Protecting Unconscious, Medically- Dependent Persons After Wendland & Schiavo

Part of Symposium: "The Schiavo Case: A Symposium

Religions, Poverty Reduction and Global Development Institutions

Religious traditions have always played a central role in supporting those experiencing poverty, through service delivery as well as the provision of spiritual resources that provide mechanisms for resilience at both the individual and community level. However, the fact that religions can be seen to support social structures and practices that contribute towards inequality and conflict, also underscores a role for religious traditions in creating conditions of poverty. While the Western-led modern global development institutions that have emerged since the Second World War have tended to be secular in nature, over the past decade or so there has been an apparent ‘turn to religion’ by these global development institutions, as well as in academic development studies. This reflects the realization that modernization and secularization do not necessarily go together, and that religious values and faith actors are important determinants in the drive to reduce poverty, as well as in structures and practices that underpin it. This paper traces three phases of engagement between religions and global development institutions. In phase one, the ‘pre-secular’ or the ‘integrated phase’ seen during the colonial era, religion and poverty reduction were intimately entwined, with the contemporary global development project being a legacy of this. The second phase is the ‘secular’ or the ‘fragmented’ phase, and relates to the era of the global development industry, which is founded on the normative secularist position that modernization will and indeed should lead to secularization. The third phase is characterized by the ‘turn to religion’ from the early 2000s. Drawing the three phases together and reflecting on the nature of the dynamics within the third phase, the ‘turn to religion’, this paper is underpinned by two main questions. First, what does this mean for the apparent processes of secularization? Is this evidence that they are being reversed and that we are witnessing the emergence of the ‘desecularization of development’ or of a ‘post-secular development praxis’? Second, to what extent are FBOs working in development to be defined as neo-liberalism’s ‘little platoons’—shaped by and instrumentalized to the service of secular neo-liberal social, political and economic systems, or do we need to develop a more sophisticated account that can contribute towards better policy and practice around poverty reduction

Twenty-first century glacier slowdown driven by mass loss in High Mountain Asia

International audienc

Molecular Biomarkers of Vascular Dysfunction in Obstructive Sleep Apnea

Untreated and long-lasting obstructive sleep apnea (OSA) may lead to important vascular abnormalities, including endothelial cell (EC) dysfunction, hypertension, and atherosclerosis. We observed a correlation between microcirculatory reactivity and endothelium-dependent release of nitric oxide in OSA patients. Therefore, we hypothesized that OSA affects (micro)vasculature and we aimed to identify vascular gene targets of OSA that could possibly serve as reliable biomarkers of severity of the disease and possibly of vascular risk. Using quantitative RT-PCR, we evaluated gene expression in skin biopsies of OSA patients, mouse aortas from animals exposed to 4-week intermittent hypoxia (IH; rapid oscillations in oxygen desaturation and reoxygenation), and human dermal microvascular (HMVEC) and coronary artery endothelial cells (HCAEC) cultured under IH. We demonstrate a significant upregulation of endothelial nitric oxide synthase (eNOS), tumor necrosis factor-alpha-induced protein 3 (TNFAIP3; A20), hypoxia-inducible factor 1 alpha (HIF-1α?? and vascular endothelial growth factor (VEGF) expression in skin biopsies obtained from OSA patients with severe nocturnal hypoxemia (nadir saturated oxygen levels [SaO2]<75%) compared to mildly hypoxemic OSA patients (SaO2 75%–90%) and a significant upregulation of vascular cell adhesion molecule 1 (VCAM-1) expression compared to control subjects. Gene expression profile in aortas of mice exposed to IH demonstrated a significant upregulation of eNOS and VEGF. In an in vitro model of OSA, IH increased expression of A20 and decreased eNOS and HIF-1α expression in HMVEC, while increased A20, VCAM-1 and HIF-1αexpression in HCAEC, indicating that EC in culture originating from distinct vascular beds respond differently to IH stress. We conclude that gene expression profiles in skin of OSA patients may correlate with disease severity and, if validated by further studies, could possibly predict vascular risk in OSA patients

GPER mediates the angiocrine actions induced by IGF1 through the HIF-1α/VEGF pathway in the breast tumor microenvironment

The G protein estrogen receptor GPER/GPR30 mediates estrogen action in breast cancer cells as well as in breast cancer-associated fibroblasts (CAFs), which are key components of microenvironment driving tumor progression. GPER is a transcriptional target of hypoxia inducible factor 1 alpha (HIF-1α) and activates VEGF expression and angiogenesis in hypoxic breast tumor microenvironment. Furthermore, IGF1/IGF1R signaling, which has angiogenic effects, has been shown to activate GPER in breast cancer cells. We analyzed gene expression data from published studies representing almost 5000 breast cancer patients to investigate whether GPER and IGF1 signaling establish an angiocrine gene signature in breast cancer patients. Next, we used GPER-positive but estrogen receptor (ER)-negative primary CAF cells derived from patient breast tumours and SKBR3 breast cancer cells to investigate the role of GPER in the regulation of VEGF expression and angiogenesis triggered by IGF1. We performed gene expression and promoter studies, western blotting and immunofluorescence analysis, gene silencing strategies and endothelial tube formation assays to evaluate the involvement of the HIF-1α/GPER/VEGF signaling in the biological responses to IGF1. We first determined that GPER is co-expressed with IGF1R and with the vessel marker CD34 in human breast tumors (n = 4972). Next, we determined that IGF1/IGF1R signaling engages the ERK1/2 and AKT transduction pathways to induce the expression of HIF-1α and its targets GPER and VEGF. We found that a functional cooperation between HIF-1α and GPER is essential for the transcriptional activation of VEGF induced by IGF1. Finally, using conditioned medium from CAFs and SKBR3 cells stimulated with IGF1, we established that HIF-1α and GPER are both required for VEGF-induced human vascular endothelial cell tube formation. These findings shed new light on the essential role played by GPER in IGF1/IGF1R signaling that induces breast tumor angiogenesis. Targeting the multifaceted interactions between cancer cells and tumor microenvironment involving both GPCRs and growth factor receptors has potential in future combination anticancer therapies