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  • 1
    Online Resource
    Online Resource
    All-Trans Retinoic Acid Induces DU145 Cell Cycle Arrest through Cdk5 Activation
    S. Karger AG ; 2014
    In:  Cellular Physiology and Biochemistry Vol. 33, No. 6 ( 2014), p. 1620-1630
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 33, No. 6 ( 2014), p. 1620-1630
    Type of Medium: Online Resource
    ISSN: 1421-9778 , 1015-8987
    URL: Article
    DOI: 10.1159/000358724
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 2
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    Effect of Ultrafiltration versus Intravenous Furosemide for Decompensated Heart Failure in Cardiorenal Syndrome: A Systematic Review with Meta-Analysis of Randomized Controlled Trials
    S. Karger AG ; 2015
    In:  Nephron Vol. 129, No. 3 ( 2015), p. 189-196
    Details
    In: Nephron, S. Karger AG, Vol. 129, No. 3 ( 2015), p. 189-196
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Ultrafiltration is an adjunctive treatment for decompensated heart failure patients with cardiorenal syndrome. The efficacy and safety of ultrafiltration in the patient cohort are still unknown. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We systematically reviewed and evaluated randomized controlled trials, comparing diuretics with ultrafiltration in adult patients with decompensated heart failure and cardiorenal syndrome through January 2014. The primary outcomes were body weight loss and total fluid removal. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 We identified 8 trials including 608 patients. In a random-effects model, the pooled difference of body weight loss was 1.44 kg between patients receiving ultrafiltration and diuretics (95% CI, 0.29-2.59; p = 0.01). The difference of fluid removal was 1.28 l between groups (95% CI, 0.43-2.12; p = 0.003). The RR for mortality was 0.90 for ultrafiltration compared with diuretics (95% CI, 0.61-1.33; p = 0.60) and the RR for renal function deterioration was 1.29 (95% CI, 0.90-1.85; p = 0.17). There is a trend toward reducing readmission rate in ultrafiltration group. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Ultrafiltration is a safe and effective strategy in the treatment of cardiorenal syndrome without increasing the risk of renal deterioration.
    Type of Medium: Online Resource
    ISSN: 1660-8151 , 2235-3186
    URL: Article
    DOI: 10.1159/000371447
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 2810853-X
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  • 3
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    Online Resource
    Hyperphosphate-Induced Myocardial Hypertrophy through the GATA-4/NFAT-3 Signaling Pathway Is Attenuated by ERK Inhibitor Treatment
    S. Karger AG ; 2015
    In:  Cardiorenal Medicine Vol. 5, No. 2 ( 2015), p. 79-88
    Details
    In: Cardiorenal Medicine, S. Karger AG, Vol. 5, No. 2 ( 2015), p. 79-88
    Abstract: 〈 b 〉 〈 i 〉 Background/Aims: 〈 /i 〉 〈 /b 〉 Numerous epidemiological studies have associated elevated serum phosphorus levels with cardiovascular disease and the risk of death in the general population as well as in chronic kidney disease (CKD) and dialysis patients. In this study, we explored whether elevated phosphate conditions induce cardiac hypertrophy and attempted to identify the molecular and cellular mechanisms in the hypertrophic response. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 H9c2 myocardial cells were incubated in high-phosphate conditions to induce hypertrophy. Pathological hypertrophic responses were measured in terms of cell size, arrangement of actin filaments, and hypertrophy markers such as atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in myocardial cells. Several transcriptional factors involved in cardiac hypertrophy development were measured to investigate the molecular pathways involved in elevated phosphate-induced cardiac hypertrophy. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 High-phosphate conditions induced cellular hypertrophy, marked by increased cell size, reorganization of actin filaments, and upregulation of both ANP and BNP in H9c2 cells. Both upstream calcineurin and downstream transcription factors, including GATA-4 and NFAT-3, were significantly increased under hyperphosphate conditions. Moreover, both MEK1/2 and ERK1/2 expression increased significantly, and cellular hypertrophy was markedly attenuated by U0126, an ERK1/2 inhibitor. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 These results suggest that hyperphosphate conditions induce myocardial hypertrophy through the ERK signaling pathway in H9c2 cells. Our findings provide a link between the hyperphosphate-induced response and the ERK/NFAT-3 signaling pathway that mediates the development of cardiac hypertrophy. In view of the potent and selective activity of the ERK inhibitor U0126, this agent warrants further investigation as a candidate for preventing hyperphosphate-induced cardiac hypertrophy in CKD and dialysis patients.
    Type of Medium: Online Resource
    ISSN: 1664-3828 , 1664-5502
    URL: Article
    DOI: 10.1159/000371454
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 2595659-0
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  • 4
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    Online Resource
    Evaluating the Effect of a Community-Based Lay Health Advisor Training Curriculum to Address Immigrant Children's Caries Disparities
    S. Karger AG ; 2015
    In:  Caries Research Vol. 49, No. 2 ( 2015), p. 147-156
    Details
    In: Caries Research, S. Karger AG, Vol. 49, No. 2 ( 2015), p. 147-156
    Abstract: Previous programs had not designed the culturally adequate Lay Health Advisor (LHA) oral health training curriculum for medically underserved population. We evaluated the effects of LHA training curriculum for addressing immigrant children's caries disparities in their access to dental care. We used a pre/post-test study design. Immigrant women were recruited from churches, schools, and immigrant centers in an urban area. Four training classes were held. Each training cycle lasted 15 consecutive weeks, consisting of 1 weekly 2-h training session for 12 weeks followed by a 3-week practicum. The curriculum included training in caries-related knowledge, oral hygiene demonstrations, teaching techniques, communication skills, and hands-on practice sessions. Thirty-seven LHA trainees completed the course and passed the post-training exam. The data were collected using self-report questionnaires. The level of oral health knowledge, self-efficacy and attitudes toward oral hygiene were significantly increased after LHA training. There was a significant and over twofold increase in trainees' oral hygiene behaviors. An increase of 〉 20% in LHA and their children's dental checkup was observed following training. After training, LHAs were more likely to have 3+ times of brushing teeth [Odds Ratio (OR) = 13.14], brushing teeth 3+ minutes (OR = 3.47), modifie d bass method use (OR = 30.60), dental flossing (OR = 4.56), fluoride toothpaste use (OR = 5.63) and child's dental visit (OR = 3.57). The cross-cultural training curriculum designed for immigrant women serving as LHAs was effective in improvement of oral hygiene behaviors and access to dental care.
    Type of Medium: Online Resource
    ISSN: 0008-6568 , 1421-976X
    URL: Article
    DOI: 10.1159/000363067
    RVK:
    XA 36250
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482046-8
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  • 5
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    Online Resource
    17β-Estradiol and/or Estrogen Receptor β Attenuate the Autophagic and Apoptotic Effects Induced by Prolonged Hypoxia Through HIF-1α-Mediated BNIP3 and IGFBP-3 Signaling Blockage
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 36, No. 1 ( 2015), p. 274-284
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 36, No. 1 ( 2015), p. 274-284
    Abstract: Background/Aims: The risk of heart disease is higher in males than in females. However, this advantage of females declines with increasing age, presumably a consequence of decreased estrogen secretion and malfunctioning of the estrogen receptor. We previously demonstrated that 17β-estradiol (E2) prevents cardiomyocyte hypertrophy, autophagy and apoptosis via estrogen receptor α (ERα), but the effects of ERβ on myocardial injury remained elusive. The present paper thus, investigated the cardioprotective effects of estrogen (E2) and ERβ against hypoxia-induced cell death. Methods: Transient transfection of Tet-On ERβ gene construct was used to overexpress ERβ in hypoxia-treated H9c2 cardiomyoblast cells. Results: Our data revealed that IGF1R, Akt phosphorylation and Bcl-2 expression are enhanced by ERβ in H9c2 cells. Moreover, ERβ overexpression reduced accumulation of hypoxia-related proteins, autophagy-related proteins and mitochondria-apoptotic proteins and enhanced the protein levels of Bcl-2, pAkt and Bad under hypoxic condition. In neonatal rat ventricular myocytes (NRVMs), we observed that hypoxia induced cell apoptosis as measured by TUNEL staining, and E2 and/or ERβ could totally abolish hypoxia-induced apoptosis. The suppressive effects of E2 and/or ERβ in hypoxia-treated NRVMs were totally reversed by ER antagonist, ICI. Taken together, E2 and/or ERβ exert the protective effect through repressed hypoxia-inducible HIF-1α, BNIP3 and IGFBP-3 levels to restrain the hypoxia-induced autophagy and apoptosis effects in H9c2 cardiomyoblast cells. Conclusion: The results suggest that females probably could tolerate better prolonged hypoxia condition than males, and E2/ERβ treatment could be a potential therapy to prevent hypoxia-induced heart damage.”
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000374070
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 6
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    Tetramethylpyrazine Ameliorated Hypoxia-Induced Myocardial Cell Apoptosis via HIF-1α/JNK/p38 and IGFBP3/BNIP3 Inhibition to Upregulate PI3K/Akt Survival Signaling
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 36, No. 1 ( 2015), p. 334-344
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 36, No. 1 ( 2015), p. 334-344
    Abstract: Background: Hemorrhagic shock (HS) is the major cause of death from trauma. Hemorrhagic shock may lead to cellular hypoxia and organ damage. Our previous findings showed that HS induced a cardiac apoptosis pathway and synergistically caused myocardial cell damage in diabetic rats under trauma-induced HS. Tetramethylpyrazine (TMP) is a major biologically active ingredient purified from the rhizome of Ligusticum wallichii (called Chuang Xiong in Chinese). Chuan Xiong rescued cells from synergistic cardiomyoblast cell injury under high-glucose (HG) conditions plus hypoxia. TMP is one of the most important active ingredients that elevated the survival rate in ischemic brain injury and prevented inducible NO synthase expression to have anti-inflammatory effects against cell damage in different cell types. Method: Here, we further investigate whether TMP can protect against hypoxic ( 〈 1% oxygen) conditions in H9c2 cardiomyoblast cells for 24 hrs. Results: Our results showed that hypoxia mediated through HIF-1α/JNK/p38 activation significantly elevated the levels of the hypoxia-related proteins HIF-1α, BNIP3 and IGFBP3, further enhanced the pro-apoptotic protein Bak and upregulated downstream Caspase 9 and 3, resulting in cell death. All of these phenomena were fully recovered under TMP treatment. We observed that TMP exerted this effect by activating the IGF1 receptor survival pathway, dependent primarily on PI3K/Akt. When PI3K (class I) was blocked by specific siRNA, the hypoxia-induced activated caspase 3 and cell apoptosis could not be reversed by TMP treatment. Conclusion: Our results strongly suggest that TMP could be used to restore hypoxia-induced myocardial cell apoptosis and cardiac hypoxic damage.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000374076
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 7
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    Elevated Phosphate Levels Trigger Autophagy-Mediated Cellular Apoptosis in H9c2 Cardiomyoblasts
    S. Karger AG ; 2018
    In:  Cardiorenal Medicine Vol. 8, No. 1 ( 2018), p. 31-40
    Details
    In: Cardiorenal Medicine, S. Karger AG, Vol. 8, No. 1 ( 2018), p. 31-40
    Abstract: Background/Aim: In chronic kidney disease (CKD), kidneys fail to maintain phosphorus homeostasis in serum. Elevated phosphorus levels in serum have been associated with cardiovascular diseases in CKD patients and in normal individuals. In this study, we evaluated the level of autophagy- and apoptosis-related markers under different concentrations of hyperphosphate in myocardial cells. Methods: Modulation inflicted on the levels of various survival-, autophagy-, and apoptosis-related markers were determined by Western blotting analysis using total protein extract. FITC-annexin V staining was performed to quantify the apoptotic cells in all groups. Results: Hyperphosphate treatments showed to induce autophagy-related proteins beclin-1, ATG7, and LC3 II through the pAMPK-ULK1 pathway in Western blotting analysis. Further, apoptosis-associated proteins such as Bax, Bid, cytochrome 〈 i 〉 c 〈 /i 〉 , and c-caspase-9 were also upregulated with hyperphosphate treatment. 3-Methyladenine, an autophagy inhibitor, inhibited apoptosis significantly in FITC-annexin V staining, and the inhibition of Bax, cytochrome 〈 i 〉 c 〈 /i 〉 , and c-caspase-3 was shown by Western blotting. Conclusion: The results suggest that hyperphosphate in H9c2 cardiomyoblasts would lead to cellular apoptosis via autophagy, which is mediated by the pAMPK signaling pathway. Our findings revealed the possible mechanism responsible for the heart damage under hyperphosphatemia.
    Type of Medium: Online Resource
    ISSN: 1664-3828 , 1664-5502
    URL: Article
    DOI: 10.1159/000479010
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 2595659-0
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  • 8
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    Low-Dose Heparin Retention in Temporary Hemodialysis Double-Lumen Catheter Does Not Increase Catheter Occlusion and Might Reduce Risk of Bleeding
    S. Karger AG ; 2011
    In:  Blood Purification Vol. 32, No. 3 ( 2011), p. 232-237
    Details
    In: Blood Purification, S. Karger AG, Vol. 32, No. 3 ( 2011), p. 232-237
    Abstract: 〈 i 〉 Background: 〈 /i 〉 The objective of this study was to assess the impact of heparin concentration retained in temporary double-lumen catheters on bleeding risk. 〈 i 〉 Methods: 〈 /i 〉 Activated partial thromboplastin time (aPTT) was measured in patients hemodialyzed via double-lumen catheters. Heparin solutions of 5,000 U/ml (group 1, n = 95) and 1,000 U/ml (group 2, n = 89) were randomly retained in catheters after placement and each hemodialysis (HD) session. Blood transfusion, bleeding episodes, and changes of hematocrit were recorded. 〈 i 〉 Results: 〈 /i 〉 The aPTT at the beginning of HD or 10 min after heparin lock was significantly prolonged, which was more prominent in the 5,000 U/ml group, whereas the aPTT declined to baseline values at the end of HD or before the next dialysis session in both groups. Infection and occlusion rates were similar in both groups. More patients suffered from major bleeding and prominent decline of hematocrit in the 5,000 U/ml group. 〈 i 〉 Conclusions: 〈 /i 〉 Low-dose heparin (1,000 U/ml) retention in double-lumen catheters for temporary HD maintains comparable catheter patency and might reduce the bleeding risk.
    Type of Medium: Online Resource
    ISSN: 0253-5068 , 1421-9735
    URL: Article
    DOI: 10.1159/000328743
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1482025-0
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  • 9
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    Online Resource
    Bioactive Peptide Improves Diet-Induced Hepatic Fat Deposition and Hepatocyte Proinflammatory Response in SAMP8 Ageing Mice
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 48, No. 5 ( 2018), p. 1942-1952
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 48, No. 5 ( 2018), p. 1942-1952
    Abstract: Background/Aims: High-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) poses therapeutic challenges in elderly subjects. Due to lack of efficient drug therapy, plant-based bioactive peptides have been studied as alternative strategy in NAFLD and for less toxicity in elderly. To mimic fatty liver in aging conditions, researchers highly commended the genetically engineered strains SAMP8 (senescence-accelerated mice prone 8). However, there is a paucity of reports about the anti-steatosis effects of bioactive peptides against fatty liver development under a combined action of high-fat diet exposure and aging process. This study was conducted to evaluate the activity of DIKTNKPVIF peptide synthesized from alcalase-generated potato protein hydrolysate (PH), on reducing HFD-driven and steatosis-associated proinflammatory reaction in ageing model. Methods: Five groups of six-month-old SAMP8 mice (n=4, each) were fed either a normal chow (NC group) for 14 weeks upon sacrifice, or induced with a 6-week HFD feeding, then treated without (HCO group) or with an 8-week simultaneous administration of peptide (HPEP group), protein (HPH group) or probucol (HRX group). Liver organs were harvested from each group for histological analysis and immunoblot assay. Results: In contrast to NC, extensive fat accumulation was visualized in the liver slides of HCO. Following the trends of orally administered PH, intraperitoneally injected peptide reduces hepatic fat deposition and causes at protein level, a significant decrease in HFD-induced proinflammatory mediators p-p38 MAPK, FGF-2, TNF-α, IL-6 with concomitant reactivation of AMPK. However, p-Foxo1 and PPAR-α levels were slightly changed. Conclusion: Oral supplementation of PH and intraperitoneal injection of derived bioactive peptide alleviate proinflammatory reaction associated with hepatosteatosis development in elderly subjects, through activation of AMPK.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000492518
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 10
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    Plasma Cell-Free Adenomatous Polyposis Coli Gene Promoter Methylation as a Prognostic Biomarker for Hepatocellular Carcinoma
    S. Karger AG ; 2024
    In:  Oncology
    Details
    In: Oncology, S. Karger AG
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Hepatocellular carcinoma (HCC) is a leading cause of cancer death worldwide. Lack of biomarkers for follow-up after treatment is a clinical challenge. DNA methylation has been proposed to be a potential biomarker in HCC. However, there is still a lack of evidence of its clinical use. This study aimed to evaluate the value of using plasma Adenomatous Polyposis Coli promoter methylation level (APC-MET) as a potential biomarker in HCC treatment. 〈 b 〉 〈 i 〉 Method: 〈 /i 〉 〈 /b 〉 A total of 96 patients with HCC at BCLC stage B who underwent local tumor ablation treatment were prospectively included in this study. APC-MET was examined in the plasma of each patient before and 1 month after treatment. The prediction value of APC-MET for survival outcome and disease status after treatment was analyzed and adjusted with alpha-fetoprotein and protein induced by vitamin K absence-II using Cox regression analysis. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Univariate Cox regression analysis showed preoperative APC-MET & gt;0 (HR, 2.9, 95% CI: 1.05–8.05, 〈 i 〉 p 〈 /i 〉 = 0.041) and postoperative APC-MET & gt;0 (HR, 3.47, 95% CI: 1.16–10.4, 〈 i 〉 p 〈 /i 〉 = 0.026) were both predictors of death, and preoperative APC-MET & gt;0 was a predictor of disease progression after treatment (HR, 2.04, 95% CI: 1.21–3.44, 〈 i 〉 p 〈 /i 〉 = 0.007). In multivariate models, preoperative APC-MET & gt;0 was a significant predictor of disease progression after adjusting with the other two traditional biomarkers (HR, 1.82, 95% CI: 1.05–3.17, 〈 i 〉 p 〈 /i 〉 = 0.034). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Hypermethylation of APC promoter appears to be a potential biomarker that could predict patient survival and disease progression outcomes in patients with intermediate-stage HCC after local ablation treatment.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    URL: Article
    DOI: 10.1159/000538455
    RVK:
    XH 3305
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2024
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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