Aktivisme dan Kesukarelawanan dalam Media Sosial Komunitas Kaum Muda YOGYAKARTA

Aktivisme dan kesukarelawanan kaum muda dalam membentuk gerakan sosial telah mengalami pergeseran dari offline menuju online. Hal ini tidak terlepas dari perkembangan teknologi informasi terutama dengan munculnya Web 2.0 yang membuat banyak realitas sosial diperlihatkan oleh media baru tersebut. Salah satu turunan media baru ini adalah media sosial yang dianggap unggul dalam kecepatan mendistribusikan pesan. Media sosial juga menjadi “ruang publik baru”kaum muda untuk berbagi atau berdiskusi mengenai isu tertentu, bahkan sampai digunakan sebagai tuntutan revolusi. Metode yang digunakan dalam penelitian media baru ini adalah wawancara mendalam dan focus group discussion. Temuannya memperlihatkan bahwa kaum muda Yogyakarta, yang terhimpun dalam berbagai komunitas, berhasil memanfaatkan media sosial sebagai penyeimbang, pengingat, dan suplemen gerakan baru komunitas kaum muda

Loss of Akt activity increases circulating soluble endoglin release in preeclampsia:identification of inter-dependency between Akt-1 and heme oxygenase-1

Aims - Endothelial dysfunction is a hallmark of preeclampsia. Desensitization of the phosphoinositide 3-kinase (PI3K)/Akt pathway underlies endothelial dysfunction and haeme oxygenase-1 (HO-1) is decreased in preeclampsia. To identify therapeutic targets, we sought to assess whether these two regulators act to suppress soluble endoglin (sEng), an antagonist of transforming growth factor-ß (TGF-ß) signalling, which is known to be elevated in preeclampsia. Methods and results - Vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor (FGF-2), angiopoietin-1 (Ang-1), and insulin, which all activate the PI3K/Akt pathway, inhibited the release of sEng from endothelial cells. Inhibition of the PI3K/Akt pathway, by overexpression of phosphatase and tensin homolog (PTEN) or a dominant-negative isoform of Akt (Aktdn) induced sEng release from endothelial cells and prevented the inhibitory effect of VEGF-A. Conversely, overexpression of a constitutively active Akt (Aktmyr) inhibited PTEN and cytokine-induced sEng release. Systemic delivery of Aktmyr to mice significantly reduced circulating sEng, whereas Aktdn promoted sEng release. Phosphorylation of Akt was reduced in preeclamptic placenta and this correlated with the elevated level of circulating sEng. Knock-down of Akt using siRNA prevented HO-1-mediated inhibition of sEng release and reduced HO-1 expression. Furthermore, HO-1 null mice have reduced phosphorylated Akt in their organs and overexpression of Aktmyr failed to suppress the elevated levels of sEng detected in HO-1 null mice, indicating that HO-1 is required for the Akt-mediated inhibition of sEng. Conclusion - The loss of PI3K/Akt and/or HO-1 activity promotes sEng release and positive manipulation of these pathways offers a strategy to circumvent endothelial dysfunction

Carbon monoxide inhibits sprouting angiogenesis and vascular endothelial growth factor receptor-2 phosphorylation

Carbon monoxide (CO) is a gaseous autacoid known to positively regulate vascular tone; however, its role in angiogenesis is unknown. The aim of this study was to investigate the effect of CO on angiogenesis and vascular endothelial growth factor (VEGF) receptor-2 phosphorylation. Human umbilical vein endothelial cells (HUVECs) were cultured on growth factor- reduced Matrigel and treated with a CO-releasing molecule (CORM-2) or exposed to CO gas (250 ppm). Here, we report the surprising finding that exposure to CO inhibits vascular endothelial growth factor (VEGF)-induced endothelial cell actin reorganisation, cell proliferation, migration and capillary-like tube formation. Similarly, CO suppressed VEGF-mediated phosphorylation of VEGFR-2 at tyrosine residue 1175 and 1214 and basic fibroblast growth factor- (FGF-2) and VEGF-mediated Akt phosphorylation. Consistent with these data, mice exposed to 250 ppm CO (1h/day for 14 days) exhibited a marked decrease in FGF-2-induced Matrigel plug angiogenesis (p<0.05). These data establish a new biological function for CO in angiogenesis and point to a potential therapeutic use for CO as an anti-angiogenic agent in tumour suppression.Fil: Ahmad, Shakil. Aston University; Reino UnidoFil: Hewett, Peter W.. University Of Birmingham; Reino UnidoFil: Fujisawa, Takeshi. University Of Birmingham; Reino UnidoFil: Sissaoui, Samir. University Of Birmingham; Reino UnidoFil: Cai, Meng. Aston University; Reino UnidoFil: Gueron, Geraldine. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Al Ani, Bahjat. University Of Birmingham; Reino UnidoFil: Cudmore, Melissa. University Of Birmingham; Reino UnidoFil: Faraz Ahmed, S.. University of Liverpool; Reino UnidoFil: Wong, Michael K. K.. University Of Southern California; Estados UnidosFil: Wegiel, Barbara. Harvard Medical School; Estados UnidosFil: Otterbein, Leo E.. Aston University; Reino Unido. Harvard Medical School; Estados UnidosFil: Vítek, Libor. Charles University; República ChecaFil: Ramma, Wenda. Harvard Medical School; Estados UnidosFil: Wang, Keqing. Aston University; Reino UnidoFil: Ahmed, Asif. Aston University; Reino Unid