GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Elsevier BV ; 2021
    In:  Journal of Hazardous Materials Vol. 406 ( 2021-03), p. 124746-
    In: Journal of Hazardous Materials, Elsevier BV, Vol. 406 ( 2021-03), p. 124746-
    Type of Medium: Online Resource
    ISSN: 0304-3894
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1491302-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Research Vol. 130, No. 10 ( 2022-05-13), p. 1586-1600
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. 10 ( 2022-05-13), p. 1586-1600
    Abstract: Pathological cardiac hypertrophy is one of the leading causes of heart failure with highly complicated pathogeneses. The E3 ligase TRIM16 (tripartite motif–containing protein 16) has been recognized as a pivotal regulator to control cell survival, immune response, and oxidativestress. However, the role of Trim16 in cardiac hypertrophy is unknown. Methods: We generated cardiac-specific knockout mice and adeno-associated virus serotype 9–Trim16 mice to evaluate the function of Trim16 in pathological myocardial hypertrophy. The direct effect of TRIM16 on cardiomyocyte enlargement was examined using an adenovirus system. Furthermore, we combined RNA-sequencing and interactome analysis that was followed by multiple molecular biological methodologies to identify the direct target and corresponding molecular events contributing to TRIM16 function. Results: We found an intimate correlation of Trim16 expression with hypertrophy-related heart failure in both human and mouse. Our functional investigations and unbiased transcriptomic analyses clearly demonstrated that Trim16 deficiency markedly exacerbated cardiomyocyte enlargement in vitro and in transverse aortic constriction–induced cardiac hypertrophy mouse model, whereas Trim16 overexpression attenuated cardiac hypertrophy and remodeling. Mechanistically, Prdx1 (peroxiredoxin 1) is an essential target of Trim16 in cardiac hypertrophy. We found that Trim16 interacts with Prdx1 and inhibits its phosphorylation, leading to a robust enhancement of its downstream Nrf2 (nuclear factor–erythroid 2–related factor 2) pathway to block cardiac hypertrophy. Trim16-blocked Prdx1 phosphorylation was largely dependent on a direct interaction between Trim16 and Src and the resultant Src ubiquitinational degradation. Notably, Prdx1 knockdown largely abolished the anti-hypertrophic effects of Trim16 overexpression. Conclusions: Our findings provide the first evidence supporting Trim16 as a novel suppressor of pathological cardiac hypertrophy and indicate that targeting the Trim16-Prdx1 axis represents a promising therapeutic strategy for hypertrophy-related heart failure.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: Journal for ImmunoTherapy of Cancer, BMJ, Vol. 9, No. Suppl 2 ( 2021-11), p. A993-A994
    Abstract: Breast cancer(BC) is the second most common cause after lung cancer of malignant pleural effusions(MPEs),in approximately one third of all MPEs.Although,MPEs are relativity easy to be collated are still not well characterized in their cellular compositions. This opens new avenues to characterize the cellular milieu comprising the MPE, as it has the potential to be highly informative about mutational markers and immune response –ultimately guiding targeted therapy and predicting therapeutic outcomes with their study. The proposed study will characterize immune landscape of the cellular composition of MPE from patients with metastatic breast carcinoma and characterize their relationship with clinicopathologic features in these patients. Abstract 945 Figure 1 Comparison between the cell block in H-E and mIF expression CK, CD68 and CD3 Abstract 945 Figure 2 Composite image in mIF expressing 8 markers. In higher magnification is possible to observe the co expression of CK+Ki67+, CK PDL1, CD3+Foxp3+ and CD3+CD8+ Abstract 945 Table 1 Results: cell phenotypes in percentage in the six cases analyzed Abstract 945 Table 2 Clinical data of the six patients. L: left . R: right , BR : Breast cáncer, CRC: Colorrectal cáncer, NE: No evaluable , IDC : Invasive ductal carcinoma , CT: chemotherapy and BT : biotherapy * Last appointment of the patient. Methods Five microns thickness paraffin cell pellet blocks from six cases randomly selected of breast carcinoma MPE were stained using a quantitative multiplex immunofluorescence(mIF) panel containing 8 markers against pancytokeratin(CK), PD-L1, PD-1, CD3, CD8, Foxp3, CD68, Ki67, and DAPI (figure 1). Representative regions of interest were scanned using a multispectral scanner (Vectra Polaris) in high magnification (20x) to capture different cell populations. Markers co-expression were processed and analyzed using a quantitative image analysis software (InForm). The final results were obtained as absolute number of cells from each phenotype and were characterized with clinicopathologic features. Results We analyzed and stained six breast cancer MPE cases with previously optimized and validated mIF panel for formalin fixed and paraffin embedded (FFPE) tumor tissues against CK, CD3, CD68, CD8, Foxp3, Ki67, PD1 and PD-L1 (figure 2). The median cellular density was 5870.53 cells. Median for each marker: CK+ was presented in 75.9% (between malignant cells and reactive mesothelial cells) in these cells the expression of Ki67 was 8% and PD-L1+ was present in 0.2%.CD3+ was 0.72% and being the cytotoxic T-cells CD3+CD8+ was 12.13% of these cells and it expression for CD3+PD1+ was in 1.14% without concomitant expression for PD-L1. The median of the macrophages CD68+ was 8.1% of the total cells (table 2). Conclusions mIF is a promising tool to study diverse corporal effusion from different origin. Although more studies are needed, this new perspective can help us to resolve some clues and possible prognosis in advanced stages of BC. Reference Nicholas D T, Matthew A. S. Diagnosis and Management of Pleural Metastases and Malignant Effusion in Breast Cancer.En: Kirby I B, Edward M C, V. Suzanne K, William J. G. The Breast (Fifth Edition): Elsevier; 2018. P 934.
    Type of Medium: Online Resource
    ISSN: 2051-1426
    Language: English
    Publisher: BMJ
    Publication Date: 2021
    detail.hit.zdb_id: 2719863-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    In: Cell Metabolism, Elsevier BV, Vol. 33, No. 10 ( 2021-10), p. 2059-2075.e10
    Type of Medium: Online Resource
    ISSN: 1550-4131
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2174469-5
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...