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  • 1
    Publication Date: 2018-05-25
    Description: Primary liver tumors and liver metastasis currently represent the leading cause of cancer-related death. Commensal bacteria are important regulators of antitumor immunity, and although the liver is exposed to gut bacteria, their role in antitumor surveillance of liver tumors is poorly understood. We found that altering commensal gut bacteria in mice induced a liver-selective antitumor effect, with an increase of hepatic CXCR6 + natural killer T (NKT) cells and heightened interferon- production upon antigen stimulation. In vivo functional studies showed that NKT cells mediated liver-selective tumor inhibition. NKT cell accumulation was regulated by CXCL16 expression of liver sinusoidal endothelial cells, which was controlled by gut microbiome-mediated primary-to-secondary bile acid conversion. Our study suggests a link between gut bacteria–controlled bile acid metabolism and liver antitumor immunosurveillance.
    Keywords: Immunology, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2018-01-03
    Description: Endothelial cells (ECs) in the tumor microenvironment have been reported to play a more active role in solid tumor growth and metastatic dissemination than simply providing the physical structure to form conduits for blood flow; however, the involvement of ECs in the process of triple-negative breast cancer (TNBC) metastasis has not been addressed. Here, we demonstrate that ECs—when mixed with TNBC cells—could increase TNBC cell metastatic potency. After treatment with TGF-β to induce endothelial–mesenchymal transition (EMT), TNBC cells could produce plasminogen activator inhibitor-1 (PAI-1) and stimulate the expression and secretion of the chemokine, CCL5, from ECs, which then acts in a paracrine fashion on TNBC cells to enhance their migration, invasion, and metastasis. CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback loop. Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 signaling via the chemokine receptor, CCR5. Of importance, key features of this pathway are manifested in patients with TNBC and in The Cancer Genome Atlas database. Taken together, our results suggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and illustrate the potential of developing new PAI-1– and CCL5-targeting therapy for patients with TNBC.—Zhang, W., Xu, J., Fang, H., Tang, L., Chen, W., Sun, Q., Zhang, Q., Yang, F., Sun, Z., Cao, L., Wang, Y., Guan, X. Endothelial cells promote triple-negative breast cancer cell metastasis via PAI-1 and CCL5 signaling.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
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  • 3
    Publication Date: 2018-11-10
    Description: Lithium (Li) metal anodes have attracted considerable interest due to their ultrahigh theoretical gravimetric capacity and very low redox potential. However, the issues of nonuniform lithium deposits (dendritic Li) during cycling are hindering the practical applications of Li metal batteries. Herein, we propose a concept of ion redistributors to eliminate dendrites by redistributing Li ions with Al-doped Li 6.75 La 3 Zr 1.75 Ta 0.25 O 12 (LLZTO) coated polypropylene (PP) separators. The LLZTO with three-dimensional ion channels can act as a redistributor to regulate the movement of Li ions, delivering a uniform Li ion distribution for dendrite-free Li deposition. The standard deviation of ion concentration beneath the LLZTO composite separator is 13 times less than that beneath the routine PP separator. A Coulombic efficiency larger than 98% over 450 cycles is achieved in a Li | Cu cell with the LLZTO-coated separator. This approach enables a high specific capacity of 140 mAh g –1 for LiFePO 4 | Li pouch cells and prolonged cycle life span of 800 hours for Li | Li pouch cells, respectively. This strategy is facile and efficient in regulating Li-ion deposition by separator modifications and is a universal method to protect alkali metal anodes in rechargeable batteries.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Kongress Medizin und Gesellschaft 2007; 20070917-20070921; Augsburg; DOC07gmds755 /20070906/
    Publication Date: 2007-09-07
    Keywords: chronic kidney disease ; prevalence ; population-based study ; systematic review ; ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
    Keywords: IN-VIVO ; MAMMALIAN-CELLS ; LIVING CELLS ; EMBRYONIC STEM-CELLS ; LYSINE-9 METHYLATION ; HP1 PROTEINS ; DNA-METHYLATION ; HISTONE H3 ; CHROMATIN-REMODELING COMPLEXES ; NUCLEOSOME MODIFICATION
    Abstract: The cell establishes heritable patterns of active and silenced chromatin via interacting factors that set, remove, and read epigenetic marks. To understand how the underlying networks operate, we have dissected transcriptional silencing in pericentric heterochromatin (PCH) of mouse fibroblasts. We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase SUV39H1/2 demarcate the PCH state. From the experimental data, we developed a predictive mathematical model that explains how chromatin-bound SUV39H1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated histone H3 lysine 9 trimethylation levels via chromatin dynamics. This "nucleation and looping" mechanism is particularly robust toward transient perturbations and stably maintains the PCH state. These features make it an attractive model for establishing functional epigenetic domains throughout the genome based on the localized immobilization of chromatin-modifying enzymes.
    Type of Publication: Journal article published
    PubMed ID: 25134515
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  • 6
    Abstract: OBJECTIVE: Chronic kidney disease (CKD) increases risk of coronary heart disease (CHD), but the impact of using different equations for estimating kidney function on CHD is not clear yet. This study described the prognostic value of CKD as defined by various creatinine- (Cr-eGFR) and cystatin C-based estimating (Cys-eGFR) equations and their combinations on subsequent cardiovascular disease (CVD) events in patients with CHD. DESIGN: Cohort study. SETTING: Patients with coronary heart disease in in-patient rehabilitation and long-term follow-up (mean 63.4 months). SUBJECTS: 1050 patients with coronary heart disease aged 30-70 years at baseline. METHODS: CKD was defined as eGFR〈60mL/min/1.73m(2) (CKD stages 3-5) estimated by three Cr-eGFR equations (Cockroft-Gault equation adjusted for body surface area (CG/BSA), Modification of Diet in Renal Disease Study (MDRD) equation, CKD-EPIcrea) and by two Cys-eGFR equations (Arnal-Dade equation, CKD-EPIcys) and a combination. The primary endpoint of our study was subsequent CVD events. RESULTS: During follow-up 118 patients (11.2%) experienced the outcome of our study. CKD assessed by the CG/BSA, MDRD, and CKD-EPIcrea equations showed no statistically significant association with subsequent CVD events after adjustment for multiple covariates (hazard ratio (HR) 1.45 [95% CI, 0.81-2.59], HR 1.47 [95% CI, 0.84-2.60], and HR 1.31 [95% CI, 0.72-2.83], respectively). By contrast, the Cys-eGFR equations were much stronger associated with subsequent CVD endpoints (Arnal-Dade: HR, 2.01 [95% CI, 1.34-3.04]; CKD-EPIcys HR, 2.22 [95% CI, 1.46-3.37]). The CKD-EPIcys also provided the highest area under the curve value. CONCLUSION: Our study shows that prevalent CKD is an independent risk factor for subsequent CVD in patients with prevalent CHD and implies that Cys-eGFR equations show a better clinical utility compared to the Cr-eGFR equations. Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
    Type of Publication: Journal article published
    PubMed ID: 20347445
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  • 7
    Abstract: Purpose: Elevated levels of neutrophils have been associated with poor survival in various cancers, but direct evidence supporting a role for neutrophils in the immunopathogenesis of human cancers is lacking.Experimental Design: A total of 573 patients with gastric cancer were enrolled in this study. Immunohistochemistry and real-time PCR were performed to analyze the distribution and clinical relevance of neutrophils in different microanatomic regions. The regulation and function of neutrophils were assessed both in vitro and in vivoResults: Increased neutrophil counts in the peripheral blood were associated with poor prognosis in gastric cancer patients. In gastric cancer tissues, neutrophils were enriched predominantly in the invasive margin, and neutrophil levels were a powerful predictor of poor survival in patients with gastric cancer. IL17+ neutrophils constitute a large portion of IL17-producing cells in human gastric cancer. Proinflammatory IL17 is a critical mediator of the recruitment of neutrophils into the invasive margin by CXC chemokines. Moreover, neutrophils at the invasive margin were a major source of matrix metalloproteinase-9, a secreted protein that stimulates proangiogenic activity in gastric cancer cells. Accordingly, high levels of infiltrated neutrophils at the invasive margin were positively correlated with angiogenesis progression in patients with gastric cancer.Conclusions: These data provide direct evidence supporting the pivotal role of neutrophils in gastric cancer progression and reveal a novel immune escape mechanism involving fine-tuned collaborative action between cancer cells and immune cells in the distinct tumor microenvironment. Clin Cancer Res; 23(6); 1575-85. (c)2016 AACR.
    Type of Publication: Journal article published
    PubMed ID: 27620275
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  • 8
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017); 20171024-20171027; Berlin; DOCPO30-1136 /20171023/
    Publication Date: 2017-10-23
    Keywords: Legg-Calve-Perthes disease ; Scottish rite brace treatment ; classification ; Waldenström ; intervention time ; ddc: 610
    Language: English
    Type: conferenceObject
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  • 9
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017); 20171024-20171027; Berlin; DOCIN13-1242 /20171023/
    Publication Date: 2017-10-23
    Keywords: core decompression ; fibular graft ; osteonecrosis ; MHHS ; ARCO ; ddc: 610
    Language: English
    Type: conferenceObject
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  • 10
    Keywords: CELL ; Germany ; GENE ; PROTEIN ; PROTEINS ; PATIENT ; COMPLEX ; COMPLEXES ; MECHANISM ; FAMILY ; primary ; mechanisms ; SIGNAL ; TRANSPORT ; MUTANT ; MUTATIONS ; FAMILIES ; ASSEMBLIES ; assembly ; DEFECTS ; POWER ; LOSSES ; cilia ; SIGNALS ; MOTILITY ; ENGLAND ; ORYZIAS-LATIPES ; ORGANELLES ; CELL MOTILITY ; POLYCYSTIC KIDNEY-DISEASE ; ARM ; ORGANELLE ; ARM DYNEIN ; CHLAMYDOMONAS-REINHARDTII ; FLUID-FLOW ; KUPFFERS VESICLE ; MEDAKA ; PRIMARY CILIARY DYSKINESIA
    Abstract: Cilia and flagella are highly conserved organelles that have diverse roles in cell motility and sensing extracellular signals. Motility defects in cilia and flagella often result in primary ciliary dyskinesia. However, the mechanisms underlying cilia formation and function, and in particular the cytoplasmic assembly of dyneins that power ciliary motility, are only poorly understood. Here we report a new gene, kintoun ( ktu), involved in this cytoplasmic process. This gene was first identified in a medaka mutant, and found to be mutated in primary ciliary dyskinesia patients from two affected families as well as in the pf13 mutant of Chlamydomonas. In the absence of Ktu/ PF13, both outer and inner dynein arms are missing or defective in the axoneme, leading to a loss of motility. Biochemical and immunohistochemical studies show that Ktu/ PF13 is one of the long- sought proteins involved in pre- assembly of dynein arm complexes in the cytoplasm before intraflagellar transport loads them for the ciliary compartment
    Type of Publication: Journal article published
    PubMed ID: 19052621
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