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  • Wiley  (3)
  • 1
    Online Resource
    Online Resource
    A meta‐analysis of neonatal outcomes in pregnant women with immune thrombocytopenic purpura
    Wiley ; 2021
    In:  Journal of Obstetrics and Gynaecology Research Vol. 47, No. 9 ( 2021-09), p. 2941-2953
    Details
    In: Journal of Obstetrics and Gynaecology Research, Wiley, Vol. 47, No. 9 ( 2021-09), p. 2941-2953
    Abstract: Thrombocytopenia is an autoimmune disorder characterized by reduced platelet counts. Neonatal thrombocytopenia incidence has been linked with immune thrombocytopenic purpura in mothers during pregnancy, possibly because antiplatelet antibodies can cross the placental barrier. To date, no study has attempted to evaluate the actual prevalence of neonatal thrombocytopenia in infants born to mothers with immune thrombocytopenic purpura. In this meta‐analysis of the available literature, we attempt to fill this gap. We want to evaluate the overall prevalence of neonatal thrombocytopenia, its severity, and the incidence of hemorrhage in infants with thrombocytopenia born from mothers with immune thrombocytopenic purpura. Methods Adhering to PRISMA guidelines, we systematically scanned four academic databases including EMBASE, CENTRAL, Scopus, and MEDLINE to identify relevant literature. We performed a meta‐analysis to summarize thrombocytopenia incidence rate and severity in newborn infants of mothers with immune thrombocytopenic purpura. Results We identified 21 eligible studies involving 1951 mothers and 1844 neonates. Meta‐analysis showed high prevalence for neonatal thrombocytopenia (24%). Within these, severe cases were the most prevalent (41.2%), followed by moderate (37.7%) and mild (17.6%) cases. Hemorrhage was only reported in 4.1% of the observed neonatal thrombocytopenia cases. Conclusion This review provides preliminary evidence that neonatal thrombocytopenia incidence is high in infants born to mothers with immune thrombocytopenic purpura. This study further reports that the largest proportion of these cases are severe.
    Type of Medium: Online Resource
    ISSN: 1341-8076 , 1447-0756
    URL: Issue
    URL: Article
    DOI: 10.1111/jog.v47.9
    DOI: 10.1111/jog.14890
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2079101-X
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  • 2
    Online Resource
    Online Resource
    Folic acid delays development of atherosclerosis in low‐density lipoprotein receptor‐deficient mice
    Wiley ; 2018
    In:  Journal of Cellular and Molecular Medicine Vol. 22, No. 6 ( 2018-06), p. 3183-3191
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 22, No. 6 ( 2018-06), p. 3183-3191
    Abstract: Many studies support the cardioprotective effects of folic acid ( FA ). We aimed to evaluate the utility of FA supplementation in preventing the development of atherosclerotic in low‐density lipoprotein receptor‐deficient ( LDLR −/−) mice and to elucidate the molecular processes underlying this effect. LDLR −/− mice were randomly distributed into four groups: control group, HF group, HF  +  FA group and the HF  +  RAPA group. vascular smooth muscle cells ( VSMC s) were divided into the following four groups: control group, PDGF group, PDGF  +  FA group and PDGF  +  FA  +  RAPA group. Blood lipid levels, oxidative stress and inflammatory cytokines were measured. Atherosclerosis severity was evaluated with oil red O staining. Haematoxylin and eosin (H & E) staining was used to assess atherosclerosis progression. Immunohistochemical staining was performed with antismooth muscle α‐actin (α‐ SMA ) antibodies and anti‐osteopontin ( OPN ) antibodies that demonstrate VSMC dedifferentiation. The protein expression of α‐ SMA , OPN and mechanistic target of rapamycin ( mTOR )/p70S6K signalling was detected by Western blot analysis. FA and rapamycin reduced serum levels of total cholesterol, triacylglycerol, LDL , inhibiting oxidative stress and the inflammatory response. Oil red O and H & E staining demonstrated that FA and rapamycin inhibited atherosclerosis. FA and rapamycin treatment inhibited VSMC dedifferentiation in vitro and in vivo, and FA and rapamycin attenuated the mTOR /p70S6K signalling pathway. Our findings suggest that FA attenuates atherosclerosis development and inhibits VSMC dedifferentiation in high‐fat‐fed LDLR −/− mice by reduced lipid levels and inhibiting oxidative stress and the inflammatory response through mTOR /p70S6K signalling pathway.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2018.22.issue-6
    DOI: 10.1111/jcmm.13599
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2076114-4
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  • 3
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    Online Resource
    Yellow Wine Polyphenolic Compounds prevents Doxorubicin‐induced cardiotoxicity through activation of the Nrf2 signalling pathway
    Wiley ; 2019
    In:  Journal of Cellular and Molecular Medicine Vol. 23, No. 9 ( 2019-09), p. 6034-6047
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 23, No. 9 ( 2019-09), p. 6034-6047
    Abstract: Doxorubicin (DOX) is considered as the major culprit in chemotherapy‐induced cardiotoxicity. Yellow wine polyphenolic compounds (YWPC), which are full of polyphenols, have beneficial effects on cardiovascular disease. However, their role in DOX‐induced cardiotoxicity is poorly understood. Due to their antioxidant property, we have been suggested that YWPC could prevent DOX‐induced cardiotoxicity. In this study, we found that YWPC treatment (30 mg/kg/day) significantly improved DOX‐induced cardiac hypertrophy and cardiac dysfunction. YWPC alleviated DOX‐induced increase in oxidative stress levels, reduction in endogenous antioxidant enzyme activities and inflammatory response. Besides, administration of YWPC could prevent DOX‐induced mitochondria‐mediated cardiac apoptosis. Mechanistically, we found that YWPC attenuated DOX‐induced reactive oxygen species (ROS) and down‐regulation of transforming growth factor beta 1 (TGF‐β1)/smad3 pathway by promoting nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) nucleus translocation in cultured H9C2 cardiomyocytes. Additionally, YWPC against DOX‐induced TGF‐β1 up‐regulation were abolished by Nrf2 knockdown. Further studies revealed that YWPC could inhibit DOX‐induced cardiac fibrosis through inhibiting TGF‐β/smad3‐mediated ECM synthesis. Collectively, our results revealed that YWPC might be effective in mitigating DOX‐induced cardiotoxicity by Nrf2‐dependent down‐regulation of the TGF‐β/smad3 pathway.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.v23.9
    DOI: 10.1111/jcmm.14466
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2076114-4
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