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  • 1
    In: Autism Research, Wiley, Vol. 11, No. 9 ( 2018-09), p. 1218-1228
    Kurzfassung: Little is currently known about the longitudinal developmental patterns of hubs in the whole‐brain white matter (WM) structural networks among toddlers with autism spectrum disorder (ASD). This study utilized diffusion tensor imaging (DTI) and deterministic tractography to map the WM structural networks in 37 ASD toddlers and 27 age‐, gender‐ and developmental quotient‐matched controls with developmental delay (DD) toddlers aged 2–3 years old at baseline (Time 1) and at 2‐year follow‐up (Time 2). Furthermore, graph‐theoretical methods were applied to investigate alterations in the network hubs in these patients at the two time points. The results showed that after 2 years, 17 hubs were identified in the ASD subjects compared to the controls, including 13 hubs that had not changed from baseline and 4 hubs that were newly identified. In addition, alterations in the properties of the hubs of the right middle frontal gyrus, right insula, left median cingulate gyri, and bilateral precuneus were significantly correlated with alterations in the behavioral data for ASD patients. These results indicated that at the stage of 2–5 years of age, ASD children showed distributions of network hubs that were relatively stable, with minor differences. Abnormal developmental patterns in the five areas mentioned above in ASD may contribute to abnormalities in the social and nonsocial characteristics of this disorder. Autism Res 2018, 11: 1218–1228 . © 2018 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary This work studied the longitudinal developmental patterns of hubs in the whole‐brain white matter (WM) structural network among toddlers with autism spectrum disorder (ASD). The findings of this study could have implications for understanding how the abnormalities in hub organization in ASD account for behavioral deficits in patients and may provide potential biomarkers for disease diagnosis and the subsequent monitoring of progression and treatment effects for patients with ASD.
    Materialart: Online-Ressource
    ISSN: 1939-3792 , 1939-3806
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2018
    ZDB Id: 2418112-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    In: Autism Research, Wiley, Vol. 10, No. 4 ( 2017-04), p. 620-630
    Kurzfassung: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder mainly showed atypical social interaction, communication, and restricted, repetitive patterns of behavior, interests and activities. Now clinic diagnosis of ASD is mostly based on psychological evaluation, clinical observation and medical history. All these behavioral indexes could not avoid defects such as subjectivity and reporter‐dependency. Therefore researchers devoted themselves to seek relatively stable biomarkers of ASD as supplementary diagnostic evidence. The goal of present study is to generate relatively stable predictive model based on anatomical brain features by using machine learning technique. Forty‐six ASD children and thirty‐nine development delay children aged from 18 to 37 months were evolved in. As a result, the predictive model generated by regional average cortical thickness of regions with top 20 highest importance of random forest classifier showed best diagnostic performance. And random forest was proved to be the optimal approach for neuroimaging data mining in small size set and thickness‐based classification outperformed volume‐based classification and surface area‐based classification in ASD. The brain regions selected by the models might attract attention and the idea of considering biomarkers as a supplementary evidence of ASD diagnosis worth exploring. Autism Res 2017, 0: 000–000 . © 2016 International Society for Autism Research, Wiley Periodicals, Inc. Autism Res 2017, 10: 620–630 . © 2016 International Society for Autism Research, Wiley Periodicals, Inc.
    Materialart: Online-Ressource
    ISSN: 1939-3792 , 1939-3806
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2017
    ZDB Id: 2418112-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    In: Aging Cell, Wiley, Vol. 19, No. 11 ( 2020-11)
    Kurzfassung: Incidence of intracerebral hemorrhage (ICH) and brain iron accumulation increases with age. Excess iron accumulation in brain tissues post‐ICH induces oxidative stress and neuronal damage. However, the mechanisms underlying iron deregulation in ICH, especially in the aged ICH model have not been well elucidated. Ferroportin1 (Fpn) is the only identified nonheme iron exporter in mammals to date. In our study, we reported that Fpn was significantly upregulated in perihematomal brain tissues of both aged ICH patients and mouse model. Fpn deficiency induced by injecting an adeno‐associated virus (AAV) overexpressing cre recombinase into aged Fpn‐floxed mice significantly worsened the symptoms post‐ICH, including hematoma volume, cell apoptosis, iron accumulation, and neurologic dysfunction. Meanwhile, aged mice pretreated with a virus overexpressing Fpn showed significant improvement of these symptoms. Additionally, based on prediction of website tools, expression level of potential miRNAs in ICH tissues and results of luciferase reporter assays, miR‐124 was identified to regulate Fpn expression post‐ICH. Higher serum miR‐124 levels were correlated with poor neurologic scores of aged ICH patients. Administration of miR‐124 antagomir enhanced Fpn expression and attenuated iron accumulation in aged mice model. Both apoptosis and ferroptosis, but not necroptosis, were regulated by miR‐124/Fpn signaling manipulation. Our study demonstrated the critical role of miR‐124/Fpn signaling in iron metabolism and neuronal death post‐ICH in aged murine model. Thus, Fpn upregulation or miR‐124 inhibition might be promising therapeutic approachs for this disease.
    Materialart: Online-Ressource
    ISSN: 1474-9718 , 1474-9726
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2020
    ZDB Id: 2099130-7
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    In: Liver International, Wiley, Vol. 42, No. 3 ( 2022-03), p. 663-673
    Kurzfassung: Epidemiological evidence linking fibroblast growth factor 21 (FGF21) with hepatocellular carcinoma (HCC) prognosis lacked. We aimed to evaluate the associations between serum FGF21 levels and HCC survival in a large prospective cohort. Methods 825 newly diagnosed, previously untreated HCC patients from the Guangdong Liver Cancer Cohort were enrolled between September 2013 and April 2017. Serum FGF21 levels were measured by ELISA. Liver cancer‐specific survival (LCSS) and overall survival (OS) were calculated. Multivariable Cox proportional hazards models were performed to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs). Results Compared with patients in the lowest tertile of serum FGF21 levels, patients in the highest tertile had inferior survival outcomes. HRs in the fully adjusted models were 1.44 (95% CI: 1.07, 1.94; P ‐trend  = .014) and 1.48 (95% CI: 1.12, 1.97; P ‐trend  = .002) for LCSS and OS, respectively. The associations were not significantly modified by selected metabolic disorder diseases or state such as arterial hypertension, diabetes, dyslipidemia, fatty liver, cirrhosis, and body mass index ≥25.0 kg/m 2 , except for that stronger associations were observed in patients co‐occurred more than three metabolic disorder diseases ( P ‐interaction  = .046 for OS and .151 for LCSS), with an HR of 2.01 (95% CI: 1.04, 3.85; P ‐trend  = .009) for OS and 1.51 (95% CI: 0.73, 3.10; P ‐trend  = .195) for LCSS. Conclusions Higher serum FGF21 levels were associated with worse survival in HCC patients, suggesting that serum FGF21 may be used as a novel metabolism‐related prognostic biomarker for HCC.
    Materialart: Online-Ressource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2022
    ZDB Id: 2124684-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 13, No. 8b ( 2009-08-02), p. 2713-2723
    Kurzfassung: This study aims to develop a new animal model of vulnerable plaques and investigate the potential mechanisms of exogenous p53‐induced plaque instability. Forty rabbits underwent aortic balloon injury, were fed a 1% cholesterol diet for 10 weeks and then normal chow for 6 weeks. Rabbits were divided into Ad5‐CMV.p53‐treated group ( n = 16), Ad5‐CMV.lac Z‐treated group ( n = 16) and blank control group ( n = 8). Under the guidance of intravascular ultrasound, a 50‐μl suspension of adenovirus containing p53 or lac Z was injected into the largest plaque of the first two groups, respectively, and these rabbits received pharmacological triggering 2 weeks later. In 76.9% of rabbits with p53 transfection, plaque rupture was found, which was significantly ( P 〈 0.05) higher than that in the Ad5‐CMV.lac Z‐treated plaques (23.1%), or blank controls plaques (0%). Increased apoptotic cells, and subsequently, decreased vascular smooth muscle cells and collagen content, enhanced intima macrophage accumulation, increased C‐reactive protein (CRP) and matrix metalloproteinases staining and high serum levels of high sensitive CRP (hs‐CRP) and monocyte chemoattractant protein‐1 (MCP‐1) were observed in Ad5‐CMV.p53‐treated rabbits. However, a binary logistic regression model revealed that hs‐CRP concentration rather than apoptosis rate played an independent role in plaque rupture with an odds ratio as 1.314 (95% CI: 1.041–1.657, P = 0.021), and there were high positive correlations between inflammatory biomarkers (hs‐CRP or MCP‐1) and apoptosis ( R 2 = 0.761, and R 2 = 0.557, respectively, both P 〈 0.01). Intraplaque injection of p53 gene provides a safe and effective method for inducing plaque vulnerability in rabbits. The destabilizing effect of p53 overexpression is mediated mainly through apoptosis‐enhanced inflammation rather than cell apoptosis itself.
    Materialart: Online-Ressource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2009
    ZDB Id: 2076114-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    Wiley ; 2014
    In:  Journal of Cellular and Molecular Medicine Vol. 18, No. 8 ( 2014-08), p. 1599-1611
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 18, No. 8 ( 2014-08), p. 1599-1611
    Kurzfassung: Autophagic dysfunction is observed in diabetes mellitus. Resveratrol has a beneficial effect on diabetic cardiomyopathy. Whether the resveratrol‐induced improvement in cardiac function in diabetes is via regulating autophagy remains unclear. We investigated the mechanisms underlying resveratrol‐mediated protection against heart failure in diabetic mice, with a focus on the role of sirtuin 1 ( SIRT 1) in regulating autophagic flux. Diabetic cardiomyopathy in mice was induced by streptozotocin ( STZ ). Long‐term resveratrol treatment improved cardiac function, ameliorated oxidative injury and reduced apoptosis in the diabetic mouse heart. Western blot analysis revealed that resveratrol decreased p62 protein expression and promoted SIRT 1 activity and Rab7 expression. Inhibiting autophagic flux with bafilomycin A1 increased diabetic mouse mortality and attenuated resveratrol‐induced down‐regulation of p62, but not SIRT 1 activity or Rab7 expression in diabetic mouse hearts. In cultured H9C2 cells, redundant or overactive H 2 O 2 increased p62 and cleaved caspase 3 expression as well as acetylated forkhead box protein O1 ( FOXO 1) and inhibited SIRT 1 expression. Sirtinol, SIRT 1 and Rab7 si RNA impaired the resveratrol amelioration of dysfunctional autophagic flux and reduced apoptosis under oxidative conditions. Furthermore, resveratrol enhanced FOXO 1 DNA binding at the Rab7 promoter region through a SIRT 1‐dependent pathway. These results highlight the role of the SIRT 1/ FOXO 1/Rab7 axis in the effect of resveratrol on autophagic flux in vivo and in vitro , which suggests a therapeutic strategy for diabetic cardiomyopathy.
    Materialart: Online-Ressource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2014
    ZDB Id: 2076114-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 18, No. 5 ( 2014-05), p. 907-918
    Kurzfassung: Cellular therapeutic neovascularization has been successfully performed in clinical trials for patients with ischaemia diseases. Despite the vast knowledge of cardiovascular disease and circadian biology, the role of the circadian clock in regulating angiogenesis in myocardial infarction ( MI ) remains poorly understood. In this study, we aimed to investigate the role and underlying mechanisms of Period 2 (Per2) in endothelial progenitor cell ( EPC ) function. Flow cytometry revealed lower circulating EPC proportion in per2 −/− than in wild‐type ( WT ) mice. PER 2 was abundantly expressed in early EPC s in mice. In vitro , EPC s from per2 −/− mice showed impaired proliferation, migration, tube formation and adhesion. Western blot analysis demonstrated inhibited PI 3k/Akt/FoxO signalling and reduced C‐X‐C chemokine receptor type 4 ( CXCR 4) protein level in EPC s of per2 −/− mice. The impaired proliferation was blocked by activated PI 3K/Akt/FoxO signalling. Direct interaction of CXCR 4 and PER 2 was detected in WT EPC s. To further study the effect of per2 on in vivo EPC survival and angiogenesis, we injected saline or DiI‐labelled WT or per2 −/− EPC intramyocardially into mice with induced MI . Per2 −/− reduced the retention of transplanted EPC s in the myocardium, which was associated with significantly reduced DiI expression in the myocardium of MI mice. Decreased angiogenesis in the myocardium of per2 −/− EPC ‐treated mice coincided with decreased LV function and increased infarct size in the myocardium. Per2 may be a key factor in maintaining EPC function in vitro and in therapeutic angiogenesis in vivo .
    Materialart: Online-Ressource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2014
    ZDB Id: 2076114-4
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    In: PROTEOMICS, Wiley, Vol. 12, No. 11 ( 2012-06), p. 1883-1891
    Materialart: Online-Ressource
    ISSN: 1615-9853
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2012
    ZDB Id: 2037674-1
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Online-Ressource
    Online-Ressource
    Wiley ; 2016
    In:  Plant Biotechnology Journal Vol. 14, No. 1 ( 2016-01), p. 206-214
    In: Plant Biotechnology Journal, Wiley, Vol. 14, No. 1 ( 2016-01), p. 206-214
    Kurzfassung: Abscisic acid ( ABA ) regulates plant adaptive responses to various environmental stresses, while l ‐ascorbic acid ( A s A ) that is also named vitamin C is an important antioxidant and involves in plant stress tolerance and the immune system in domestic animals. Transgenic tobacco ( Nicotiana tabacum L.) and stylo [ Stylosanthes guianensis (Aublet) Swartz], a forage legume, plants co‐expressing stylo 9‐ cis ‐epoxycarotenoid dioxygenase (Sg NCED 1) and yeast d ‐arabinono‐1,4‐lactone oxidase ( ALO ) genes were generated in this study, and tolerance to drought and chilling was analysed in comparison with transgenic tobacco overexpressing Sg NCED 1 or ALO and the wild‐type plants. Compared to the Sg NCED 1 or ALO transgenic plants, in which only ABA or AsA levels were increased, both ABA and AsA levels were increased in transgenic tobacco and stylo plants co‐expressing Sg NCED 1 and ALO genes. Compared to the wild type, an enhanced drought tolerance was observed in Sg NCED 1 transgenic tobacco plants with induced expression of drought‐responsive genes, but not in ALO plants, while an enhanced chilling tolerance was observed in ALO transgenic tobaccos with induced expression of cold‐responsive genes, but not in Sg NCED 1 plants. Co‐expression of Sg NCED 1 and ALO genes resulted in elevated tolerance to both drought and chilling in transgenic tobacco and stylo plants with induced expression of both drought and cold‐responsive genes. Our result suggests that co‐expression of Sg NCED 1 and ALO genes is an effective way for use in forage plant improvement for increased tolerance to drought and chilling and nutrition quality.
    Materialart: Online-Ressource
    ISSN: 1467-7644 , 1467-7652
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2016
    ZDB Id: 2136367-5
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
    In: Experimental Dermatology, Wiley, Vol. 19, No. 11 ( 2010-11), p. 958-964
    Materialart: Online-Ressource
    ISSN: 0906-6705
    URL: Issue
    RVK:
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2010
    ZDB Id: 2026228-0
    Standort Signatur Einschränkungen Verfügbarkeit
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