GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Ovid Technologies (Wolters Kluwer Health)  (28)
  • 1
    Online Resource
    Online Resource
    Epidemiology and Clinical Long-term Outcome of Childhood Aplastic Anemia in Korea for 15 Years : Retrospective Study of the Korean Society of Pediatric Hematology Oncology (KSPHO)
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Journal of Pediatric Hematology/Oncology Vol. 33, No. 3 ( 2011-04), p. 172-178
    Details
    In: Journal of Pediatric Hematology/Oncology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 3 ( 2011-04), p. 172-178
    Type of Medium: Online Resource
    ISSN: 1077-4114
    URL: Article
    DOI: 10.1097/MPH.0b013e31820826a8
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2047125-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Abstract 12429: Grade Of CRS is Associated With Cardiac Dysfunction in the Acute Phase, but Do Not Predict the Prognosis of Diffuse Large B Cell Lymphoma Patients Who Underwent CAR-T Therapy
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Introduction: As Chimeric Antigen Receptor T cell (CAR-T) therapy gains advantage in the management of diffuse large B cell lymphoma (DLBCL), accumulating evidence shows that it frequently accompanies cardiac dysfunction. Previous retrospective studies indicated the potential involvement of cytokine release syndrome (CRS) in cardiac dysfunction after CAR-T therapy, but no prospective study has reported the time course of cardiac dysfunction and its association with prognosis. Purpose: To prospectively examine the sequential changes in cardiac markers over time after CAR-T therapy and to clarify their association between the grade of CRS, cardiac markers, and prognosis.   Methods: In this prospective study, 30 DLBCL patients who underwent CAR-T therapy were enrolled. Before and after the treatment, the level of cardiac biomarkers and echocardiographic index were sequentially collected. We classified all patients into two groups according to the severity of CRS after CAR-T therapy, namely Low-CRS group (CRS 〈 2) and High-CRS group (CRS≧2). Cardiac biomarkers, echocardiographic index, and long-term survival prognosis were further analyzed in both groups.   Results: The average age of participants was 59.6 years, and 9 (30%) were female. The number of patients in Low- and High-CRS group was 13 and 17, respectively. At the baseline before CAR-T therapy, there were no significant differences in cardiac parameters between two groups. In High-CRS group, NT-proBNP levels were significantly increased on day 3 and 7 compared to the baseline and were significantly higher than Low-CRS group at both timepoints, whereas troponin T level did not show any differences. Likewise, in High-CRS group, GLS was significantly decreased on day 7 and 14 compared to the baseline and recovered toward baseline on day 28. GLS and EF did not show significant differences between Low- and High-CRS groups throughout the follow-up. The Kaplan-Meier analysis demonstrated that there was no significant difference in long-term survival prognosis according to the severity of CRS. Conclusion:    This study revealed that CAR-T therapy induced transient changes in NT-proBNP level and GLS especially in High-CRS group in the first 2 weeks, but they did not predict the long-term prognosis. 
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.12429
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Abstract 10168: Association Between the Grade of Cytokine Release Syndrome and Cardiac Dysfunction After Chimeric Antigen Receptor T Cell Therapy for Diffuse Large B Cell Lymphoma Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. Suppl_1 ( 2021-11-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: As Chimeric Antigen Receptor T cell (CAR-T) therapy gains its clinical advantage in the management of diffuse large B cell lymphoma (DLBCL), accumulating evidence shows that it often accompanies cardiac dysfunction. Previous retrospective studies indicated the involvement of cytokine release syndrome (CRS) in cardiac dysfunction after CAR-T therapy, but their association is not fully investigated. Therefore, we designed a prospective study to clarify the association between the grade of CRS and cardiac dysfunction in the DLBCL patients after CAR-T therapy. Methods: In this prospective study, 14 DLBCL patients who underwent CAR-T therapy from July 2020 to May 2021 were enrolled. Before and after CAR-T therapy, we collected the levels of troponin T (TnT) as a marker for myocardial damage, left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) as markers for systolic function, and E/e’ and left atrial volume index (LAVI) as markers for diastolic function. We classified all patients into two groups according to the severity of CRS after CAR-T therapy, namely the low-CRS Group (CRS 〈 3) and the high-CRS Group (CRS≧3). The markers for cardiac injury and dysfunction were further analyzed in both groups. Results: Average age was 56.4 years and 7 patients (50%) were female. The number of patients in the low-CRS and high-CRS Group were 11 and 3, respectively. Before CAR-T therapy, there were no differences in cardiac function between the two groups. From the hyper-early phase of CAR-T therapy, the increase of TnT, E/e’ and LAVI from the baseline were significantly larger in the high-CRS Group compared to the low-CRS Group (P=0.023, 0.039, and 0.024, respectively). Subsequently, the decrease of GLS from the baseline became significantly larger in the high-CRS Group compared to the low-CRS Group (P=0.049). These results indicated that cardiac dysfunction after CAR-T therapy occurred in the order of myocardial damage, diastolic dysfunction, and systolic dysfunction. Conclusion: We for the first time demonstrated the association between high-grade CRS and cardiac dysfunction after CAR-T therapy through a prospective study.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.144.suppl_1.10168
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    The Cancer Therapy-Related Clonal Hematopoiesis Driver Gene Ppm1d Promotes Inflammation and Non-Ischemic Heart Failure in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 129, No. 6 ( 2021-09-03), p. 684-698
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 129, No. 6 ( 2021-09-03), p. 684-698
    Abstract: Cancer therapy can be associated with short- and long-term cardiac dysfunction. Patients with cancer often exhibit therapy-related clonal hematopoiesis (t-CH), an aggressive form of clonal hematopoiesis that can result from somatic mutations in genes encoding regulators of the DNA-damage response (DDR) pathway. Gain-of-function mutations in exon 6 of the protein phosphatase Mg2+/Mn2+ dependent 1D ( PPM1D ) gene are the most frequently mutated DNA-damage response gene associated with t-CH. Whether t-CH can contribute to cardiac dysfunction is unknown. Objective: We evaluated the causal and mechanistic relationships between Ppm1d -mediated t-CH and nonischemic heart failure in an experimental system. Methods and Results: To test whether gain-of-function hematopoietic cell mutations in Ppm1d can increase susceptibility to cardiac stress, we evaluated cardiac dysfunction in a mouse model where clonal hematopoiesis-associated mutations in exon 6 of Ppm1d were produced by CRISPR-Cas9 technology. Mice transplanted with hematopoietic stem cells containing the mutated Ppm1d gene exhibited augmented cardiac remodeling following the continuous infusion of Ang II (angiotensin II). Ppm1d -mutant macrophages were impaired in DDR pathway activation and displayed greater DNA damage, higher reactive oxygen species generation, and an augmented proinflammatory profile with elevations in IL (interleukin)-1β and IL-18. The administration of an NLRP3 (NLR family pyrin domain containing 3) inflammasome inhibitor to mice reversed the cardiac phenotype induced by the Ppm1d -mutated hematopoietic stem cells under conditions of Ang II–induced stress. Conclusions: A mouse model of Ppm1d -mediated t-CH was more susceptible to cardiac stress. Mechanistically, disruption of the DDR pathway led to elevations in inflammatory cytokine production, and the NLRP3 inflammasome was shown to be essential for this augmented cardiac stress response. These data indicate that t-CH involving activating mutations in PPM1D can contribute to the cardiac dysfunction observed in cancer survivors, and that anti-inflammatory therapy may have utility in treating this condition.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.121.319314
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Abstract 10950: Prognostic Utility of Left Atrio-Ventricular Deformation Analysis in Heart Failure Patients Underwent Cardiac Resynchronization Therapy
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Introduction: Left atrial (LA) adverse remodeling is a prognostic marker in patients with heart failure. Although left ventricular (LV) deformation analysis by speckle tracking method has been shown as a useful predictive marker after cardiac resynchronization therapy (CRT), the prognostic impact of baseline left atrio-ventricular functional deterioration on the outcome of patients underwent CRT implantation. Hypothesis: We hypothesized that a combination of LV and LA deformation assessments by speckle-tracking strain is of additive prognostic value in patients with CRT. Methods: We retrospectively analyzed 71 participants who received CRT implantation in the clinical guidelines. Global longitudinal strain (GLS) was defined as averaged strain from 3 apical views. LA strain (LAS) was calculated as the average strain using apical two- and four-chamber views. The endpoint was composite outcome of death, hospitalization due to worsening HF for 5 years after CRT implantation. Results: Out of 71 patients aged 68 ± 11 years with 162±24ms of QRS duration and 30±8% of LV ejection fraction, 40 patients (56%) met the endpoint. The patients were stratified using median value of LAS (-15%) and GLS (-8%). LAS and GCS remained significantly associated with poor outcome after adjusting for LVEF (LAS hazard ratio, 0.92; p 〈 0.001; GLS hazard ratio, 1.15; p = 0.01). Kaplan-Meier analysis showed that the subgroup of patients with both lower median values of LAS and GLS had the worst outcomes over 5 years (Figure, Log-rank, p = 0.008). In the sequential Cox model, predictive value of baseline LV ejection fraction (χ2 = 4.9) was improved by the addition of GLS (χ2 = 9.2, p = 0.037), and further improved by the addition of LAS (χ2 = 15.8, p = 0.005). C-statistics also improved from 0.62 to 0.73. Conclusions: Baseline left atrio-ventricular functional deterioration by deformation analysis were significantly associated with poor outcome after CRT implantation.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.146.suppl_1.10950
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Identification of the Mtus1 Splice Variant as a Novel Inhibitory Factor Against Cardiac Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Heart Association Vol. 5, No. 7 ( 2016-07-06)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 7 ( 2016-07-06)
    Abstract: In cardiac hypertrophy and failure, there is a widespread alteration in mRNA splicing, but the role of splice variants in cardiac hypertrophy has not yet been fully elucidated. In this study, we used an exon array to identify novel splice variants associated with cardiac hypertrophy. Methods and Results We performed genome‐wide exon array analysis and developed a splicing profile in murine hearts with hypertrophy induced by transverse aortic constriction for 8 weeks. Following global analysis of splice variants using the Mouse Exon 1.0 ST Array, we identified 46 spliced genes and narrowed our focus to 1 gene, mitochondrial tumor suppressor 1 ( Mtus1 ), whose splice variants were registered in the NCBI RefSeq database. Notably, one of the splice variants Mtus1A was specifically upregulated, although the total expression of the Mtus1 gene remained unchanged. We showed that Mtus1A was localized in the mitochondria, and its expression level increased with the degree of cardiac hypertrophy. In cultured cardiomyocytes, Mtus1A overexpression reduced phenylephrine‐induced reactive oxygen species production and consequent ERK phosphorylation, resulting in a decrease in both cell size and protein synthesis. In vivo, cardiac‐specific Mtus1A transgenic mice showed left ventricle wall thinning and a reduced hypertrophic response to pressure overload and phenylephrine treatment. Conclusions We found that Mtus1 is specifically spliced in hypertrophic hearts and that the Mtus1A variant has an inhibitory effect on cardiac hypertrophy. Mtus1A is, therefore, a possible diagnostic and therapeutic target for cardiac hypertrophy and failure.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.003521
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2653953-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Experimental ASXL1 ‐Mediated Clonal Hematopoiesis Promotes Inflammation and Accelerates Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of the American Heart Association Vol. 11, No. 19 ( 2022-10-04)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 11, No. 19 ( 2022-10-04)
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.122.026154
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2653953-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Abstract 46: Temporal Ubiquitin-Proteasomal Degradation of Smad9 Mediated by its Specific E3 Ligase Asb2 is Required for Cardiac Development through the Regulation of Tbx2 Expression
    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)
    Abstract: Background: The bone morphogenetic protein (BMP) pathway plays crucial roles in cardiac development. Recent studies have reported that mutations in Smad9, one of the regulatory Smad specific for the BMP pathway, might result in cardiovascular diseases. However, both regulation and function of Smad9 in the cardiovascular system have not been elucidated. Methods and Results: We conducted DNA microarray using P19CL6 cells with forced expression of Smad9. Microarray analysis using Ingenuity Pathway Analysis elucidated that 19 genes including Tbx2 were related to BMP pathway and showed significantly altered expression levels by transient expression of Smad9. We confirmed by qRT-PCR that only Tbx2, but not other Tbx families, were induced by Smad9. Importantly, the expression of Tbx2 was more up-regulated by Smad9 than by Smad1. Moreover, we identified Asb2 as a specific E3 ligase that targets Smad9, but not Smad1/5, for proteasomal degradation. The in situ hybridization using murine embryo revealed that Asb2 is expressed predominantly in the heart during embryonic development, suggesting that Asb2 quantitatively regulates Smad9 in the developing heart. Biochemical analysis demonstrated that Tbx2 expression induced by Smad9 was attenuated by Asb2, which was restored by the treatment with proteasome inhibitor, lactacystin. Developmental studies using both P19CL6 cells and zebrafish showed that the ablation of Asb2 leads accumulation of Smad9 resulting in the up-regulation of Tbx2, which attenuates myocardial development while induces non-myocardial tissue including cardiac cushion. Indeed, alcian blue staining of morpholino-mediated knockdown of zebrafish Asb2 showed significantly dilated ventricle and thinned ventricular wall, accompanied with decreased myocardium and increased cardiac jelly. Conclusions: Smad9 induces the expression of Tbx2 during cardiac development and is temporally and quantitatively regulated by its specific E3 ligase Asb2. This is the first study to show both the target gene and specific E3 ligase of Smad9.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.115.suppl_1.46
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Abstract 12381: Ast-120, an Adsorbent of Uremic Toxins Normalized the Cardiac Hypertrophic/pro- Apoptotic And Cardioprotective/anti-apoptotic Signaling in Pacing-induced Heart Failure in Dogs
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Vol. 132, No. suppl_3 ( 2015-11-10)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. suppl_3 ( 2015-11-10)
    Abstract: Background: Renal dysfunction increases the plasma levels of indoxyl sulfate (IS), a uremic toxin excreted from the kidney. Interestingly, IS is reported to directly stimulate both collagen synthesis and cardiomyocyte hypertrophy in vitro via the modulation of ERK and p38-MAPK. However, it is unclear whether the pathophysiology of heart failure (HF) changes such intracellular signaling via the IS-dependent pathways. AST-120 is known to inhibit the uptake of indole and decrease the plasma IS levels. Hypothesis: We tested the hypothesis that the removal of plasma IS by using AST-120 modulates the intracellular signaling for hypertrophy, collagen synthesis and apoptosis of the myocardium in the canine HF model in vivo. Method: A canine HF model was produced by continuous rapid ventricular pacing at 230 bpm for 6 weeks. We treated the canine with oral AST-120 (1g/kg/day) administration between 4th and 6th week following the onset of rapid pacing (HF with AST-120 group, HF without AST-120 group, n=7 in each). We also set a control (Control group, n=7) without pacing for 6 weeks. We extracted the protein from the hearts and analyzed it by Western blotting. Result: AST-120 treatment reduced both plasma IS elevated in the canine HF model. HF without AST-120 group showed the activation of ERK signaling and the deactivation of both Akt and p38-MAPK signaling compared with Control group. The treatment with AST-120 increased the phosphorylation levels of Akt and p38-MAPK, and suppressed the ERK phosphorylation. HF without AST-120 group also showed an increased expression of pro-apoptotic Bax protein, and a decreased expression of anti-apoptotic Bcl-2 protein. The increased Bcl-2/Bax ratio was significantly ameliorated by AST-120 treatment. Conclusion: The decreases in plasma levels of indoxyl sulfate by the treatment with AST-120 1) deactivates the cardiac hypertrophic signaling, 2) activates the cardiac survival and anti-apoptotic signals and 3) suppresses the pro-apoptotic signals in failing heart in vivo. Indoxyl sulfate may become a sensitive and novel biomarker/mediator of heart failure explaining the cardio-renal syndrome that links renal dysfunction to heart failure.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.132.suppl_3.12381
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1466401-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Osteosarcoma Developed in the Period of Maximal Growth Rate Have Inferior Prognosis
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Journal of Pediatric Hematology/Oncology Vol. 30, No. 6 ( 2008-06), p. 419-424
    Details
    In: Journal of Pediatric Hematology/Oncology, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 6 ( 2008-06), p. 419-424
    Type of Medium: Online Resource
    ISSN: 1077-4114
    URL: Article
    DOI: 10.1097/MPH.0b013e318168e7dc
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 2047125-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...