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  • 1
    Online Resource
    Online Resource
    Does a Carbon Ion-Implanted Surface Reduce the Restenosis Rate of Coronary Stents?
    S. Karger AG ; 2005
    In:  Cardiology Vol. 104, No. 2 ( 2005), p. 72-75
    Details
    In: Cardiology, S. Karger AG, Vol. 104, No. 2 ( 2005), p. 72-75
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Neointimal hyperplasia and resulting restenosis limit the long-term success of coronary stenting. Heavy metal ions induce an inflammatory and allergic reaction, and result in in-stent restenosis. However, a carbon ion-implanted surface might prevent heavy metal ions from diffusing into surrounding tissue. 〈 i 〉 Methods: 〈 /i 〉 140 lesions in 140 patients with coronary lesions underwent implantation of carbon-implanted surface stents (Arthos 〈 sup 〉 inert 〈 /sup 〉 stent group, n = 70) or control stents (Arthos stent group, n = 70). The primary end point was the in-stent restenosis and the secondary end point was the value of hs-CRP at 48 h and 6 months after coronary stenting. Clinical and angiographic follow-ups were performed at 6 months. 〈 i 〉 Results: 〈 /i 〉 The rate of in-stent restenosis was lower in the Arthos 〈 sup 〉 inert 〈 /sup 〉 stent group (15.9%, 10/63) than in the Arthos stent group (20.9%, 13/62), but there were no significant differences between both groups (p = 0.56). The value of hs-CRP at 48 h was lower in the Arthos 〈 sup 〉 inert 〈 /sup 〉 stent group (13.9 ± 13.4 mg/dl) than in the Arthos stent group (24.5 ± 26.0 mg/dl) with significant differences (p = 0.04). However, the differences between two groups were not statistically significant at 6 months (p = 0.76). 〈 i 〉 Conclusions: 〈 /i 〉 As compared with a standard coronary stent, a carbon ion-implanted stent shows no considerable benefit for the prevention of in-stent restenosis within the range of this study. Despite all the limitations of this study, a positive effect of a carbon ion-implanted stent in reducing inflammatory reaction after coronary revascularization seems likely.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000086688
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2005
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  • 2
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    Online Resource
    Outcomes of Cardiac Involvement in Patients with Late-Stage Duchenne Muscular Dystrophy under Management in the Pulmonary Rehabilitation Center of a Tertiary Referral Hospital
    S. Karger AG ; 2012
    In:  Cardiology Vol. 121, No. 3 ( 2012), p. 186-193
    Details
    In: Cardiology, S. Karger AG, Vol. 121, No. 3 ( 2012), p. 186-193
    Abstract: 〈 i 〉 Objectives: 〈 /i 〉 The purpose of this study was to investigate the clinical outcome as well as the sequential changes of cardiac function in late-stage Duchenne muscular dystrophy (DMD) patients by 2-dimensional echocardiography. 〈 i 〉 Methods: 〈 /i 〉 A total of 31 individuals (initial age: 21.6 ± 5.0 years, range: 15–35 years) with late-stage DMD (Swinyard-Deaver’s stage 7 or 8) were enrolled. All of these patients had respiratory insufficiency and were on ventilator support. Sequential echocardiographic data were collected over at least 3 years. Repeated measures analysis of variance was used to compare changes in left ventricular ejection fraction (LVEF) over time. 〈 i 〉 Results: 〈 /i 〉 The sequential change in the mean LVEF showed no significant differences with initial, 1-, 2-, and 3-year follow-up LVEFs which were 42.2, 42.9, 43.8 and 42.6%, respectively (p = 0.320). In terms of the clinical outcome, all but 1 patient survived during the follow-up period of 46.5 ± 9.1 months. 〈 i 〉 Conclusions: 〈 /i 〉 The cardiac function in late-stage DMD patients showed a stabilization of LVEF on adequate ventilatory support and optimal cardiac medication therapy until their mid-30s. In addition, considering the favorable clinical outcome in our study, the process of cardiac involvement in late-stage DMD may demonstrate that in some patients it is nonprogressive.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000336810
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
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  • 3
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    The Valsalva Maneuver Can Misdiagnose ‘Normal' as ‘Pseudonormal': A Word of Caution for an Echocardiographic Evaluation of Diastolic Function
    S. Karger AG ; 2014
    In:  Cardiology Vol. 128, No. 4 ( 2014), p. 355-362
    Details
    In: Cardiology, S. Karger AG, Vol. 128, No. 4 ( 2014), p. 355-362
    Abstract: 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 To identify differences in cardiac hemodynamic changes between the Valsalva maneuver and nitroglycerin (NTG) administration. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Fifty-three subjects (37 men, 43 ± 12 years) with normal cardiac function [left ventricular ejection fraction ≥55%, early to late mitral inflow velocity ratio (E/A) ≥1, left atrial volume index ≤34 ml/m 〈 sup 〉 2 〈 /sup 〉 and early diastolic mitral annulus velocity (E') ≥8 cm/s] were enrolled. Doppler parameters were determined at rest, during the Valsalva maneuver and after NTG administration. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Decreased E, A and E/A were observed both during the Valsalva maneuver and after NTG administration (p 〈 0.0001 for all). However, the reduction in E ( & #x0394;E 〈 sub 〉 Valsalva 〈 /sub 〉 : -30 ± 16 cm/s vs. & #x0394;E 〈 sub 〉 NTG 〈 /sub 〉 : -17 ± 17 cm/s) and E/A ( & #x0394;E/A 〈 sub 〉 Valsalva 〈 /sub 〉 : -0.37 ± 0.28 vs. & #x0394;E/A 〈 sub 〉 NTG 〈 /sub 〉 : -0.19 ± 0.25) and the prolongation of the deceleration time (DT) of E ( & #x0394;DT 〈 sub 〉 Valsalva 〈 /sub 〉 : 105 ± 74 ms vs. & #x0394;DT 〈 sub 〉 NTG 〈 /sub 〉 : 83 ± 63 ms) were more prominent during the Valsalva maneuver than with NTG administration (p 〈 0.0001 for all). Particularly, a greater decrease in E' was observed during the Valsalva maneuver ( & #x0394;E' 〈 sub 〉 Valsalva 〈 /sub 〉 : -3 ± 2 cm/s vs. & #x0394;E' 〈 sub 〉 NTG 〈 /sub 〉 : -2 ± 2 cm/s, p 〈 0.0001). Eighteen subjects (34%) showed & #x0394;E/A ≥0.5 during the Valsalva maneuver; thus, they were mislabeled as ‘pseudonormal', while only 3 subjects (6%) showed & #x0394;E/A ≥0.5 after NTG administration. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The Valsalva maneuver not only decreases preload but also affects myocardial performance, thus, its use can result in the mislabeling of normal subjects as pseudonormal.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000358376
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
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  • 4
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    Online Resource
    Left Ventricular Hypercontractility Immediately after Tilting Triggers a Disregulated Cardioinhibitory Reaction in Vasovagal Syncope: Echocardiographic Evaluation during the Head-Up Tilt Test
    S. Karger AG ; 2010
    In:  Cardiology Vol. 117, No. 2 ( 2010), p. 118-123
    Details
    In: Cardiology, S. Karger AG, Vol. 117, No. 2 ( 2010), p. 118-123
    Abstract: 〈 i 〉 Objectives: 〈 /i 〉 Vasovagal syncope (VVS) has been believed to occur when mechanoreceptors are discharged by vigorous ventricular contraction. However, previous investigators have reported divergent observations regarding the presence of left ventricular (LV) hypercontractility in VVS. Because the autonomic nervous system can be promptly activated after certain stimuli, we postulated that instantaneously increased LV contractility at the time of venous pooling may trigger the disregulated vasovagal reaction in VVS. 〈 i 〉 Methods: 〈 /i 〉 Forty-seven patients (31 males, mean age 41 ± 18 years) with unexplained syncope were enrolled. Echocardiography was performed during the head-up tilt test (HUTT) as follows: baseline, passive tilting (0 and 20 min), and tilting with isoproterenol administration (5 and 10 min). Patients were divided into 2 groups according to the results of the HUTT; group 1 (n = 12) had a positive result and group 2 had a negative response. 〈 i 〉 Results: 〈 /i 〉 LV ejection fraction (LVEF), determined immediately after tilting, increased in group 1, whereas LVEF decreased in group 2 (p = 0.032). Although left atrial and LV volumes decreased similarly during the test, group 1 showed a progressive reduction in LVEF, while LVEF progressively increased in group 2 (p = 0.007). 〈 i 〉 Conclusion: 〈 /i 〉 Patients with HUTT-induced VVS presented LV hypercontractions immediately after tilting and a subsequent decrease in LV contractility. An instantaneous activation of the sympathetic nervous system at the time of venous pooling may trigger an early disregulated vasovagal reflex via an increase in LV contractility in VVS.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000320141
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
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  • 5
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    Phenotypic Spectrum and Clinical Characteristics of Apical Hypertrophic Cardiomyopathy: Multicenter Echo-Doppler Study
    S. Karger AG ; 2008
    In:  Cardiology Vol. 110, No. 1 ( 2008), p. 53-61
    Details
    In: Cardiology, S. Karger AG, Vol. 110, No. 1 ( 2008), p. 53-61
    Abstract: 〈 i 〉 Objectives: 〈 /i 〉 The aim of this study was to define the phenotypic spectrum of apical hypertrophic cardiomyopathy (ApHCM) and clinical characteristics pertaining to identified subtypes. 〈 i 〉 Methods: 〈 /i 〉 In 182 consecutive ApHCM patients (58.9 ± 11.2 years; 142 men) with left ventricular ejection fraction ≧50%, we measured end-diastolic wall thickness of all 16 left ventricular segments to determine patterns of hypertrophy. Echo-Doppler parameters, electrocardiography patterns, and clinical findings were analyzed. 〈 i 〉 Results: 〈 /i 〉 ApHCM was classified into three types as pure focal (n = 81), pure diffuse (n = 70) and mixed type (n = 31) according to patterns of hypertrophy. Incidence of atrial fibrillation (5% for pure focal vs. 11% for pure diffuse vs. 23% for mixed type, p 〈 0.05) and left atrial volume index (30.9 ± 11.8, 35.7 ± 14.8, and 41.3 ± 15.9 ml/m 〈 sup 〉 2 〈 /sup 〉 , respectively, p 〈 0.001) were significantly different among subtypes. Peak systolic (6.6 ± 1.0 vs. 6.3 ± 1.2 vs. 5.9 ± 1.1 cm/s, respectively, p 〈 0.05), diastolic (5.1 ± 1.8 vs. 5.0 ± 1.2 vs. 4.1 ± 1.3 cm/s, respectively, p 〈 0.05) mitral annular velocity, E/E′ (13.3 ± 4.2 vs. 13.7 ± 5.4 vs. 16.1 ± 6.1, respectively, p 〈 0.05) were also significantly different. 〈 i 〉 Conclusions: 〈 /i 〉 ApHCM contains three morphologically distinct phenotypes and detailed subtyping is important in the prediction of development of atrial fibrillation, left atrial volume index and left ventricular longitudinal function.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000109407
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
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  • 6
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    1,2,4,5-Tetramethoxybenzene Suppresses House Dust Mite-Induced Allergic Inflammation in BALB/c Mice
    S. Karger AG ; 2016
    In:  International Archives of Allergy and Immunology Vol. 170, No. 1 ( 2016), p. 35-45
    Details
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 170, No. 1 ( 2016), p. 35-45
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Atopic dermatitis (AD) is the most common allergic inflammatory skin disease. The activation of innate immunity by house dust mite ( 〈 i 〉 Dermatophagoides farinae 〈 /i 〉 extract, DFE) allergen plays an important role in the pathogenesis of AD. We previously showed the inhibitory effect of an extract of 〈 i 〉 Amomum xanthioides 〈 /i 〉 on allergic diseases, and isolated 1,2,4,5-tetramethoxybenzene (TMB) as a major active component. In this study, we investigated whether TMB relieves DFE-induced allergic inflammation symptoms. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We established a DFE-induced allergic inflammation model in BALB/c mice by repeated skin exposure to DFE. To define the underlying mechanisms of action, we used a tumor necrosis factor-α and interferon- & #947;-activated human keratinocytes (HaCaT cell line) and mouse keratinocytes (3PC cell line) cell line model. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Oral administration of TMB suppressed allergic inflammation symptoms, such as histopathological analysis and ear thickness, in addition to serum IgE, DFE-specific IgE and IgG2a levels. TMB decreased the serum histamine levels and tissue infiltration of inflammatory cells, including mast cells and eosinophils. TMB also inhibited CD4 〈 sup 〉 + 〈 /sup 〉 IFN- & #947; 〈 sup 〉 + 〈 /sup 〉 , CD4 〈 sup 〉 + 〈 /sup 〉 IL-4 〈 sup 〉 + 〈 /sup 〉 , and CD4 〈 sup 〉 + 〈 /sup 〉 IL-17A 〈 sup 〉 + 〈 /sup 〉 lymphocyte expansion in the draining lymph nodes and expression of the Th2 cytokines in the ear tissue. TMB significantly inhibited the expression of cytokines and chemokines by the downregulation of the mitogen-activated protein kinases and nuclear factor of activated cytoplasmic T cells in HaCaT cells. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 TMB improved DFE-induced allergic inflammation by suppressing the production of proinflammatory cytokines and chemokines. Our results suggest that TMB might be a potential therapeutic agent for AD.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    URL: Article
    DOI: 10.1159/000446510
    RVK:
    XA 49650
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482722-0
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  • 7
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    Online Resource
    Urinary Soluble HLA Class I Antigen in Patients with Minimal Change Disease: A Predictor of Steroid Response
    S. Karger AG ; 1998
    In:  Nephron Vol. 79, No. 1 ( 1998), p. 44-49
    Details
    In: Nephron, S. Karger AG, Vol. 79, No. 1 ( 1998), p. 44-49
    Abstract: In primary minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS), increased lymphocyte reactivity to renal antigens has been defined. Soluble HLA class I antigen (sHLA-I) is actively secreted by T and B lymphocytes when they are stimulated by mitogens, antigens and lymphokines. To determine if serum and urine sHLA-I levels could predict steroid response in patients with MCD and differentiate those from FSGS, we have investigated 45 healthy controls, biopsy-proven 17 patients with MCD (edema and 24-hour urine protein 〉 3.5 g/day), 8 patients with FSGS (24-hour urine protein 〉 1 g/day) and 10 patients with membranous nephropathy (MGN) (24-hour urine protein 〉 1 g/day). Before and after prednisone therapy (1 mg/kg/day or 2 mg/kg/EOD for 8 weeks), the levels of serum and urinary sHLA-I were measured by ELISA (sHLA-STAT; Sangstat Co., Calif., USA). After 8 weeks of treatment, 10 patients with MCD were responders (MCD-CR) while the other 7 patients with MCD were nonresponders (MCD-NR). Three of 7 patients with MCD-NR were re-biopsied and finally diagnosed as FSGS. They were included in the data of patients with FSGS. In healthy controls, serum sHLA-I was detected (415 ± 256 ng/ml), but urinary sHLA-I was not. At entry, there were no differences in age, sex, serum Cr and 24-hour urine protein among the patients with MCD-CR, MCD-NR and FSGS, but serum albumin was significantly elevated in patients with FSGS and MGN (p 〈 0.05). Serum sHLA-I levels were notably elevated in MCD-CR (1,040 ± 1,066 ng/ml), in MCD-NR (668 ± 315 ng/ml) and in FSGS (713 ± 790 ng/ml), but not in patients with MGN (444 ± 86 ng/ml) when compared with controls (p 〈 0.05). On the other hand, urinary sHLA-I levels in MCD-NR (541 ± 239 ng/mg Cr) and in FSGS (457 ± 239 ng/mg Cr) were significantly higher than those in MGN (125 ± 28 ng/mg Cr) and in MCD-CR (100 ± 42 ng/mg Cr, p 〈 0.05) and these substantial differences were maintained for 8 weeks. In all patients, serum and urinary sHLA-I levels were not reduced during 8 weeks of steroid therapy. We conclude that elevated serum and urinary sHLA-I levels reflect increased cellular immune response and disease activity in patients with MCD and FSGS. In patients with MCD, urinary sHLA-I may be an easily measurable indicator of predicting steroid response, while MCD-NR with high urinary sHLA-I levels might be re-evaluated for the possibility of FSGS.
    Type of Medium: Online Resource
    ISSN: 1660-8151 , 2235-3186
    URL: Article
    DOI: 10.1159/000044990
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 2810853-X
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  • 8
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    Exogenous Hydrogen Peroxide Induces Lipid Raft-Mediated STAT-6 Activation in T Cells
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 42, No. 6 ( 2017), p. 2467-2480
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 42, No. 6 ( 2017), p. 2467-2480
    Abstract: Background/Aims: CD4+ T cells are a critical component of the adaptive immune response. While the mechanisms controlling the differentiation of the Th1, Th17, and regulatory T cell subsets from naïve CD4+ T cells are well described, the factors that induce Th2 differentiation are still largely unknown. Methods: The effects of treatment with exogenous H2O2 on STAT-6 phosphorylation and activation in T cells were examined by immunoblotting, immunofluorescence and gel shift assay. Anti-CD3 antibody and methyl-β-cyclodextrin were utilized to induce lipid raft assembly and to investigate the involvement of lipid rafts, respectively. Results: Jurkat and EL-4 T cells that were exposed to H2O2 showed rapid and strong STAT-6 phosphorylation, and the extent of STAT-6 phosphorylation was enhanced by co-treatment with anti-CD3 antibody. The effect of H2O2 on STAT-6 phosphorylation and translocation was inhibited by disruption of lipid rafts. STAT-6 activation in response to H2O2 treatment regulated IL-4 gene expression, and this response was strengthened by treatment with anti-CD3. Conclusion: Our results indicate that reactive oxygen species such as H2O2 can act on upstream and initiating factors for activation of STAT-6 in T cells and contribute to formation of a positive feedback loop between STAT-6 and IL-4 in the Th2 differentiation process.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000480210
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 9
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    Rag2 Deficiency Enhances Susceptibility to Systemic Mouse Adenovirus Type 1 Infection
    S. Karger AG ; 2022
    In:  Intervirology Vol. 65, No. 3 ( 2022), p. 134-143
    Details
    In: Intervirology, S. Karger AG, Vol. 65, No. 3 ( 2022), p. 134-143
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Recombination-activating gene ( 〈 i 〉 Rag 〈 /i 〉 ) 1 and 〈 i 〉 Rag2 〈 /i 〉 , which are essential in V(D)J recombination, play a crucial role in B- and T-cell maturation. 〈 b 〉 〈 i 〉 Method: 〈 /i 〉 〈 /b 〉 We investigated the effects of 〈 i 〉 Rag2 〈 /i 〉 deficiency in clustered regularly interspaced short palindromic repeats/Cas9-mediated FVB- 〈 i 〉 Rag2 〈 /i 〉 knockout (KO) and wild-type (WT) mice infected with mouse adenovirus type 1 (MAV-1) via the intranasal route. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 MAV-1 infection caused more severe histopathological changes in FVB- 〈 i 〉 Rag2 〈 /i 〉 KO mice than in WT mice. FVB- 〈 i 〉 Rag2 〈 /i 〉 KO mice exhibited moderate to severe inflammation on day 4 and severe inflammation on day 8 post infection. In contrast, WT mice showed mild inflammation on day 4 and mild to severe inflammation on day 8 post infection, including interstitial pneumonia and inflammatory cell infiltration in the lungs and liver. Viral loads in the spleen and kidneys were significantly higher in FVB- 〈 i 〉 Rag2 〈 /i 〉 KO mice than in WT mice on day 8 post infection. Levels of cytokines and chemokines, including macrophage inflammatory protein-1α, induced protein 10, interferon (IFN)-α, IFN-γ, and tumor necrosis factor alpha, were upregulated in the spleens of FVB- 〈 i 〉 Rag2 〈 /i 〉 KO mice compared with those of WT mice. The upregulation of several cytokines occurred concurrently with the histopathological changes. MAV-1 infection induced more severe systemic infection in FVB- 〈 i 〉 Rag2 〈 /i 〉 KO mice than in WT mice. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 In mice, 〈 i 〉 Rag2 〈 /i 〉 deficiency induces inflammatory cell recruitment via the upregulation of cytokine and chemokine levels. The MAV-1 infection model can be utilized to assess the efficacy and safety of therapeutic agents for human adenoviral diseases.
    Type of Medium: Online Resource
    ISSN: 0300-5526 , 1423-0100
    URL: Article
    DOI: 10.1159/000520463
    RVK:
    XA 10000
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1482863-7
    SSG: 12
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  • 10
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    Protective Role for bcl-2 in Experimentally Induced Cell Death of Bovine Corneal Endothelial Cells
    S. Karger AG ; 1999
    In:  Ophthalmic Research Vol. 31, No. 4 ( 1999), p. 287-296
    Details
    In: Ophthalmic Research, S. Karger AG, Vol. 31, No. 4 ( 1999), p. 287-296
    Abstract: To characterize the pattern of cell death and to investigate the potential role of bcl-2 in a death paradigm of corneal endothelial cells, primary cultures of bovine corneal endothelial (BCEN) cells were first established and treated with 0.01–1 µ 〈 i 〉 M 〈 /i 〉 staurosporine, a nonspecific protein kinase inhibitor. The pattern of BCEN cell death induced by staurosporine was apoptotic in nature, characterized by shrinkage of the cytoplasmic membrane, nuclear condensation and DNA fragmentation. Cotreatment of BCEN cells with Z-VAD-fmk (a caspase inhibitor) but not cycloheximide (a protein synthesis inhibitor) prevented staurosporine-induced cell death. To investigate the potential role of bcl-2, BCEN cells were transferred with a eukaryotic expression vector containing anti-apoptotic bcl-2 cDNA and characterized by reverse transcription-polymerase chain reaction (RT-PCR; BCEN/bcl-2). As measured by the MTT reduction assay after treatment with staurosporine, the survival rate of BCEN/bcl-2 cells was 48.0 ± 4.8% compared to 7.4 ± 2.1% in control BCEN cells. As determined by light microscopy, apoptotic changes such as nuclear condensation and apoptotic bodies were largely attenuated in BCEN/bcl-2 cells after staurosporine treatment although arborization of processes and rounding up of the cell body were not affected by overexpression of bcl-2. These results suggest that staurosporine induces apoptosis in a cycloheximide-independent but caspase-dependent manner and bcl-2 acts as a negative regulator in staurosporine-induced apoptosis of BCEN cells.
    Type of Medium: Online Resource
    ISSN: 0030-3747 , 1423-0259
    URL: Article
    DOI: 10.1159/000055549
    RVK:
    XA 10000
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1999
    detail.hit.zdb_id: 1483177-6
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