,and repeat revascularization.Follow up was carried out by telephone or outpatient interview.To overcome the defect of non-randomized comparisons,multivariable Cox proportional-hazards regression was carried out to adjust for potential confounding factors.Results:The average follow-up was(28.4±7.4) months.A toal of 915 appropriate patients were divided to two groups: 12-month DAPT group(362) and 12-month DAPT group(553).Rates of MACCE(3.6% VS.4.3%,P=0.87) and TVR(2.2% VS.2.5%,P=0.97) did not differ between 12-month DAPT group and 12-month DAPT group.After adjusted by the multivariable Cox proportional-hazards regression,still no significant differences of the endpoints mentioned above were observed between the two groups.Rates of death MI or stroke were not significantly different between the two groups either.Conclusion:The use of dual antiplatelet therapy for a period longer than 12 months in patients who had received zotarolimus-eluting stents was not significantly more effective than aspirin monotherapy in reducing adverse cardiac or cerebrovascular event.

128 citations

Journal ArticleDOI
TL;DR: Peripapillary RNFL vascular microcirculation measured as blood flux index by OMAG showed significant differences among OAG, glaucoma suspect, and normal controls and was significantly correlated with functional and structural defects.
Abstract: Purpose To investigate the vascular microcirculation changes in the retinal nerve fiber layer (RNFL) in normal, glaucoma suspect, and open-angle glaucoma (OAG) groups using optical coherence tomography-based microangiography (OMAG). Methods One eye from each subject was scanned with a Cirrus HD-OCT 5000-based OMAG prototype system montage scanning protocol centered at the optic nerve head (ONH). Blood flow signals were extracted using OMAG algorithm. Retinal nerve fiber layer vascular microcirculation was measured by calculating the blood flux index and vessel area density within a 1.2-mm width annulus centered at the ONH with exclusion of big retinal vessels. One-way ANOVA were performed to analyze the RNFL microcirculation among groups. Linear-regression models were constructed to analyze the correlation between RNFL microcirculation and clinical parameters. Discrimination capabilities of the flow metrics were assessed with the area under the receiver operating characteristic curve (AROC). Results Twenty normal, 26 glaucoma suspect, and 42 OAG subjects were enrolled. Eyes from OAG subjects and glaucoma suspects showed significantly lower blood flux index compared with normal eyes (P ≤ 0.0015). Retinal nerve fiber layer blood flow metrics showed significant correlations with visual field indices and structural changes in glaucomatous eyes (P ≤ 0.0123). Similar discrimination capability of blood flux index compared with RNFL thickness was found in both disease groups. Conclusions Peripapillary RNFL vascular microcirculation measured as blood flux index by OMAG showed significant differences among OAG, glaucoma suspect, and normal controls and was significantly correlated with functional and structural defects. Retinal nerve fiber layer microcirculation measurement using OMAG may help physicians monitor glaucoma.

128 citations

Journal ArticleDOI
TL;DR: It is shown that targeted disruption of PTEN leads to neoplastic transformation of human neural stem cells (NSCs), but not mesenchymal stem cells, and a cellular platform is established to identify factors involved in NSC transformation, potentially permitting personalized treatment of glioblastoma.
Abstract: PTEN is a tumour suppressor frequently mutated in many types of cancers. Here we show that targeted disruption of PTEN leads to neoplastic transformation of human neural stem cells (NSCs), but not mesenchymal stem cells. PTEN-deficient NSCs display neoplasm-associated metabolic and gene expression profiles and generate intracranial tumours in immunodeficient mice. PTEN is localized to the nucleus in NSCs, binds to the PAX7 promoter through association with cAMP responsive element binding protein 1 (CREB)/CREB binding protein (CBP) and inhibits PAX7 transcription. PTEN deficiency leads to the upregulation of PAX7, which in turn promotes oncogenic transformation of NSCs and instates 'aggressiveness' in human glioblastoma stem cells. In a large clinical database, we find increased PAX7 levels in PTEN-deficient glioblastoma. Furthermore, we identify that mitomycin C selectively triggers apoptosis in NSCs with PTEN deficiency. Together, we uncover a potential mechanism of how PTEN safeguards NSCs, and establish a cellular platform to identify factors involved in NSC transformation, potentially permitting personalized treatment of glioblastoma.

128 citations

Journal ArticleDOI
01 Nov 2013-Glia
TL;DR: The data suggest that by targeting a pro‐apoptotic BCL2 family member, increasing levels of miR‐29a might emerge as a strategy for protection against ischemia‐reperfusion injury.
Abstract: Following transient forebrain ischemia, astrocytes play a key role in determining whether or not neurons in the hippocampal CA1 sector go on to die in a delayed fashion. MicroRNAs (miRNAs) are a novel class of RNAs that control gene expression at the post-transcriptional level and the miR-29 family is highly expressed in astrocytes. In this study we assessed levels of miR-29 in hippocampus following forebrain ischemia and found that after transient forebrain ischemia and short periods of reperfusion, miR-29a significantly increased in the resistant dentate gyrus, but decreased in the vulnerable CA1 region of the hippocampus. We demonstrate that miR-29a targets BH3-only proapoptotic BCL2 family member PUMA by luciferase reporter assay and by Western blot. Comparing primary neuron and astrocyte cultures, and postnatal brain, we verified the strongly astrocytic expression of miR-29a. We further found that miR-29a mimic protects and miR-29a inhibitor aggravates cell injury and mitochondrial function after ischemia-like stresses in vitro. Lastly, by overexpressing and reducing miR-29a we demonstrate the protective effect of miR-29a on CA1 delayed neuronal death after forebrain ischemia. Our data suggest that by targeting a pro-apoptotic BCL2 family member, increasing levels of miR-29a might emerge as a strategy for protection against ischemia-reperfusion injury.

128 citations


Authors

Showing all 56323 results

NameH-indexPapersCitations
Yang Yang1712644153049
Hua Zhang1631503116769
Matthias Egger152901184176
Jost B. Jonas1321158166510
Shuai Liu129109580823
Yang Liu1292506122380
Chao Zhang127311984711
Michael Wang117142856282
Wei Lu111197361911
Yan Zhang107241057758
Claus Bachert10684249557
Nan Lin10568754545
Banglin Chen10539355287
Ming Li103166962672
George F. Gao10279382219
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202379
2022296
20217,328
20206,584
20195,064
20184,202