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  • 1
    Online Resource
    Online Resource
    Reduced default mode network functional connectivity in patients with recurrent major depressive disorder
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 18 ( 2019-04-30), p. 9078-9083
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 18 ( 2019-04-30), p. 9078-9083
    Abstract: Major depressive disorder (MDD) is common and disabling, but its neuropathophysiology remains unclear. Most studies of functional brain networks in MDD have had limited statistical power and data analysis approaches have varied widely. The REST-meta-MDD Project of resting-state fMRI (R-fMRI) addresses these issues. Twenty-five research groups in China established the REST-meta-MDD Consortium by contributing R-fMRI data from 1,300 patients with MDD and 1,128 normal controls (NCs). Data were preprocessed locally with a standardized protocol before aggregated group analyses. We focused on functional connectivity (FC) within the default mode network (DMN), frequently reported to be increased in MDD. Instead, we found decreased DMN FC when we compared 848 patients with MDD to 794 NCs from 17 sites after data exclusion. We found FC reduction only in recurrent MDD, not in first-episode drug-naïve MDD. Decreased DMN FC was associated with medication usage but not with MDD duration. DMN FC was also positively related to symptom severity but only in recurrent MDD. Exploratory analyses also revealed alterations in FC of visual, sensory-motor, and dorsal attention networks in MDD. We confirmed the key role of DMN in MDD but found reduced rather than increased FC within the DMN. Future studies should test whether decreased DMN FC mediates response to treatment. All R-fMRI indices of data contributed by the REST-meta-MDD consortium are being shared publicly via the R-fMRI Maps Project.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1900390116
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
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    SSG: 11
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Fluorescent Proteins Expressed in Mouse Transgenic Lines Mark Subsets of Glia, Neurons, Macrophages, and Dendritic Cells for Vital Examination
    Society for Neuroscience ; 2004
    In:  The Journal of Neuroscience Vol. 24, No. 49 ( 2004-12-08), p. 10999-11009
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 24, No. 49 ( 2004-12-08), p. 10999-11009
    Abstract: To enable vital observation of glia at the neuromuscular junction, transgenic mice were generated that express proteins of the green fluorescent protein family under control of transcriptional regulatory sequences of the human S100B gene. Terminal Schwann cells were imaged repetitively in living animals of one of the transgenic lines to show that, except for extension and retraction of short processes, the glial coverings of the adult neuromuscular synapse are stable. In other lines, subsets of Schwann cells were labeled. The distribution of label suggests that Schwann cells at individual synapses are clonally related, a finding with implications for how these cells might be sorted during postnatal development. Other labeling patterns, some present in unique lines, included astrocytes, microglia, and subsets of cerebellar Bergmann glia, spinal motor neurons, macrophages, and dendritic cells. We show that lines with labeled macrophages can be used to follow the accumulation of these cells at sites of injury.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3934-04.2004
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2004
    detail.hit.zdb_id: 1475274-8
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  • 3
    Online Resource
    Online Resource
    Rehabilitative Training Interacts with Ischemia-Instigated Spine Dynamics to Promote a Lasting Population of New Synapses in Peri-Infarct Motor Cortex
    Society for Neuroscience ; 2019
    In:  The Journal of Neuroscience Vol. 39, No. 43 ( 2019-10-23), p. 8471-8483
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 39, No. 43 ( 2019-10-23), p. 8471-8483
    Abstract: After subtotal infarcts of primary motor cortex (M1), motor rehabilitative training (RT) promotes improvements in paretic forelimb function that have been linked with its promotion of structural and functional reorganization of peri-infarct cortex, but how the reorganization unfolds is scantly understood. Cortical infarcts also instigate a prolonged period of dendritic spine turnover in peri-infarct cortex. Here we investigated the possibility that synaptic structural responses to RT in peri-infarct cortex reflect, in part, interactions with ischemia-instigated spine turnover. This was tested after artery-targeted photothrombotic M1 infarcts or Sham procedures in adult (4 months) C57BL/6 male and female GFP-M line ( n = 24) and male yellow fluorescent protein-H line ( n = 5) mice undergoing RT in skilled reaching or no-training control procedures. Regardless of training condition, spine turnover was increased out to 5 weeks postinfarct relative to Sham, as was the persistence of new spines formed within a week postinfarct. However, compared with no-training controls, new spines formed during postinfarct weeks 2–4 in mice undergoing RT persisted in much greater proportions to later time points, by a magnitude that predicted behavioral improvements in the RT group. These results indicate that RT interacts with ischemia-instigated spine turnover to promote preferential stabilization of newly formed spines, which is likely to yield a new population of mature synapses in peri-infarct cortex that could contribute to cortical functional reorganization and behavioral improvement. The findings newly implicate ischemia-instigated spine turnover as a mediator of cortical synaptic structural responses to RT and newly establish the experience dependency of new spine fates in the postischemic turnover context. SIGNIFICANCE STATEMENT Motor rehabilitation, the main treatment for motor impairments after stroke, is far from sufficient to normalize function. A better understanding of neural substrates of rehabilitation-induced behavioral improvements could be useful for understanding how to optimize it. Here, we investigated the nature and time course of synaptic responses to motor rehabilitative training in vivo . Focal ischemia instigated a period of synapse turnover in peri-infarct motor cortex of mice. Rehabilitative training increased the stability of new synapses formed during the initial weeks after the infarct, the magnitude of which was correlated with improvements in skilled motor performance. Therefore, the maintenance of new synapses formed after ischemia could represent a structural mechanism of rehabilitative training efficacy.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1141-19.2019
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2019
    detail.hit.zdb_id: 1475274-8
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  • 4
    Online Resource
    Online Resource
    Spine Neck Plasticity Controls Postsynaptic Calcium Signals through Electrical Compartmentalization
    Society for Neuroscience ; 2008
    In:  The Journal of Neuroscience Vol. 28, No. 50 ( 2008-12-10), p. 13457-13466
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 28, No. 50 ( 2008-12-10), p. 13457-13466
    Abstract: Dendritic spines have been proposed to function as electrical compartments for the active processing of local synaptic signals. However, estimates of the resistance between the spine head and the parent dendrite suggest that compartmentalization is not tight enough to electrically decouple the synapse. Here we show in acute hippocampal slices that spine compartmentalization is initially very weak, but increases dramatically upon postsynaptic depolarization. Using NMDA receptors as voltage sensors, we provide evidence that spine necks not only regulate diffusional coupling between spines and dendrites, but also control local depolarization of the spine head. In spines with high-resistance necks, presynaptic activity alone was sufficient to trigger calcium influx through NMDA receptors and R-type calcium channels. We conclude that calcium influx into spines, a key trigger for synaptic plasticity, is dynamically regulated by spine neck plasticity through a process of electrical compartmentalization.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2702-08.2008
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2008
    detail.hit.zdb_id: 1475274-8
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  • 5
    Online Resource
    Online Resource
    CAG RNAs induce DNA damage and apoptosis by silencing NUDT16 expression in polyglutamine degeneration
    Proceedings of the National Academy of Sciences ; 2021
    In:  Proceedings of the National Academy of Sciences Vol. 118, No. 19 ( 2021-05-11)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 118, No. 19 ( 2021-05-11)
    Abstract: DNA damage plays a central role in the cellular pathogenesis of polyglutamine (polyQ) diseases, including Huntington’s disease (HD). In this study, we showed that the expression of untranslatable expanded CAG RNA per se induced the cellular DNA damage response pathway. By means of RNA sequencing (RNA-seq), we found that expression of the Nudix hydrolase 16 ( NUDT16 ) gene was down-regulated in mutant CAG RNA-expressing cells. The loss of NUDT16 function results in a misincorporation of damaging nucleotides into DNAs and leads to DNA damage. We showed that small CAG (sCAG) RNAs, species generated from expanded CAG transcripts, hybridize with CUG-containing NUDT16 mRNA and form a CAG-CUG RNA heteroduplex, resulting in gene silencing of NUDT16 and leading to the DNA damage and cellular apoptosis. These results were further validated using expanded CAG RNA-expressing mouse primary neurons and in vivo R6/2 HD transgenic mice. Moreover, we identified a bisamidinium compound, DB213, that interacts specifically with the major groove of the CAG RNA homoduplex and disfavors the CAG-CUG heteroduplex formation. This action subsequently mitigated RNA-induced silencing complex (RISC)-dependent NUDT16 silencing in both in vitro cell and in vivo mouse disease models. After DB213 treatment, DNA damage, apoptosis, and locomotor defects were rescued in HD mice. This work establishes NUDT16 deficiency by CAG repeat RNAs as a pathogenic mechanism of polyQ diseases and as a potential therapeutic direction for HD and other polyQ diseases.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2022940118
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2021
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Coding mutations in NUS1 contribute to Parkinson’s disease
    Proceedings of the National Academy of Sciences ; 2018
    In:  Proceedings of the National Academy of Sciences Vol. 115, No. 45 ( 2018-11-06), p. 11567-11572
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 115, No. 45 ( 2018-11-06), p. 11567-11572
    Abstract: Whole-exome sequencing has been successful in identifying genetic factors contributing to familial or sporadic Parkinson’s disease (PD). However, this approach has not been applied to explore the impact of de novo mutations on PD pathogenesis. Here, we sequenced the exomes of 39 early onset patients, their parents, and 20 unaffected siblings to investigate the effects of de novo mutations on PD. We identified 12 genes with de novo mutations ( MAD1L1 , NUP98 , PPP2CB , PKMYT1 , TRIM24 , CEP131 , CTTNBP2 , NUS1 , SMPD3 , MGRN1 , IFI35 , and RUSC2 ), which could be functionally relevant to PD pathogenesis. Further analyses of two independent case-control cohorts (1,852 patients and 1,565 controls in one cohort and 3,237 patients and 2,858 controls in the other) revealed that NUS1 harbors significantly more rare nonsynonymous variants ( P = 1.01E-5, odds ratio = 11.3) in PD patients than in controls. Functional studies in Drosophila demonstrated that the loss of NUS1 could reduce the climbing ability, dopamine level, and number of dopaminergic neurons in 30-day-old flies and could induce apoptosis in fly brain. Together, our data suggest that de novo mutations could contribute to early onset PD pathogenesis and identify NUS1 as a candidate gene for PD.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1809969115
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2018
    detail.hit.zdb_id: 209104-5
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    SSG: 11
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    The color-word Stroop effect driven by working memory maintenance
    Springer Science and Business Media LLC ; 2019
    In:  Attention, Perception, & Psychophysics Vol. 81, No. 8 ( 2019-11), p. 2722-2731
    Details
    In: Attention, Perception, & Psychophysics, Springer Science and Business Media LLC, Vol. 81, No. 8 ( 2019-11), p. 2722-2731
    Type of Medium: Online Resource
    ISSN: 1943-3921 , 1943-393X
    URL: Article
    DOI: 10.3758/s13414-019-01780-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2480891-X
    SSG: 5,2
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  • 8
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    Online Resource
    Construal level among poor children: Executive function implications
    Wiley ; 2023
    In:  British Journal of Psychology Vol. 114, No. 3 ( 2023-08), p. 638-661
    Details
    In: British Journal of Psychology, Wiley, Vol. 114, No. 3 ( 2023-08), p. 638-661
    Abstract: Poverty impedes children's executive function (EF). Therefore, it is necessary to mitigate the negative effect of poverty by developing efficient interventions to improve poor children's cognitive function. In three studies, we examined whether high‐level construals can improve EF among poor children in China. In Study 1, we observed a positive relationship between family socioeconomic status and children's EF, which was moderated by construal level ( n  = 206; M age  = 9.71; 45.6% girls). In Study 2a, we experimentally induced high‐ versus low‐level construals and found that poor children with high‐level construals exhibited better EF than those with low‐level construals ( n  = 65; M age  = 11.32; 47.7% girls). However, the same intervention did not affect the performance of affluent children in Study 2b ( n  = 63; M age  = 10.54; 54% girls). Moreover, we found that the interventional effects of high‐level construals improved the ability of children living in poverty to make healthy decisions and delayed gratification in Study 3 ( n  = 74; M age  = 11.10; 45.9% girls). These findings may have implications for using high‐level construals as an effective intervention to improve poor children's EF and cognitive capacity.
    Type of Medium: Online Resource
    ISSN: 0007-1269 , 2044-8295
    URL: Issue
    URL: Article
    DOI: 10.1111/bjop.v114.3
    DOI: 10.1111/bjop.12642
    RVK:
    CL 1000
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1493663-X
    SSG: 5,2
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  • 9
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    Online Resource
    Effects of electrodes on performance figures of thin film bulk acoustic resonators
    Acoustical Society of America (ASA) ; 2007
    In:  The Journal of the Acoustical Society of America Vol. 122, No. 3 ( 2007-09-01), p. 1646-1651
    Details
    In: The Journal of the Acoustical Society of America, Acoustical Society of America (ASA), Vol. 122, No. 3 ( 2007-09-01), p. 1646-1651
    Abstract: The effects of mechanical losses and elastic properties of the electrodes on the performance figures of a thin film bulk acoustic resonator (FBAR) are analyzed by numerical simulation. Results indicate that the material loss of the electrode has no visible effect on the characterization of the effective electromechanical coupling factor, keff2. The acoustic impedance ratio of the electrode to the piezo-film dominantly determines the behaviors of the keff2 variation with the electrode thickness. The resonance Q value, Qs, of the FBAR closely relies on the material Q values of film and of electrodes as expected. Besides, the variation of Qs versus the thickness of the electrodes crucially depends on the acoustic impedance ratio as well. Especially, three characteristic parameters, i.e., the maximum value of keff2, the sectional mass ratio of the electrode to the piezo film corresponding to the maximum keff2, and the tolerance range of the ratio to keep keff2 near the maximum, are calculated for some typical samples. These results would be useful for optimizing FBAR designs and performances.
    Type of Medium: Online Resource
    ISSN: 0001-4966 , 1520-8524
    URL: Article
    DOI: 10.1121/1.2764473
    RVK:
    EQ 1000
    Language: English
    Publisher: Acoustical Society of America (ASA)
    Publication Date: 2007
    detail.hit.zdb_id: 1461063-2
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  • 10
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    Online Resource
    RNA editing of SLC22A3 drives early tumor invasion and metastasis in familial esophageal cancer
    Proceedings of the National Academy of Sciences ; 2017
    In:  Proceedings of the National Academy of Sciences Vol. 114, No. 23 ( 2017-06-06)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 114, No. 23 ( 2017-06-06)
    Abstract: Like many complex human diseases, esophageal squamous cell carcinoma (ESCC) is known to cluster in families. Familial ESCC cases often show early onset and worse prognosis than the sporadic cases. However, the molecular genetic basis underlying the development of familial ESCC is mostly unknown. We reported that SLC22A3 is significantly down-regulated in nontumor esophageal tissues from patients with familial ESCC compared with tissues from patients with sporadic ESCCs. A-to-I RNA editing of the SLC22A3 gene results in its reduced expression in the nontumor esophageal tissues of familial ESCCs and is significantly correlated with lymph node metastasis. The RNA-editing enzyme ADAR2 , a familial ESCC susceptibility gene identified by our post hoc genome-wide association study, is positively correlated with the editing level of SLC22A3 . Moreover, functional studies showed that SLC22A3 is a metastasis suppressor in ESCC, and deregulation of SLC22A3 facilitates cell invasion and filopodia formation by reducing its direct association with α-actinin-4 (ACTN4), leading to the increased actin-binding activity of ACTN4 in normal esophageal cells. Collectively, we now show that A-to-I RNA editing of SLC22A3 contributes to the early development and progression of familial esophageal cancer in high-risk individuals.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1703178114
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2017
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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