Penggunaan Media Gambar Dalam Meningkatkan Kemampuan Membaca Permulaan Siswa Kelas I SDN Uwedaka Kecamatan Pagimana Kabupaten Banggai

Pokok permasalahan dalam penelitian ini adalah rendahnya tingkat kemampuan membaca permulaan siswa kelas I SDN Uwedaka dalam pembelajaran Bahasa Indonesia. Tujuan Penelitian adalah untuk meningkatkan kemampuan membaca permulaan siswa kelas I SDN Uwedaka Kecamatan Pagimana Kabupaten Banggai. Berdasarkan hasil observasi yang didapatkan masih terdapat beberapa siswa yang sama sekali belum bisa membaca. Pembelajaran membaca permulaan di SDN Uwedaka selama ini hanya menggunakan media pembelajaran yang konvensional yaitu dengan menggunakan papan tulis, pembelajaran yang hanya berpusat pada guru, penggunaan media dalam pembelajaran sebagai alat bantu masih sangat terbatas, hal ini menyebabkan kemampuan membaca permulaan yang masih rendah dan terlihat hampir 65% siswa masih mengalami kesulitan membaca dalam proses belajar mengajar. Metode yang digunakan adalah metode deskriptif kualitatif dan kuantitatif. Data kualitatif didapatkan dari hasil tes dan observasi siswa dan guru. data kuantitatif didapatkan dari hasil tes belajar. Desain penelitian ini mengacu pada desain oleh Kemmis dan Mc Taggart yang terdiri dari empat tahapan, yaitu perencanaan, pelaksanaan tindakan, observasi dan refleksi. Data dikumpulkan melalui penilaian proses dan penilaian hasil setiap akhir tindakan. Penelitian ini dilakukan dalam dua siklus. Pada siklus I diperoleh nilai rata-rata siswa yaitu sebesar 67 dengan ketuntasan belajar klasikal sebesar 40% serta daya serap 66,6%. Pada siklus II, nilai rata-rata meningkat menjadi 83 dengan ketuntasan klasikal sebesar 100% serta daya serap klasikal sebesar 83,3%. Bersarkan hasil penelitian maka dapat disimpulkan bahwa penggunaan media gambar dapat meningkatkan kemampuan membaca permulaan terhadap siswa kelas I SDN Uwedaka Kecamatan Pagimana Kabupaten Banggai

Effects of miR-204, -211, and -379 on Smad signaling.

<p>Smad signaling was quantified using a luciferase construct which encodes the firefly luciferase reporter gene under the control of a minimal (m)CMV promoter and tandem repeats of the Smad transcriptional response element. The luciferase reporter construct and miRNA precursors were co-transfected into MDA-MB-231(SA) cells (n = 3), and the medium was replaced with serum-free medium 16 hours after transfection. TGF-β was added 8 hours later. Activity of the firefly luciferase reporter and Renilla luciferase was measured after 16 hour TGF-β induction. * p<0.05, ** p<0.01, as compared to the Pre-miR negative control and Smad reporter-transfected cells.</p

<i>IL11</i> 3′ UTR luciferase assay.

<p>Luciferase reporter constructs, each containing one fragment of the <i>IL11</i> 3′ UTR, were co-transfected with a Renilla luciferase construct and the miRNA precursors into MDA-MB-231(SA) cells (n = 5), and luciferase activity was measured 28 hours later. * p<0.05, ** p<0.01, *** p<0.001, as compared to the negative control Pre-miR.</p

Effects of 55 miRNA precursors and a negative control on IL-11 secretion in MDA-MB-231(SA) cells.

<p>Cells were transfected with miRNA precursors in 96-well plates. Medium was changed 24 hours after transfection (+/− TGF-β), and IL-11 concentration in the conditioned medium was measured 24 hours later. IL-11 concentration was normalized to the number of viable cells in the well. The scale of reduction (blue) or increase (red) in IL-11 concentration in the conditioned medium is represented in the color graph in the upper right hand corner of the figure.</p

A schematic representation of the complex interplay of TGF-β-signaling pathways regulating TIMP-3 expression in human fibroblasts.

<p>Stimulation of human gingival fibroblasts with TGF-β results in activation of Smad3, ERK1/2 and p38 MAPK pathways. Activation of all three pathways is required for induction of TIMP-3 expression by TGF-β Smad3 associates with Smad4 and mediates induction of TIMP-3 expression by TGF-β. ERK1/2 and p38 MAPK pathways both co-operate with Smad3 in mediating the induction of TIMP-3 expression by TGF-β.</p

Genes over 1.5-fold downregulated in response to miR-204 and/or -379 versus negative control Pre-miR.

<p>RNA samples for genome-wide gene expression analysis were collected 24 hours after MDA-MB-231(SA) cells had been transfected with miRNA precursors. The predicted targets of miR-204 are typed in red and the predicted targets of miR-379 in blue. Expression fold changes, gene names, and more detailed information about the target predictions are listed in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037361#pone.0037361.s004" target="_blank">Tables S3</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0037361#pone.0037361.s005" target="_blank">S4</a>.</p

Expression of Smad4 rescues the TGF-β response of TIMP-3 and PAI-1 in Smad4 null fibroblasts.

<p>(<b>A</b>) EF7WT (wild-type) and EF7KO (Smad4 deficient) fibroblasts were transduced with recombinant adenovirus for HA-tagged Smad4 (RAdSmad4), or with empty control virus RAd66 at MOI 100 (EF7WT) or 300 (EF7KO). After 36 h incubation cell lysates were harvested and analyzed by Western blotting to detect the levels of endogenous and exogenous Smad4. Anti-HA antibody was used to detect adenovirally delivered Smad4 (upper panel) and anti-Smad4 to detect endogenous Smad4 (lower panel). (<b>B</b>) EF7KO fibroblasts were infected with adenoviruses RAdSmad4 or RAd66. After 36 h incubation the cells were stimulated with TGF-β1 (5 ng/ml) for different periods of time, as indicated. Total RNA was extracted and analyzed by qRT-PCR to determine TIMP-3 and PAI-1 mRNA levels. mRNA expression (mean ± SEM from two separate experiments, both run with duplicates) is shown relative to 18S ribosomal RNA. *p<0.05, t-test).</p

Smad3 mediates TGF-β-elicited induction of TIMP-3 expression in human fibroblasts.

<p>(<b>A</b>) Normal human gingival fibroblasts were transduced with recombinant adenoviruses for Smad2 (RAdSmad2), Smad3 (RAdSmad3), dominant negative Smad3 (RAdSmad3DN), or with empty control virus (RAd66) at MOI 500, and incubated for 18 h. Thereafter, the cells were treated with TGF-β1 for 24 h. The cell layers were harvested for RNA extraction and analyzed for the expression of TIMP-3 or GAPDH by Northern blot hybridizations. (<b>B</b>) Normal human gingival fibroblasts were infected with RAdSmad3, RAdSmad3DN, adenovirus for Smad7 (RAdSmad7), or with empty control virus (RAdpCA3) as in (<b>A</b>). Cells were treated with TGF-β1 for 24 h, the cell layers harvested and analyzed for the expression of TIMP-3 by Western blotting. Equal loading was confirmed by stripping and reprobing the same filter for β-actin.</p

Smad3, p38α and ERK1/2 cooperate in the induction of TIMP-3 gene expression in human fibroblasts.

<p>(<b>A</b>) Human gingival fibroblasts were serum starved for 18 h, and treated for 1 h with PD98059 (30 µM), or SB203580 (10 µM), specific chemical inhibitors for MEK1 or p38, respectively. Subsequently, TGF-β1 (5 ng/ml) was added, and the cultures incubated for 16 h. Total cellular RNAs were harvested and analyzed for the levels of TIMP-3, TIMP-1, PAI-1 and GAPDH mRNAs by Northern blot hybridizations. (<b>B</b>) Human gingival fibroblasts were transduced with recombinant adenoviruses for wild-type p38α (RAdp38α), constitutively active MKK3b (RAdMKK3bE), Smad3 (RAdSmad3), Smad4 (RAdSmad4), or with empty control virus (RAd66) at MOI 500, and incubated for 24 h. Total cellular RNA was analyzed with Northern blot hybridizations for the expression of TIMP-3, TIMP-1, PAI-1, and GAPDH mRNAs. (<b>C</b>) Human gingival fibroblasts were transduced with recombinant adenoviruses for constitutively active MEK1 (RAdMEK1CA), constitutively active MKK3b (RAdMKK3bE), Smad3 (RAdSmad3) and control virus RAd66 as in (<b>B</b>). Total cellular RNA was analyzed with Northern blot hybridizations for the expression of TIMP-3, TIMP-1, PAI-1, and GAPDH mRNAs.</p

TGF-β induces TIMP-3 gene expression in a Smad-dependent manner in fibroblasts.

<p>(<b>A</b>) Human gingival fibroblasts were treated with TGF-β1 (5 ng/ml) for 24 h. Thereafter, total cellular RNAs were harvested and analyzed for the expression of TIMP-3, TIMP-1, PAI-1, and GAPDH mRNAs by Northern blotting. (<b>B</b>) EF7WT and EF7Smad4KO (Smad4 deficient) cells were treated with TGF-β1 (5 ng/ml) for 3 h and 12 h or left untreated (control). Total RNA was extracted and TIMP-3 and PAI-1 gene expression was determined by qRT-PCR. mRNA expression (mean+SD) is shown relative to 18S ribosomal RNA (n = 4). *p<0.05, **p<0.005 (t-test) for TGF-β vs. control cultures.</p