1,721,366 research outputs found

    Modulation of vascular responses by non-genomic actions of 17{221}-estradiol

    No full text
    published_or_final_versionabstractPharmacologyDoctoralDoctor of Philosoph

    Effects of homocysteine and puerarin on coronary vasomotor responses

    No full text
    published_or_final_versionabstracttocPharmacologyMasterMaster of Philosoph

    Effect of gender and age on the vascular actions of flavonoids in the rat mesenteric artery

    No full text
    published_or_final_versionPharmacology and PharmacyMasterMaster of Philosoph

    Vascular effects and signaling mechanisms of flavonoids in porcine coronary arteries

    No full text
    published_or_final_versionabstractPharmacologyDoctoralDoctor of Philosoph

    Cleavable cysteine modification by electron-deficient alkynes and molecular imaging of cysteine and homocysteine

    No full text
    published_or_final_versionChemistryDoctoralDoctor of Philosoph

    Mechanisms of acute actions of 17B-estradiol in the vascular system

    No full text
    published_or_final_versionabstracttocPharmacologyMasterMaster of Philosoph

    Effects of Salviae miltiorrhizae radix, a herbal medicine, on vascularconstriction and dilatation

    No full text
    published_or_final_versionPharmacologyMasterMaster of Philosoph

    Effects of human mesenchymal stem cells on cigarette smoke-induced lung damage

    No full text
    Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by persistent airway obstruction that is only partially reversible. It is the fourth leading cause of death and is predicted to be the third by 2030. The progression of the disease involves chronic inflammation, oxidative stress, excess protease activity, increased lung cell apoptosis and accelerated lung aging, but the exact pathogenesis is still unclear. The major cause of COPD is cigarette smoking(CS). Although COPD is associated with increasing social and economical burden, there have been few advances in pharmacological therapy of COPD. Mesenchymal stem cells (MSCs) are fibroblast-like multipotent stem cells which can be isolated from a broad range of sources including bone marrow (BM) and adipose tissue. Administration of BM-derivedMSCs (BM-MSC) or adipose tissue-derived MSCs was reported to attenuate CS-induced emphysema in murine models. Induced pluripotent stem cell-derived MSC (IPSC-MSC) are MSCs differentiated from induced pluripotent stem cells(IPSCs), which are pluripotent cells generated by somatic cell reprogramming in vitro. IPSC-MSCs have several advantages over BM-MSC, including more abundant sources and high capacity of doubling without loss of differentiation potency. A general exploration and comparison on the effects of human IPSC-MSC and BM-MSC treatments were carried out in a 56-day CS-exposed rat model. Compared to BM-MSC, IPSC-MSC showed a higher capacity to reside in lung tissue. The two treatments shared similar efficacy to attenuate CS-induced lung cell apoptosis, to restore CS-induced reduction of lungIL-10and to alleviate CS-induced elevation of systemic TGF-β1. In addition, IPSC-MSC was found to cause reduction in CS-induced elevation of systemic oxidative stress and reversal of CS-induced reduction of lung adiponectin. Furthermore, in order to understand the possible paracrine mechanism involved, human airway epithelial cells were treated with IPSC-MSC or BM-MSC-conditioned medium in a cell culture system in the presence of cigarette smoke medium (CSM). Potentiation rather than attenuation of CSM-induced release of pro-inflammatory cytokine IL-8, MCP-1 and IL-6 was observed with IPSC-MSC or BM-MSC conditioned medium. It is currently unknown whether cultured IPSC-MSCs or BM-MSCs will release pro-inflammatory mediators into the conditioned medium or not. In order to study CS-induced oxidative stress and inflammation in a short time frame, anacute (5-day) CS-exposed rat model was established in juvenile and adult groups. An age-dependent alteration of CS-induced oxidative and inflammatory responses was demonstrated in this model. In summary, our in vivo rat model provides a platform for elucidating the effects of stem cell treatment in CS-induced oxidative stress and inflammation, leading to lung damage. Our findings suggest that treatment of IPSC-MSC or BM-MSC might be able to slow down CS-induced disease progression, possibly through anti-oxidant, anti-inflammatory and anti-apoptotic properties. However, caution should be taken as our in vitro data revealed that conditioned medium from MSCs may provoke pro-inflammatory responses. Further studies on the regulation of the activity of MSCs in vivo will be needed before developing IPSC-MSC into cell therapies for COPD to halt the progression over time.published_or_final_versionMedicineMasterMaster of Philosoph

    Endothelial dysfunction and changes in vascular smooth muscle responsiveness in femoral arteries of rats with type I diabetes

    No full text
    published_or_final_versionabstractPharmacologyDoctoralDoctor of Philosoph

    Modulation of vascular reactivity by flavonoids: effect of kaempferol

    No full text
    published_or_final_versionPharmacology and PharmacyMasterMaster of Philosoph
    corecore