Bentuk Marginalisasi Terhadap Perempuan Dalam Novel Tarian Bumi Karya Oka Rusmini

Penelitian ini mendeskripsikan bentuk marginalisasi terhadap perempuan dalam novel Tarian Bumi karya Oka Rusmini. Penelitian ini merupakan penelitian kualitatif deskriptif. Sumber data penelitian ini berupa novel Tarian Bumi karya Oka Rusmini. Data dalam penelitiaan ini adalah berupa kalimat, paragraf, kutipankutipan dialog, dan wacana yang menggambarkan bentuk marginalisasi. Teknik pengumpulan data yang digunakan adalah teknik dokumentasi. Teknik analisis data yang digunakan dalam penelitian ini adalah teknik analisis model interaktif, seperti yang dikemukakan oleh Miles dan Huberman. Hasil penelitian menunjukkan bentuk marginalisasi terhadap kaum perempuan tidak hanya terjadi di tempat pekerjaan, melainkan juga terjadi dalam rumah tangga, masyarakat atau kultur, dan bahkan negara. Kesimpulan yang didapat yakni marginalisasi terhadap perempuan dalam novel Tarian Bumi terjadi karena peran dominan dari adat istiadat maupun tafsir keagamaan

LATIHAN CIRCUIT TRAINING TERHADAP PENINGKATAN DAYA TAHAN AEROBIK (VO2 MAX)

Penelitian ini dilaksanakan dengan tujuan untuk mengetahui pengaruh latihan circuit training terhadap Vo2 max siswa. Pada metode penelitian yang akan dibahas akdalah penelitian eksperimen dengan teknisk analisi data yakni uji t dengan prasyarat yakni Uji Normalitas, Uji Homogenitas. Instrumen yang digunakan adalah bleep test. Implikasi dalam penelitian ini adalah setelah diberikan perlakuan terhadap sampel terdapat pengaruh terhadap peningkatan  VO2max. Jumlah sampel dalam penelitian ini berjumlah 25 siswa. Penelitian ini dilaksanakan dengan mengadakan treatment atau perlakuan selama 26 kali.  instrumen penelitian yang digunakan adalah bleep test  untuk mengetahui kemampuan VO2max  siswa. Berdasarkan dari hasil analisis data Pengujian Hipotesis dan pembahasan yang telah dikemukakan  memiliki kesimpulan dalam penelitian ini adalah terdapat pengaruh latihan sirkuit training Terhadap Peningkatan daya tahan aerobik siswa kelas XII SMAN 17 Surabaya

Inflammation mobilizes copper metabolism to promote colon tumorigenesis via an IL-17-STEAP4-XIAP axis.

Copper levels are known to be elevated in inflamed and malignant tissues. But the mechanism underlying this selective enrichment has been elusive. In this study, we report a axis by which inflammatory cytokines, such as IL-17, drive cellular copper uptake via the induction of a metalloreductase, STEAP4. IL-17-induced elevated intracellular copper level leads to the activation of an E3-ligase, XIAP, which potentiates IL-17-induced NFκB activation and suppresses the caspase 3 activity. Importantly, this IL-17-induced STEAP4-dependent cellular copper uptake is critical for colon tumor formation in a murine model of colitis-associated tumorigenesis and STEAP4 expression correlates with IL-17 level and XIAP activation in human colon cancer. In summary, this study reveals a IL-17-STEAP4-XIAP axis through which the inflammatory response induces copper uptake, promoting colon tumorigenesis

Induction of IFN-β and the Innate Antiviral Response in Myeloid Cells Occurs through an IPS-1-Dependent Signal That Does Not Require IRF-3 and IRF-7

Interferon regulatory factors (IRF)-3 and IRF-7 are master transcriptional factors that regulate type I IFN gene (IFN-α/β) induction and innate immune defenses after virus infection. Prior studies in mice with single deletions of the IRF-3 or IRF-7 genes showed increased vulnerability to West Nile virus (WNV) infection. Whereas mice and cells lacking IRF-7 showed reduced IFN-α levels after WNV infection, those lacking IRF-3 or IRF-7 had relatively normal IFN-b production. Here, we generated IRF-3−/−× IRF-7−/− double knockout (DKO) mice, analyzed WNV pathogenesis, IFN responses, and signaling of innate defenses. Compared to wild type mice, the DKO mice exhibited a blunted but not abrogated systemic IFN response and sustained uncontrolled WNV replication leading to rapid mortality. Ex vivo analysis showed complete ablation of the IFN-α response in DKO fibroblasts, macrophages, dendritic cells, and cortical neurons and a substantial decrease of the IFN-β response in DKO fibroblasts and cortical neurons. In contrast, the IFN-β response was minimally diminished in DKO macrophages and dendritic cells. However, pharmacological inhibition of NF-κB and ATF-2/c-Jun, the two other known components of the IFN-β enhanceosome, strongly reduced IFN-β gene transcription in the DKO dendritic cells. Finally, a genetic deficiency of IPS-1, an adaptor involved in RIG-I- and MDA5-mediated antiviral signaling, completely abolished the IFN-β response after WNV infection. Overall, our experiments suggest that, unlike fibroblasts and cortical neurons, IFN-β gene regulation after WNV infection in myeloid cells is IPS-1-dependent but does not require full occupancy of the IFN-β enhanceosome by canonical constituent transcriptional factors

2′-O Methylation of the Viral mRNA Cap by West Nile Virus Evades Ifit1-Dependent and -Independent Mechanisms of Host Restriction In Vivo

Prior studies have shown that 2′-O methyltransferase activity of flaviviruses, coronaviruses, and poxviruses promotes viral evasion of Ifit1, an interferon-stimulated innate immune effector protein. Viruses lacking 2′-O methyltransferase activity exhibited attenuation in primary macrophages that was rescued in cells lacking Ifit1 gene expression. Here, we examined the role of Ifit1 in restricting pathogenesis in vivo of wild type WNV (WNV-WT) and a mutant in the NS5 gene (WNV-E218A) lacking 2′-O methylation of the 5′ viral RNA cap. While deletion of Ifit1 had marginal effects on WNV-WT pathogenesis, WNV-E218A showed increased replication in peripheral tissues of Ifit1−/− mice after subcutaneous infection, yet this failed to correlate with enhanced infection in the brain or lethality. In comparison, WNV-E218A was virulent after intracranial infection as judged by increased infection in different regions of the central nervous system (CNS) and a greater than 16,000-fold decrease in LD50 values in Ifit1−/− compared to wild type mice. Ex vivo infection experiments revealed cell-type specific differences in the ability of an Ifit1 deficiency to complement the replication defect of WNV-E218A. In particular, WNV-E218A infection was impaired in both wild type and Ifit1−/− brain microvascular endothelial cells, which are believed to participate in blood-brain barrier (BBB) regulation of virus entry into the CNS. A deficiency of Ifit1 also was associated with increased neuronal death in vivo, which was both cell-intrinsic and mediated by immunopathogenic CD8+ T cells. Our results suggest that virulent strains of WNV have largely evaded the antiviral effects of Ifit1, and viral mutants lacking 2′-O methylation are controlled in vivo by Ifit1-dependent and -independent mechanisms in different cell types