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  • 1
    Online Resource
    Online Resource
    Non-Hodgkin's Lymphoma following Acute Myeloid Leukemia in Complete Remission
    S. Karger AG ; 1998
    In:  Acta Haematologica Vol. 100, No. 2 ( 1998), p. 97-98
    Details
    In: Acta Haematologica, S. Karger AG, Vol. 100, No. 2 ( 1998), p. 97-98
    Type of Medium: Online Resource
    ISSN: 0001-5792 , 1421-9662
    URL: Article
    DOI: 10.1159/000040875
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1481888-7
    detail.hit.zdb_id: 80008-9
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  • 2
    Online Resource
    Online Resource
    Hypoxia Promotes Extravillous Trophoblast Cell Invasion through the Hypoxia-Inducible Factor Urokinase-Type Plasminogen Activator Receptor Pathway
    S. Karger AG ; 2022
    In:  Gynecologic and Obstetric Investigation Vol. 87, No. 3-4 ( 2022), p. 232-241
    Details
    In: Gynecologic and Obstetric Investigation, S. Karger AG, Vol. 87, No. 3-4 ( 2022), p. 232-241
    Abstract: 〈 b 〉 〈 i 〉 Objectives: 〈 /i 〉 〈 /b 〉 Hypoxia is a common feature of extravillous trophoblast (EVT) cells that promote invasion during the early stages of human placentation. This study aimed to examine whether hypoxia-induced an invasive phenotype in EVT cells in vitro and explore the underlying molecular mechanisms. 〈 b 〉 〈 i 〉 Design: 〈 /i 〉 〈 /b 〉 The invasiveness of primary EVT cells isolated from the first trimester placental tissues during weeks 5–8 of gestation was examined under hypoxic (5% O 〈 sub 〉 2 〈 /sub 〉 ) and normoxic (20% O 〈 sub 〉 2 〈 /sub 〉 ) conditions. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Invasiveness was determined by transwell and wound-healing invasion assays using the IncuCyte ZOOM™ Live-Cell Imaging System. Protein expression of the urokinase plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor of hypoxia or normoxia-treated cells was measured using Western blot analysis. Knockdown of hypoxia-inducible factor-1 alpha (HIF-1α) was assessed using small interfering RNA (siRNA). 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Hypoxia enhanced EVT cell invasion but did not affect apoptosis. The stimulatory effect of hypoxia on EVT cell invasiveness was associated with induction of the uPA-uPAR pathway. The synthetic inhibitor of uPAR significantly inhibited hypoxia-induced EVT cell invasion. Silencing of HIF-1α by siRNA abolished the stimulatory effect of hypoxia and inhibited the upregulation of uPAR expression, suggesting that the HIF-1α-uPAR signal is the key mediator for hypoxia-induced EVT cell invasion. Further experiments need to be performed to elucidate the HIF-1α-uPAR signal pathways. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The low oxygen-regulated early events of EVT invasion may be mediated by the HIF-1α-uPAR pathway.
    Type of Medium: Online Resource
    ISSN: 0378-7346 , 1423-002X
    URL: Article
    DOI: 10.1159/000525851
    RVK:
    XA 45603
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1482695-1
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  • 3
    Online Resource
    Online Resource
    Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism
    S. Karger AG ; 2010
    In:  Gynecologic and Obstetric Investigation Vol. 70, No. 2 ( 2010), p. 138-144
    Details
    In: Gynecologic and Obstetric Investigation, S. Karger AG, Vol. 70, No. 2 ( 2010), p. 138-144
    Abstract: 〈 i 〉 Aims: 〈 /i 〉 To identify factors leading to fatality of patients with amniotic fluid embolism (AFE). 〈 i 〉 Methods: 〈 /i 〉 Patients who had fatal or nonfatal AFE were registered at the Hamamatsu University School of Medicine in the Department of Obstetrics and Gynecology from 1992 to 2006. Data collected included information about demographics and clinical characteristics. The fatal factors among these data were identified using χ 〈 sup 〉 2 〈 /sup 〉 analysis and the Mann-Whitney test. 〈 i 〉 Results: 〈 /i 〉 One hundred and thirty-five patients met the criteria, which included fatal (n = 65) and nonfatal AFE (n = 70). Maternal full-term gestational weeks, multiparous and noncesarean sections were the risk factors for death found in this study (p 〈 0.01). Sialyl Tn levels (mean ± SD) in the serum of patients with fatal AFE (69.7± 126.4 U/ml) were higher compared to those with nonfatal AFE (48.3± 161.8 U/ml; p = 0.003). Each of three items (cardiac arrest, dyspnea or loss of consciousness) was more common in fatal AFE (p 〈 0.01). Maternal pregnancy and labor complications were not associated with the distinction between fatal and nonfatal AFE. 〈 i 〉 Conclusion: 〈 /i 〉 Factors associated with patients with fatal AFE were identified. These included multiparity, noncesarean section at full-term and the three symptoms mentioned above. Sialyl Tn levels could be a possible prognostic fatality factor.
    Type of Medium: Online Resource
    ISSN: 0378-7346 , 1423-002X
    URL: Article
    DOI: 10.1159/000313302
    RVK:
    XA 45603
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1482695-1
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  • 4
    Online Resource
    Online Resource
    Anticytokine Therapy in Preterm Labor: Current Knowledge and Future Perspectives
    S. Karger AG ; 2011
    In:  Gynecologic and Obstetric Investigation Vol. 71, No. 1 ( 2011), p. 1-10
    Details
    In: Gynecologic and Obstetric Investigation, S. Karger AG, Vol. 71, No. 1 ( 2011), p. 1-10
    Abstract: 〈 i 〉 Aims: 〈 /i 〉 Up to 10% of pregnant women have preterm birth that might be refractory to current therapy. Infections and asphyxia related to preterm birth are the causes of death in the majority of neonates and therefore represent an urgent clinical need. 〈 i 〉 Methods: 〈 /i 〉 The present article reviews the English language literature for preclinical and clinical trials and promising molecular targets on preterm labor. 〈 i 〉 Results: 〈 /i 〉 Preterm birth is a complex heterogeneous condition. There is no current treatment for the fetal membranes once they have ruptured; therefore, essentially any treatment has to be preventative to quiesce preterm labor and prevent any spread of infection to the fetus. Modulating the pro-inflammatory process-mediated cytokine network may present a new paradigm for preterm labor treatment. There are many reports on the role of β-adrenergic agonists (betamimetics), magnesium sulfate, progesterone, oxytocin antagonist, calcium channel blocker or the Kunitz inhibitor bikunin in the treatment of preterm labor. In the present review, we have focused on the preclinical and clinical anticytokine therapy for preterm labor. The preclinical and clinical trials with bikunin reducing preterm labor exacerbations have raised the importance of usefulness and safety considerations related to this novel therapy. 〈 i 〉 Conclusion: 〈 /i 〉 Anticytokine therapy is ready for the clinic.
    Type of Medium: Online Resource
    ISSN: 0378-7346 , 1423-002X
    URL: Article
    DOI: 10.1159/000317268
    RVK:
    XA 45603
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1482695-1
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  • 5
    Online Resource
    Online Resource
    Antiangiogenic-Induced Hypertension: The Molecular Basis of Signaling Network
    S. Karger AG ; 2012
    In:  Gynecologic and Obstetric Investigation Vol. 73, No. 2 ( 2012), p. 89-98
    Details
    In: Gynecologic and Obstetric Investigation, S. Karger AG, Vol. 73, No. 2 ( 2012), p. 89-98
    Abstract: 〈 i 〉 Problem: 〈 /i 〉 Preeclampsia, a pregnancy-related hypertensive disorder, is one of the leading causes of fetal and maternal death globally. Angiogenic factors including vascular endothelial growth factor (VEGF) are involved in the formation of new blood vessels required for placental development and function. The hallmark of preeclampsia is similar to the toxicities related to antiangiogenesis therapy. VEGF inhibitors or antagonists promote vasoconstriction, hypertension and proteinuria. VEGF plays a role in attenuating hypertension and improving kidney damage in an animal model; however, the mechanisms underlying this effect remain poorly defined. The aim of this paper is to summarize recent advances in VEGF-mediated signaling and the target molecules, and provide new insights into treatment strategies for preeclampsia. 〈 i 〉 Method of Study: 〈 /i 〉 This article reviews the English-language literature for pathogenesis of preeclampsia based on VEGF signaling and hypertension. 〈 i 〉 Results: 〈 /i 〉 VEGF activates downstream signaling molecules, including Ca 〈 sup 〉 2+ 〈 /sup 〉 /CAMKK, Rac1/NOX, ROS/ERK, Ezrin/Calpain/PI3K/Akt, PLCγ/PKC and Src/HSP90. Among these signalings, important pathways for receptor-triggered intracellular signaling are (1) the PI3K/Akt-dependent, (2) the PLCγ-dependent and (3) the ERK/Egr-1-dependent pathway. VEGF is closely involved in receptor-activated signaling events, leading to eNOS-dependent NO synthesis and eNOS-independent endothelial cell proliferation, respectively, and thus modulates vasoactive function and angiogenic response. 〈 i 〉 Conclusion: 〈 /i 〉 This review highlights the potential role of NO in vasodilation, while stress-related ERK activation might act to strengthen angiogenesis, migration and proliferation. We discuss the similarity between preeclampsia and VEGF-targeted therapy-induced hypertension.
    Type of Medium: Online Resource
    ISSN: 0378-7346 , 1423-002X
    URL: Article
    DOI: 10.1159/000334458
    RVK:
    XA 45603
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
    detail.hit.zdb_id: 1482695-1
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