Implementasi Permendagri Nomor 15 Tahun 2008 Tentang Pengarusutamaan Gender pada Jenjang Pendidikan Dasar di Kota Malang

Windra Rizkiyana1 & Wahyu Widodo21 Mahasiswa & 2Staf Pengajar Program Pasca Sarjana, Universitas Muhammadiyah MalangAlamat Korespondensi : Jl. Bandung No.1 MalangEmail: [email protected] education, still found a gender gap regarding both aspects of the expansion of educationalaccess and equity, quality and relevance of education and management. The purpose of this studywere: (1) describe the substance Permendagri No. 15 of 2008 on Gender Mainstreaming; (2) describethe implementation of Permendagri No. 15 of 2008 on Gender Mainstreaming in Elementary Educationin Malang; (3) Analyze the obstacles encountered in implementation Permendagri No. 15 of 2008 onGender Mainstreaming in Elementary Education in Malang. This type of research is a descriptiveanalysis, using a qualitative approach that is supported by a quantitative approach. And the techniquesof data acolllection through by interviews and the documents. Study sites are in Malang EducationDepartment. Analysis of the data used is descriptive analysis of qualitative and quantitative theorysupported by Gender Analysis Pathway (GAP), Content Analysis and Root Analysis. Implementationof Permendagri No 15 of 2008 about gender mainstreaming in basic education levels in Malang hasnot been optimal. These proved by the remains of gender inequality or gap that occurs in all threeaspects, that access and educational equity, quality and relevance of education, as well as accountabilityand governance. Constraints encountered in implementation Permendagri No. 15 of 2008 on gendermainstreaming in elementary education in Malang include: (a) Outreach activities that are specificallyabout the PUG in primary education has not been done; (b) The budget is not specifically formainstreaming activities; (c) newly formed working group PUG.Key word: Permendagri No. 15 of 2008, gender mainstreaming, basic educatio

Are Viral Infections Key Inducers of Autoimmune Diseases? Focus on Epstein–Barr Virus

It is generally accepted that certain viral infections can trigger the development of autoimmune diseases. However, the exact mechanisms by which these viruses induce autoimmunity are still not understood. In this review, we first describe hypothetical mechanisms by which viruses induce some representative autoimmune diseases. Then, we focus on Epstein–Barr virus (EBV) and discuss its role in the pathogenesis of rheumatoid arthritis (RA). The discussion is mainly based on our own previous findings that (A) EBV DNA and its products EBV-encoded small RNA (EBER) and latent membrane protein 1 (LMP1) are present in the synovial lesions of RA, (B) mRNA expression of the signaling lymphocytic activation molecule-associated protein (SAP)/SH2D1A gene that plays a critical role in cellular immune responses to EBV is reduced in the peripheral T cells of patients with RA, and (C) EBV infection of mice reconstituted with human immune system components (humanized mice) induced erosive arthritis that is pathologically similar to RA. Additionally, environmental factors may contribute to EBV reactivation as follows: Porphyromonas gingivalis peptidylarginine deiminase (PAD), an enzyme required for citrullination, engenders antigens leading to the production of citrullinated peptides both in the gingiva and synovium. Anti-citrullinated peptides autoantibody is an important marker for diagnosis and disease activity of RA. These findings, as well as various results obtained by other researchers, strongly suggest that EBV is directly involved in the pathogenesis of RA, a typical autoimmune disease

Glutamine depletion induces murine neonatal melena with increased apoptosis of the intestinal epithelium

AIM: To investigate the possible biological outcome and effect of glutamine depletion in neonatal mice and rodent intestinal epithelial cells

Dual tyrosine kinase inhibitor for focal adhesion kinase and insulin-like growth factor-I receptor exhibits anticancer effect in esophageal adenocarcinoma in vitro and in vivo.

PURPOSE: Focal adhesion kinase (FAK) regulates integrin and growth factor-mediated signaling pathways to enhance cell migration, proliferation, and survival, and its up-regulation correlates malignant grade and poor outcome in several types of cancer. In this study, we aimed to raise a potential therapeutic strategy using a FAK inhibitor for Barrett's esophageal adenocarcinoma. EXPERIMENTAL DESIGN: The expression status of FAK in clinical Barrett's esophageal adenocarcinoma tissues was determined by immunohistochemistry. Cultured esophageal adenocarcinoma cells were treated with TAE226, a specific FAK inhibitor with an additional effect of inhibiting insulin-like growth factor-I receptor (IGF-IR), to assess its anticancer effect in vitro. Western blot was carried out to explore a participating signaling pathway for TAE226-induced cell death. Furthermore, TAE226 was orally administered to s.c. xenograft animals to investigate its anticancer effect in vivo. RESULTS: Strong expression of FAK was found in 94.0% of Barrett's esophageal adenocarcinoma compared with 17.9% of Barrett's epithelia, suggesting that FAK might play a critical role in the progression of Barrett's esophageal adenocarcinoma. When esophageal adenocarcinoma cells were treated with TAE226, cell proliferation and migration were greatly inhibited with an apparent structural change of actin fiber and a loss of cell adhesion. The activities of FAK, IGF-IR, and AKT were suppressed by TAE226 and subsequent dephosphorylation of BAD at Ser(136) occurred, resulting in caspase-mediated apoptosis. In vivo tumor volume was significantly reduced by oral administration of TAE226. CONCLUSIONS: These results suggest that TAE226, a dual tyrosine kinase inhibitor for FAK and IGF-IR, could become a new remedy for Barrett's esophageal adenocarcinoma

Fucoganglioside α-fucosyl(α-galactosyl)-GM1: a novel member of lipid membrane microdomain components involved in PC12 cell neuritogenesis

In order to search for novel components of lipid membrane microdomains involved in neural signalling pathways, mAbs (monoclonal antibodies) were raised against the detergent-insoluble membrane fraction of PC12 (pheochromocytoma) cells. Among the 22 hybrid clones, mAb PR#1 specifically detected a fucoganglioside Fuc(Gal)-GM1 [α-fucosyl(α-galactosyl)-GM1], a ganglioside homologous with GM1a (II3NeuAc,GgOse4Cer), as a novel member of microdomain components with biological functions. In the presence of mAb PR#1 in the culture medium, the outgrowth of neurites was induced in PC12 cells in a dose-dependent manner, with no effects on cell proliferation, suggesting that Fuc(Gal)-GM1 is preferentially involved in PC12 cell neuritogenesis. Effects through Fuc(Gal)-GM1 were different from those through GM1a during differentiation, e.g. under PR#1 treatment on Fuc(Gal)-GM1, round cell bodies with thinner cell processes were induced, whereas treatment with CTB (cholera toxin B subunit), a specific probe for GM1a, produced flattened cell bodies with thicker pro-cesses. Molecular analysis demonstrated that the PR#1–Fuc(Gal)-GM1 pathway was associated with Fyn and Yes of the Src family of kinases, although Src itself was not involved. No association was found with TrkA (tropomyosin receptor kinase A) and ERKs (extracellular-signal-regulated kinases), which are responsible for GM1a-induced differentiation. From these findings, it is suggested that a fucoganglioside Fuc(Gal)-GM1 provides a functional platform distinct from that of GM1a for signal transduction in PC12 cell differentiation

Measurement of membrane stiffness using optical tweezers

<p>. A. Diagram of the displacement of the bead by the optical tweezers. A collagen-coated bead (2 μm in diameter) was attached to the cell membrane using optical tweezers and held in position for a short time. ‘Laser on’, the path of the bead forced by the laser; ‘laser off’, the path of the bead without laser force. Blue arrow, forced direction of the bead; arrow outlined in black, displacement of the bead. Colored forms, membrane proteins; red bars, structural proteins; hemispheres, beads; I, initial position of the bead; S, stopping position of the bead; B, tracing of the bead with the laser on or off; C, tracing of the displacement of the bead for 1000 ms.</p

PB1 and PB2 mRNA in single-virus infected cells.

<p>Detection of PB1, PB2 mRNA in single virus infected cells by RT-PCR. Individual cells, either infected with DiI-labeled influenza virus using optical tweezers or uninfected (n = 5 for each cells, virus bound and unbound cells), were removed by suction at 6 hpi and assayed for mRNA of PB1 and PB2, and 18S rRNA. The numbers in parentheses indicate standard deviation from n = 5.</p

Attachment of DiI-labeled influenza virus particles to cells at different phases of the cell cycle.

<p>A. H292 cells were transfected with pFucci-S/G2/M Green vector and cultured overnight. GFP expression was observed only in S/G2/M-phase. DiI-labeled virus particles were added to cultured cells and incubated for 15 min at 34°C. Unbound virus was washed off with PBS and the cells were fixed with 4% paraformaldehyde and observed under a Nikon Ti E confocal microscope fitted with a 100× objective lens. The red particles are DiI-labeled viruses. The green colored cells express GFP. B. Cartoon of virus trapping and release on a cell using optical tweezers. Yellow triangle represents optical tweezers; red circle represents virus; light green colored teardrop shape represents the cell. C. Trapping potential was calculated under the indicated conditions. n, refractive index; NA, numerical aperture; T, absolute temperature; blue, red, and green lines represent laser power is at 100 mW, 30 mW, and 10 mW, respectively. D. The cells in the microchip were observed through the objective lens (×100). The DiI-labeled virus is trapped in the chamber of the microchip and transported to the apical membrane of a mitotic cell (arrow 1) but was unable to attach. The same particle was recaptured and then transported to the apical membrane of a G1-phase cell (arrow 2). E. Trace showing virus particle movement after transportation to a dividing (left) or resting (right) cell. White circle (red-cross) in the left panel represents the recaptured virus, whereas that in the right panel represents that the brownian motion of the virus particle on the cell membrane has stopped.</p