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  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 31, No. 9 ( 2011-09), p. 2063-2069
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 9 ( 2011-09), p. 2063-2069
    Abstract: Bariatric surgery is emerging as an effective method to alleviate a multitude of medical conditions associated with morbid obesity and type 2 diabetes. However, little is known about the effects and mechanisms of bariatric surgery on visceral fat inflammation and endothelial dysfunction in type 2 diabetes. We hypothesize that bariatric surgery ameliorates interferon-γ–mediated adipose tissue inflammation/oxidative stress and improves endothelial function in type 2 diabetic mice. Methods and Results— Control mice (m Lepr db ) and diabetic mice (Lepr db ) were treated with either sham surgery or improved gastric bypass surgery and then were evaluated at 5, 10, 20, and 30 days to assess postsurgical effects. Surgery reduced body weight, abdominal adiposity, blood glucose level, and food intake in Lepr db . The surgery-induced decrease in visceral adiposity was accompanied by amelioration of T-lymphocytes and macrophage infiltration, as well as reduction in the expression of interferon-γ and other inflammatory cytokines in the mesenteric adipose tissue (MAT) of Lepr db mice. Furthermore, surgery improved endothelium-dependent, but not endothelium-independent, vasorelaxation in small mesenteric arteries (SMA) of Lepr db mice. The improvement in endothelial function was largely attenuated by nitric oxide synthase inhibitor (L-NAME) incubation. Interferon-γ treatment increased the mRNA expression of tumor necrosis factor-α in the MAT of control mice and incubation of SMA of control mice with tumor necrosis factor-α caused impairment of endothelial function. Superoxide production in MAT/SMA and nitrotyrosine protein level in SMA were elevated in diabetic mice. Surgery reduced MAT/SMA oxidative stress in Lepr db mice. Conclusion— The amelioration of adipose tissue inflammation and the improvement of endothelial function may represent important mechanisms that result in cardiovascular benefits after bariatric surgery.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1494427-3
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  • 2
    Online Resource
    Online Resource
    American Society for Microbiology ; 2022
    In:  Journal of Virology Vol. 96, No. 20 ( 2022-10-26)
    In: Journal of Virology, American Society for Microbiology, Vol. 96, No. 20 ( 2022-10-26)
    Abstract: Peste des petits ruminants virus (PPRV) infection leads to autophagy, and the molecular mechanisms behind this phenomenon are unclear. Here, we demonstrate that PPRV infection results in morphological changes of the endoplasmic reticulum (ER) and activation of activating transcription factor 6 (ATF6) of the ER stress unfolded protein response (UPR). Knockdown of ATF6 blocked the autophagy process, suggesting ATF6 is necessary for PPRV-mediated autophagy induction. Further study showed that PPRV infection upregulates expression of the ER-anchored adaptor protein stimulator of interferon genes (STING), which is well-known for its pivotal roles in restricting DNA viruses. Knockdown of STING suppressed ATF6 activation and autophagy induction, implying that STING functions upstream of ATF6 to induce autophagy. Moreover, the STING-mediated autophagy response originated from the cellular pattern recognition receptor melanoma differentiation-associated gene 5 (MDA5). The absence of MDA5 abolished the upregulation of STING and the activation of autophagy. The deficiency of autophagy-related genes (ATG) repressed the autophagy process and PPRV replication, while it had no effect on MDA5 or STING expression. Overall, our work revealed that MDA5 works upstream of STING to activate ATF6 to induce autophagy. IMPORTANCE PPRV infection induces cellular autophagy; however, the intracellular responses and signaling mechanisms that occur upon PPRV infection are obscure, and whether innate immune responses are linked with autophagy to regulate viral replication is largely unknown. Here, we uncovered that the innate immune sensor MDA5 initiated the signaling cascade by upregulating STING, which is best known for its role in anti-DNA virus infection by inducing interferon expression. We first provide evidence that STING regulates PPRV replication by activating the ATF6 pathway of unfolded protein responses (UPRs) to induce autophagy. Our results revealed that in addition to mediating responses to foreign DNA, STING can cross talk with MDA5 to regulate the cellular stress response and autophagy induced by RNA viruses; thus, STING works as an adaptor protein for cellular stress responses and innate immune responses. Modulation of STING represents a promising approach to control both DNA and RNA viruses.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2022
    detail.hit.zdb_id: 1495529-5
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  • 3
    In: Acta Biomaterialia, Elsevier BV, Vol. 146 ( 2022-07), p. 421-433
    Type of Medium: Online Resource
    ISSN: 1742-7061
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2173841-5
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Institute of Electrical and Electronics Engineers (IEEE) ; 2023
    In:  IEEE Transactions on Circuits and Systems II: Express Briefs Vol. 70, No. 10 ( 2023-10), p. 3872-3876
    In: IEEE Transactions on Circuits and Systems II: Express Briefs, Institute of Electrical and Electronics Engineers (IEEE), Vol. 70, No. 10 ( 2023-10), p. 3872-3876
    Type of Medium: Online Resource
    ISSN: 1549-7747 , 1558-3791
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2023
    detail.hit.zdb_id: 2028232-1
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 29, No. 8 ( 2009-08), p. 1164-1171
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 29, No. 8 ( 2009-08), p. 1164-1171
    Abstract: We tested whether the naturally occurring polyphenol resveratrol protects against oxidative stress–induced endothelial dysfunction in type 2 diabetes. Our data demonstrate that resveratrol restored endothelial function in type 2 diabetic mice by inhibiting TNFα-induced activation of NAD(P)H oxidase and preserving eNOS (Ser1177) phosphorylation.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 1494427-3
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  • 6
    In: International Journal of Nanomedicine, Informa UK Limited, Vol. Volume 17 ( 2022-09), p. 3809-3820
    Type of Medium: Online Resource
    ISSN: 1178-2013
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2377464-2
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  • 7
    Online Resource
    Online Resource
    Frontiers Media SA ; 2022
    In:  Frontiers in Pharmacology Vol. 13 ( 2022-2-14)
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 13 ( 2022-2-14)
    Abstract: Purpose: Wolfiporia cocos is frequently used in traditional Chinese medicine to treat depression. However, antidepressant-like effects of the main active ingredients of Wolfiporia cocos , total triterpenes of Wolfiporia cocos (TTWC), are not well studied. This study aimed to investigate those effects and explore their specific mechanisms of action in depth. Methods: Chemical components of TTWC were analyzed using LC-MS. Depression-like behavior in rats were induced by chronic unpredictable mild stress (CUMS). The suppressive effects of TTWC (60, 120, 240 mg/kg) against CUMS-induced depression-like behavior were evaluated using the forced swimming test (FST), open field test (OFT) and sucrose preference test (SPT). Levels of 5-hydroxytryptamine (5-HT), glutamate (GLU), corticotropin-releasing hormone (CRH), interleukin-1 beta (IL-1beta), interleukin-18 (IL-18), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in different groups were determined by ELISA. Western blotting (WB) was used to detect the expression of NLRP3, ASC, pro-caspase-1, caspase-1, pro-IL-1beta, IL-1beta, pro-IL-18, and IL-18 in the prefrontal cortex. Additionally, the mRNA levels of NLRP3, ASC, caspase-1, IL-1beta and IL-18 were detected by RT-PCR. Results: A total of 69 lanostane-type triterpene acids of TTWC were identified. The results showed that TTWC exhibited an antidepressant-like effect in CUMS rats, reversed the decreased sugar preference in the SPT, reduction of immobility time in the FST, reduced the rest time, increased the total moving distance in the OFT. TTWC increased 5-HT levels and decreased GLU levels in the hippocampus. Moreover, TTWC decreased CRH levels in serum, indicating the regulation of over-activation of the hypothalamic-pituitary-adrenal (HPA) axis. In addition, reduced serum levels of IL-1beta, IL-18, IL-6, and TNF-alpha. The WB results implied that TTWC inhibited the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 in the prefrontal cortex and enhanced the expression of pro-caspase-1, pro-IL-1beta, and pro-IL-18. Although most of the results were not significant, PCR results showed that TTWC inhibited the expression of NLRP3, ASC, caspase-1, IL-1beta, and IL-18 in the prefrontal cortex. Conclusion: TTWC treatment exerted an antidepressant-like effect and regulates neurotransmitters, HPA axis and NLRP3 signaling pathway. These results indicated the potential of TTWC in preventing the development of depression.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    MDPI AG ; 2022
    In:  Applied Sciences Vol. 12, No. 20 ( 2022-10-12), p. 10270-
    In: Applied Sciences, MDPI AG, Vol. 12, No. 20 ( 2022-10-12), p. 10270-
    Abstract: The working environment of contemporary mechanical products is becoming more complex, and the working conditions are becoming more extreme. This has led to a significant increase in the frequency of problems in mechanical products. In order to reduce the frequency of human repair after problems, the application of the self-recovery concept has become a hot research topic in the area of smart design. However, the current application of the self-recovery concept is mostly limited to the structural and parametric levels, with less research at the functional level, which may lead to a waste of resources within products. To solve this problem, this research combines the functional-level product research method with the self-recovery concept and establishes a design process model of complex products under functional self-recovery. This model extends the application scope of the self-recovery concept and improves the efficiency of resource utilization in the product. The design process model has six steps. First, according to the user requirements and the existing product, the initial function solving is carried out, and the initial function model of the product is established. Next, the main functions of the product are determined based on the initial function model of the product. Then, according to the determined main functions of the product, combined with the parameters marked in the function structure, the self-diagnosis function is designed. After that, the LT matrix and effect library are used to design the self-regulation function corresponding to the main functions, and the parameters are used to screen the self-regulation function design scheme. Finally, according to the design scheme of the self-diagnosis function and self-regulation function, the functional period oriented to self-recovery is constructed to ensure the realization of the main functions of the product. The effectiveness of the design process model is proved through the design process of an intelligent photovoltaic power generation system at the end of the paper.
    Type of Medium: Online Resource
    ISSN: 2076-3417
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2704225-X
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  • 9
    Online Resource
    Online Resource
    Institute of Electrical and Electronics Engineers (IEEE) ; 2022
    In:  IEEE Transactions on Very Large Scale Integration (VLSI) Systems Vol. 30, No. 12 ( 2022-12), p. 1928-1932
    In: IEEE Transactions on Very Large Scale Integration (VLSI) Systems, Institute of Electrical and Electronics Engineers (IEEE), Vol. 30, No. 12 ( 2022-12), p. 1928-1932
    Type of Medium: Online Resource
    ISSN: 1063-8210 , 1557-9999
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2022
    detail.hit.zdb_id: 2034318-8
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  • 10
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. suppl_1 ( 2015-05)
    Abstract: Loss-of-function mutations of lysosomal acid lipase ( LIPA or LAL) are the cause of the rare lysosomal disorders, Wolman disease and Cholesteryl Ester Storage Disease (CESD), which manifest with hepatomegaly, hyperlipidemia and premature atherosclerosis due to lysosomal cholesteryl ester (CE) accumulation mainly in hepatocytes and macrophages. Surprisingly, recent genome-wide association studies (GWAS) have implicated LIPA alleles, which associate with higher LIPA mRNA, also associate with increased risk of coronary artery disease (CAD). To date, the mechanistic insights into the role of human LIPA were largely derived from skin fibroblasts of CESD patients. Here we use CRISPR/Cas techniques to knock-out LIPA in human iPSC, and then differentiate to macrophage (IPSDM) to explore human macrophage LIPA phenotypes. LIPA mRNA was markedly induced by ~20 fold upon iPSC to IPSDM differentiation, was comparable between IPSDM and peripheral blood mononuclear cells (PBMC)-derived macrophages (HMDM, n=9) and was ~7 fold higher than in skin fibroblasts. Knock-out LIPA ( LIPA -/- ) IPSDM had barely detectable LIPA mRNA. Control and LIPA -/- IPSDM were loaded with [ 3 H]-cholesteryl oleate (CO)-labeled acetylated-LDL ([ 3 H]CO-ac-LDL) followed by efflux to apolipoprotein-AI (apoA-I) in the presence of ACAT inhibitor (n=5). Efflux of [ 3 H]-cholesterol was abolished in LIPA -/- IPSDM with massive lysosomal [ 3 H]-CE accumulation, indicating deficiency in LIPA-mediated lysosomal CE hydrolysis. In non-lipid loading state, LIPA -/- IPSDM had high levels of CE mass compared with minute amounts in control IPSDM (11.34±0.49 vs. 2.42±0.44 ug/mg protein, n=3). Yet, with ac-LDL loading, CE mass was similarly increased in both control and LIPA -/- IPSDM (22.34±1.70 vs. 21.96±2.18 ug/mg). LIPA -/- also did not impact IPSDM lysosomal apoB degradation or [ 3 H]-labeled free cholesterol efflux to apoA-I (4h and 20h) with ac-LDL loading. In conclusion, LIPA -/- IPSDM reveals macrophage-specific hallmarks of human LIPA LOF. CRISPR/Cas and IPSDM provide critical tools in assessing the impact of human LIPA genetic variation in diseases including the impact of GWAS CAD alleles in macrophage-specific functions in atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1494427-3
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