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  • 1
    Online-Ressource
    Online-Ressource
    Novel Susceptibility Loci for Moyamoya Disease Revealed by a Genome-Wide Association Study
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Stroke Vol. 49, No. 1 ( 2018-01), p. 11-18
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 49, No. 1 ( 2018-01), p. 11-18
    Kurzfassung: Moyamoya disease (MMD) is a rare cerebral vasculopathy characterized by bilateral internal carotid artery stenosis and often leads to stroke in children or young adults. Although familial inheritance is well recognized, the genetic basis of MMD remains poorly understood. Methods— A 2-stage genome-wide association study was conducted involving 1492 cases and 5084 controls. In the discovery stage, logistic regression was used to test associations, and imputation was conducted based on genotyped single-nucleotide polymorphisms (SNPs). In the validation stage, the top significant SNPs were again genotyped in an independent cohort. Fixed-effects inverse variance-weighted meta-analysis was used in the combined discovery and validation samples. Furthermore, association analysis was conducted in subgroups using patient clinical data. Results— The study identified 10 novel risk loci with genome-wide significance ( P 〈 5×10 −8 ) and confirmed a previously reported locus on 17q25. No significant SNP showed evidence of heterogeneity between the 2 stages. Cumulatively, these SNPs explained 14.76% of disease risk variance—a substantial proportion of the 39.02% of risk variance explained by all genome-wide genotyped SNPs. One SNP, rs9916351 in RNF213 ( P combined =4.57×10 −54 ; odds ratio, 1.96), showed a stronger genetic effect on early-onset than late-onset MMD ( P =0.003). Two novel SNPs in genes regulating homocysteine metabolism, rs9651118 in MTHFR ( P combined =2.49×10 −19 ; odds ratio, 0.65) and rs117353193 in TCN2 ( P combined =6.15×10 −13 ; odds ratio, 1.43), were associated with high-serum homocysteine in MMD cases. Additionally, another SNP associated with MMD (rs2107595 in HDAC9 ; P combined =1.49×10 −29 ; odds ratio, 1.64) was previously implicated in large-vessel disease. Tissue enrichment analysis showed that the genes of associated loci were highly expressed in the immune system (false discovery rate, 〈 0.05). Conclusions— This study identifies several novel susceptibility genes for MMD. The association with homocysteine metabolism and the immune system enrichment of susceptibility gene expression suggest that therapeutic interventions targeting these pathways may be effective approaches for MMD treatment.
    Materialart: Online-Ressource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.117.017430
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2018
    ZDB Id: 1467823-8
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    Spiroplasma eriocheiris Enters Drosophila Schneider 2 Cells and Relies on Clathrin-Mediated Endocytosis and Macropinocytosis
    American Society for Microbiology ; 2019
    In:  Infection and Immunity Vol. 87, No. 11 ( 2019-11)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 87, No. 11 ( 2019-11)
    Kurzfassung: Spiroplasma eriocheiris causes great economic losses in the crustacean aquaculture industry. However, the mechanism of S. eriocheiris infecting host cells has been poorly studied. We established a Spiroplasma -infected Drosophila Schneider 2 (S2) cell model and investigated its pathogenic mechanism. First, S. eriocheiris induced S2 cell apoptosis and necrosis, seriously decreased cell viability, and increased the production of intracellular reactive oxygen species. Further research showed that S. eriocheiris can invade S2 cells, and the number of copies of intracellular spiroplasmas is sharply increased by 12 h postinfection. In addition, S. eriocheiris can cause S2 cells to form typical inclusion bodies and exhibit large vacuoles. Second, S. eriocheiris is internalized into S2 cells and strongly inhibited through blocking clathrin-mediated endocytosis using chlorpromazine and dynasore. Inhibitors of macropinocytosis, protein kinase C and myosin II, cause a significant reduction in S. eriocheiris in S2 cells. In contrast, disruption of cellular cholesterol by methyl-β-cyclodextrin and nystatin has no effect on S. eriocheiris infection. These results suggest that the entry of S. eriocheiris into S2 cells relies on clathrin-dependent endocytosis and macropinocytosis, but not via the caveola-mediated endocytic pathway. In addition, the intracellular numbers of S. eriocheiris are dramatically reduced after S2 cells are treated with cytoskeleton-depolymerizing agents, including nocodazole and cytochalasin B. Thus, cellular infection by S. eriocheiris is related to microtubules and actin filaments. This research successfully shows for the first time that S. eriocheiris can invade Drosophila S2 cells and provides a process for S. eriocheiris infection.
    Materialart: Online-Ressource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00233-19
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2019
    ZDB Id: 1483247-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    A blood flow–dependent klf2a-NO signaling cascade is required for stabilization of hematopoietic stem cell programming in zebrafish embryos
    American Society of Hematology ; 2011
    In:  Blood Vol. 118, No. 15 ( 2011-10-13), p. 4102-4110
    Details
    In: Blood, American Society of Hematology, Vol. 118, No. 15 ( 2011-10-13), p. 4102-4110
    Kurzfassung: Blood flow has long been thought to be important for vessel development and function, but its role in HSC development is not yet fully understood. Here, we take advantage of zebrafish embryos with circulation defects that retain relatively normal early development to illustrate the combinatorial roles of genetic and hemodynamic forces in HSC development. We show that blood flow is not required for initiation of HSC gene expression, but instead is indispensable for its maintenance. Knockdown of klf2a mimics the silent heart (sih/tnnt2a) phenotype while overexpression of klf2a in tnnt2a morphant embryos can rescue HSC defects, suggesting that klf2a is a downstream mediator of blood flow. Furthermore, the expression of NO synthase (nos) was reduced in klf2a knockdown embryos, and ChIP analysis showed that endogenous Klf2a is bound to the promoters of nos genes in vivo, indicating direct gene regulation. Finally, administration of the NO agonist S-nitroso N-acetylpenicillamine (SNAP) can restore HSC development in tnnt2a and klf2a morphants, suggesting that NO signaling is downstream of Klf2a which is induced by hemodynamic forces. Taken together, we have demonstrated that blood flow is essential for HSC development and is mediated by a klf2a-NO signaling cascade in zebrafish.
    Materialart: Online-Ressource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2011-05-353235
    RVK:
    XA 33000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Society of Hematology
    Publikationsdatum: 2011
    ZDB Id: 1468538-3
    ZDB Id: 80069-7
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    Impact of shoulder subluxation on peripheral nerve conduction and function of hemiplegic upper extremity in stroke patients: A retrospective, matched-pair study
    Informa UK Limited ; 2021
    In:  Neurological Research Vol. 43, No. 6 ( 2021-06-03), p. 511-519
    Details
    In: Neurological Research, Informa UK Limited, Vol. 43, No. 6 ( 2021-06-03), p. 511-519
    Materialart: Online-Ressource
    ISSN: 0161-6412 , 1743-1328
    URL: Article
    DOI: 10.1080/01616412.2020.1870360
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Informa UK Limited
    Publikationsdatum: 2021
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    Distinct Interactions of EBP1 Isoforms with FBXW7 Elicits Different Functions in Cancer
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 8 ( 2017-04-15), p. 1983-1996
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 8 ( 2017-04-15), p. 1983-1996
    Kurzfassung: The ErbB3 receptor–binding protein EBP1 encodes two alternatively spliced isoforms P48 and P42. While there is evidence of differential roles for these isoforms in tumorigenesis, little is known about their underlying mechanisms. Here, we demonstrate that EBP1 isoforms interact with the SCF-type ubiquitin ligase FBXW7 in distinct ways to exert opposing roles in tumorigenesis. EBP1 P48 bound to the WD domain of FBXW7 as an oncogenic substrate of FBXW7. EBP1 P48 binding sequestered FBXW7α to the cytosol, modulating its role in protein degradation and attenuating its tumor suppressor function. In contrast, EBP1 P42 bound to both the F-box domain of FBXW7 as well as FBXW7 substrates. This adapter function of EBP1 P42 stabilized the interaction of FBXW7 with its substrates and promoted FBXW7-mediated degradation of oncogenic targets, enhancing its overall tumor-suppressing function. Overall, our results establish distinct physical and functional interactions between FBXW7 and EBP1 isoforms, which yield their mechanistically unique isoform-specific functions of EBP1 in cancer. Cancer Res; 77(8); 1983–96. ©2017 AACR.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-16-2246
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2017
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    Abstract 249: Mir-211 Regulates Bone Marrow Mesenchymal Stem Cells Migration Through Stat5a
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Research Vol. 115, No. suppl_1 ( 2014-07-18)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 115, No. suppl_1 ( 2014-07-18)
    Kurzfassung: Background: Efficacy of intravenous mesenchymal stem cells (MSCs) administration for myocardial infarction (MI) is limited by low cell migration to the damaged myocardium. Our previous study demostrated that migration ability of MSCs enhanced by hypoxia preconditioning (HPC). miRNA microarray displayed that miR-211 exhibited most significant change between HPC and normoxia cultured MSCs. The aim of this study is to study whether and how miR-211 regulate MSCs migration. Methods: In vitro, transwell assay were used to assess the migration ability of MSC moduated by miR-211 using overexpressing and knockdown lentivirus. The target gene of miR-211 predicted by Targetscan were verified by PCR, western blot and lucifurase assay. Chromatin immunoprecitation (ChiP) were used to explore the transcription factors that regulate the expression of miR-211. To evaluate the effect of miR-211 on MSCs migration in vivo, miR-211-mimic and miR-211-shRNA male MSCs were intravenously delivered 24h after MI, the engraft cells were detected by RT-PCR of SRY gene. Results: Quatitative RT-PCR showed that miR-211 expression of MSCs upregulated by HPC. MiR-211 mimic improved MSCs migration by 31.03% (p 〈 0.05), however, knockdown miR-211 using shRNA attenuated MSCs migration ability significantly. Signal transducer and activator of transcription 5A (STAT5A) was predicted as one of miR-211 target genes, PCR and Western blot showed miR-211 overexpression dramatically decreased STAT5A expression, while miR-211 knockdown upregulated STAT5A. The luciferase assay showed the similar results. Transwell assay showed that STAT5A knockdown reverse the inhibition of MSCs migration induced by miR-211-shRNA. Intrestingly, ChiP assay showed that STAT5A can combine to the promoter of miR-211, which lead to the regulation of miR-211 transcription. In vivo data showed that MiR-211 overexpression enhanced MSCs homing to ischemic myocardium, and miR-211 overexprssing MSCs improved cardiac function 28days post-MI. However, miR-211 knockdown decreased MSCs homing and hampered cardiac function recovery. Conclusions: These results indicate that miR-211 has important role in regulating MSCs migration through targeting STAT5A, meanwhile STAT5A regulated miR-211 transcription.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.115.suppl_1.249
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2014
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    DISPARITIES IN HYPERTENSION PREVALENCE, AWARENESS, TREATMENT, CONTROL, AND ASSOCIATED FACTORS BETWEEN TUJIA AND HAN ETHNIC IN SOUTHWEST CHINA
    Elsevier BV ; 2019
    In:  Journal of the American College of Cardiology Vol. 73, No. 9 ( 2019-03), p. 1859-
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 73, No. 9 ( 2019-03), p. 1859-
    Materialart: Online-Ressource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(19)32465-9
    RVK:
    XA 17760
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2019
    ZDB Id: 1468327-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Online-Ressource
    Online-Ressource
    Aberrant Expansion and Function of Follicular Helper T Cell Subsets in IgG4‐Related Disease
    Wiley ; 2018
    In:  Arthritis & Rheumatology Vol. 70, No. 11 ( 2018-11), p. 1853-1865
    Details
    In: Arthritis & Rheumatology, Wiley, Vol. 70, No. 11 ( 2018-11), p. 1853-1865
    Kurzfassung: To determine the number and function of follicular helper T (Tfh) cell subsets in IgG4‐related disease (IgG4‐ RD ). Methods Mononuclear cells from the peripheral blood and involved tissue of patients with IgG4‐ RD were assessed for Tfh cells and their subsets, and levels of B cell lymphoma 6 (Bcl‐6), B lymphocyte–induced maturation protein 1 ( BLIMP ‐1), and interleukin‐21 ( IL ‐21) messenger RNA ( mRNA ). Immunohistochemical and immunofluorescence techniques were used to assess the involved tissue of patients to determine the location of IL ‐21, Bcl‐6, and CD 4+ CXCR 5+ Tfh cells. Furthermore, the ability of circulating Tfh ( cT fh) cell subsets to induce B cell proliferation, apoptosis, and differentiation and to produce IgG4 was explored in cell cocultures in vitro. Results Frequencies of cT fh cells were significantly increased in the peripheral blood of patients with IgG4‐ RD , and even higher frequencies were observed in the involved tissue. Percentages of programmed cell death protein 1 in CD 4+ CXCR 5+ ICOS + cT fh cells were positively correlated with the serum levels of IgG and IgG4, IgG4:IgG ratio, number of involved organs, and frequency of CD 19+ CD 24− CD 38 high plasmablasts/plasma cells. Levels of BLIMP ‐1 and IL ‐21 mRNA in peripheral CD 4+ T cells were increased in patients with IgG4‐ RD compared to healthy controls, and this was correlated with the levels of serum IgG4. Moreover, in the involved tissue, Bcl‐6, IL ‐21, and Tfh cells were highly expressed. Compared to cT fh cells from healthy controls, cT fh cells from patients with IgG4‐ RD could facilitate B cell proliferation and inhibit B cell apoptosis more efficiently, and enhanced the differentiation of naive B cells into switched memory B cells and plasmablasts/plasma cells, with a resultant increase in the secretion of IgG4. Notably, the cTfh1 and cTfh2 cell subsets were the most effective at providing B cell help. Conclusion Tfh cell subsets are expanded in IgG4‐ RD and may play pivotal roles in the pathogenesis of the disease.
    Materialart: Online-Ressource
    ISSN: 2326-5191 , 2326-5205
    URL: Issue
    URL: Article
    DOI: 10.1002/art.2018.70.issue-11
    DOI: 10.1002/art.40556
    RVK:
    XA 10000
    RVK:
    XA 30325
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2018
    ZDB Id: 2754614-7
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Online-Ressource
    Online-Ressource
    Proteomic analyses of plasma-derived exosomes in immunoglobulin (Ig) G4-related disease and their potential roles in B cell differentiation and tissue damage
    Elsevier BV ; 2021
    In:  Journal of Autoimmunity Vol. 122 ( 2021-08), p. 102650-
    Details
    In: Journal of Autoimmunity, Elsevier BV, Vol. 122 ( 2021-08), p. 102650-
    Materialart: Online-Ressource
    ISSN: 0896-8411
    URL: Article
    DOI: 10.1016/j.jaut.2021.102650
    RVK:
    XA 52099
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2021
    ZDB Id: 1468989-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
    Online-Ressource
    Online-Ressource
    3D-printed vertebral body for anterior spinal reconstruction in patients with thoracolumbar spinal tumors
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2022
    In:  Journal of Neurosurgery: Spine Vol. 37, No. 2 ( 2022-08-01), p. 274-282
    Details
    In: Journal of Neurosurgery: Spine, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 37, No. 2 ( 2022-08-01), p. 274-282
    Kurzfassung: A 3D-printed vertebral prosthesis can be used to reconstruct a bone defect more precisely because of its tailored shape, with its innermost porous structure inducing bone ingrowth. The aim of this study was to evaluate the clinical outcomes of using a 3D-printed artificial vertebral body for spinal reconstruction after en bloc resection of thoracolumbar tumors. METHODS This was a retrospective analysis of 23 consecutive patients who underwent surgical treatment for thoracolumbar tumors at our hospital. En bloc resection was performed in all cases, based on the Weinstein-Boriani-Biagini surgical staging system, and anterior reconstruction was performed using a 3D-printed artificial vertebral body. Prosthesis subsidence, fusion status, and instrumentation-related complications were evaluated. Stability of the anterior reconstruction method was evaluated by CT, and CT Hounsfield unit (HU) values were measured to evaluate fusion status. RESULTS The median follow-up was 37 (range 24–58) months. A customized 3D-printed artificial vertebral body was used in 10 patients, with an off-the-shelf 3D-printed artificial vertebral body used in the other 13 patients. The artificial vertebral body was implanted anteriorly in 5 patients and posteriorly in 18 patients. The overall fusion rate was 87.0%. The average prosthesis subsidence at the final follow-up was 1.60 ± 1.79 mm. Instrument failure occurred in 2 patients, both of whom had substantial subsidence (8.47 and 3.69 mm, respectively). At 3 months, 6 months, and 1 year postoperatively, the mean CT HU values within the artificial vertebral body were 1930 ± 294, 1997 ± 336, and 1994 ± 257, respectively, with each of these values being significantly higher than the immediate postoperative value of 1744 ± 321 (p 〈 0.05). CONCLUSIONS The use of a 3D-printed artificial vertebral body for anterior reconstruction after en bloc resection of the thoracolumbar spinal tumor may be a feasible and reliable option. The low incidence of prosthesis subsidence of 3D-printed endoprostheses can provide good stability instantly. Measurement of HU values with CT is a valuable method to evaluate the osseointegration at the bone-metal interface of a 3D-printed vertebral prosthesis.
    Materialart: Online-Ressource
    ISSN: 1547-5654
    URL: Article
    DOI: 10.3171/2022.1.SPINE21900
    RVK:
    XA 55270.1
    Sprache: Unbekannt
    Verlag: Journal of Neurosurgery Publishing Group (JNSPG)
    Publikationsdatum: 2022
    Standort Signatur Einschränkungen Verfügbarkeit
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